Short Notes and Short Cases in Ophthalmology PDF

Short Notes and
Short Cases in
Ophthalmology
Short Notes and
Short Cases in
Ophthalmology
UN Panda
MD
Senior Physician
New Delhi
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Short Notes and Short Cases in Ophthalmology

© 2003, UN Panda
All rights reserved. No part of this publication should be reproduced,

stored in a retrieval system, or transmitted in any form or by any
means: electronic, mechanical, photocopying, recording, or otherwise,
without the prior written permission of the author and the publisher.
This book has been published in good faith that the material pro-
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of material, but the publisher, printer and author will not be held
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First Edition: 2003
Publishing Director: RK Yadav
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Preface
Eyes are the precious gifts of God. Eye diseases have to

diagnosed accurately and very early failing which one
may loose them permanently. Hence understanding
diagnosis and management of common eye diseases is
essential part of primary care physicians.
This handbook Short Notes and Short Cases in
Ophthalmology presents diseases of eye in question
answer format in a crisp and compact manner for quick
revision and recollection. Commonly eye diseases for
clinical discussion at undergraduate level are presented
under short cases.
The book will be of immense help for final MBBS
students preparing for their examination both clinical
and viva voce.
UN Panda
Contents
SHORT NOTES
1. Diseases of Conjunctiva ................................. 3
2. Corneal Diseases .............................................. 8
3. Diseases of Eyelids and Orbit ......................... 16
4. Ocular Tumors .................................................... 22
5. Glaucoma ............................................................. 25
6. Uveitis .................................................................. 34
7. Retinal Diseases ................................................. 39
8. Cataract................................................................. 48
9. Retinopathy of Prematurity ............................. 52
10. Pupil ..................................................................... 53
11. Differential Diagnosis of Ocular
Symptoms and Signs ......................................... 55
12. Ocular Trauma .................................................... 60
13. Diagnostic Tests in Ophthalmology .............. 64
SHORT CASES
Cases 1 to 10 ........................................................ 65
Short Notes
1 Diseases of
Conjunctiva
1. Red eyes—causes of
• Conjunctivitis
• Episcleritis and scleritis
• Anterior uveitis
• Keratitis
• Acute congestive glaucoma
2. Watery, itchy eyes with swollen lids- differential
diagnosis
• Allergic conjunctivitis (hay fever)
• Viral conjunctivitis
• Trachoma
• Drug allergy—local eyedrops/systemic use
3. Viral conjunctivitis- characteristics (usually adeno-
virus)
• Follicles in inferior palpebral conjunctiva, associated
URI
• Enlarged preauricular nodes
• Membrane/pseudomembrane formation
• Epidemic form, itching,burning, watery discharge
• Subepithelial infiltrates (SEI)
• Very contagious
• Treat with naphazoline eyedrops, steroid eyedrop if
SEI or pseudomembrane are present.
4. Gonococcal conjunctivitis
• Purulent discharge
• Tender enlarged preauricular nodes
• Marked chemosis
• Gram –ve intracellular diplococci in conjunctival
discharge.
5. Trachoma
• Evolves in 4 phases, beginning with superior tarsal
follicles, SPK and pannus
4 Short Notes and Short Cases in Ophthalmology
• Complications include corneal opacity, trichiasis,

scarring of tarsal conjunctiva, severe dry eye,
entropion, Herberts pits (scarred limbal follicles).
• Treatment is with doxycyline 100 mg bid/tetracyline
250 mg QID x 3 weeks along with tetracycline/
erythromycin eye ointment and sulfacetamide 20-
30% eyedrops.
6. Treatment of gonococcal conjunctivitis in adults
• Ceftriaxone 1 gm IM ( in absence of corneal involve-
ment) or 1 gm IV bid when corneal involvement
suspected or can not be ruled out
• Ciprofloxacin eyedrop 2 hourly
• Bacitracin/erythromycin eye oint.
• Doxycycline 100 mg bid x 2 weeks for associated
chlamydia infection
7. Red eye with diminished/ misty vision
• HSV keratitis
• Acute congestive glaucoma
• Dry eye syndrome
8. HSV kerato conjunctivitis
• Dendritic ulcer with terminal bulbs in fluorescent
staining
• Cells in anterior chamber and aqueous flare
• Treatment is with local trifluuridine, vidarabine 3%
oints and systemic acyclovir
9. Dry eye syndrome
• Collagen vascular diseases (RA, Sjögren’s syndrome,
SLE, Wegener’s)
• Vitamin A deficiency
• Infiltration of lacrimal gland by sarcoid/tumor
• Drugs—antihistamines, beta blockers, phenothia-
zines
• Idiopathic
• Trachoma, Steven Johnson syndrome
10. Superficial punctate keratopathy—causes of
• Dry eye syndrome
• Ectropion/ entropion
• Trichiasis
• Ultraviolet burn (Welder’s, snow blindness)
• Floppy lid syndrome
• Alkali burn (dye, cement, plaster)
Diseases of Conjunctiva 5
11. Pterygium
It is a wing shaped fibrovascular tissue nasally in both
eyes that extends into cornea, probably arising from UV
exposure, dust and wind. They may be associated with
dellen, an area of corneal thinning secondary to drying.
It is necessary to rule out conjunctival intraepithelial
neoplasia which is unilateral, often elevated but not in
a wing shaped configuration. Removal of pterygium is
necessary when it disturbs vision or causes irritation.
Recurrence after surgery is usual; hence bare sclera
dissection with conjunctival autograft reduces
recurrence rate.
12. Vernal catarrh (atopic conjunctivitis)
• Itching, thick ropy discharge, history of atopy
• Large conjunctival papillae under upper eyelid or
along the limbus
• Horner Tranta’s dots (limbal or palpebral), SPK
• Superficial corneal shield ulcer
• Treatment is with local vasoconstrictors, antiallergics
cromolyn sodium 4% or iodoxamide/olopatadine
0.1%.
• If shield ulcer is present- topical steroid
13. Inclusion conjunctivitis
• Sexually transmitted (chlamydial), history of cervi-
citis, urethritis
• Inferior tarsal conjunctival follicles, superior corneal
pannus, stringy mucous discharge, enlarged PAN,
Peripheral sub-epithelial infiltrates
• Treatment is with oral doxycycline/tetracycline/
erythromycin for 3 weeks; tetracycline/ sulface-
tamide eye ointment/ eye drops.
14. Perinaud’s oculoglandular conjunctivitis
• Red eye, mucopurulent discharge
• Granulomatous nodules on palpebral conjunctiva,
enlarged PAN, follicular reaction
• Causative agents can be of tularaemia, cat scratch
disease, tuberculosis, sarcoidosis, syphilis
• Establish diagnosis by conjunctival culture, histo-
logy of scraping, serology, etc
• Treatment is dependent upon cause
15. Superficial limbic keratoconjunctivitis
• Red eye, burning, pain, tearing, mild photophobia,
frequent blinking
• Chronic course with exacerbation and remission

• Thickening and inflammation of superior bulbar
conjunctiva especially at limbus
• Fine papillae on the superior palpebral conjunctiva,
superior corneal micropannus, fine SPK of superior
cornea and limbus.
• Fifty percent have associated thyroid disease.
• Treatment is with geneous artificial tear, (if need be
punctal occlusion), silver nitrate 0.5-1% cauterisation
(after topical anesthesia with proparacaine); else
cautery/ surgical resection or recession of superior
bulbar conjunctiva.
16. Episcleritis
• Redness and mild pain but no discharge; cornea and
iris are normal
• Mostly idiopathic but can be due to collagen vascular
disease, gout, HSV , HBV, IBD, rosacea, atopy,
dysthyroid state
• Treatment is with artificial tear, mild topical steroid,
NSAID
17. Scleritis
• Severe and boring eye pain with wide radiation
• Inflammation of scleral, episcleral and conjunctival
vessels. The sclera has blue appearance, may be thin
or edematous
• Scleral vessels are large, deep and can be moved with
a cotton swab; do not shrink with topical phenyl-
ephrine
• Associated keratitis, uveitis.
• Classification (1) diffuse anterior scleritis (2) nodular
anterior scleritis (3) necrotising anterior scleritis
(4) posterior scleritis (with restricted extraocular
movements, proptosis, RD, disc swelling, retinal/
choroidal haemorrhage – usually idiopathic)
• Half the cases are due to collagen vascular disease,
TB, parasite.
• Treatment is with NSAID, oral corticosteroid or
immunosuppressants depending upon severity.
• Scleromalacia perforans may demand scleral patch
grafting
• Topical steroids are ineffective and subconjunctival
steroid can cause scleral thinning and perforation
Diseases of Conjunctiva 7
18. Blepharitis
• Itching, burning, tearing, crusting, FB sensation
• Crusty red, thickened eyelid margins
• Conjunctival injection, mild mucous discharge, SPK
may be there.
• Treatment is with tetracycline/ doxycyclin PO for 1-
2 weeks; erythromycin/ bacitracin oint; scrubbing
eyelid margins with baby shampoo, etc.
• Remember: Unilateral intractable or asymmetric
blepharitis is the only manifestation of sebaceous cell
carcinoma
19. Subconjunctival haemorrhage
• Usually asymptomatic except for red eye, mild
irritation
• Can be due to coughing, straining, hypertension,
trauma, bleeding disorder.
• Can be confused with conjunctival Kaposi sarcoma
(AIDS) where lesion is beneath the conjunctiva;
conjunctival lymphoma with secondary haemor-
rhage.
• Treatment is not required except for artificial tear for
mild irritation.
20. Pingueculum
• Yellow white flat or raised conjunctival lesion
usually in interpalpebral fissure adjacent to limbus
but not involving cornea.
• Elastotic degeneration of deep conjunctival layers.
Most common to equatorial regions- likely due to
sunlight.
• Should be distinguished from (1) conjunctival
intraepithelial neoplasia (unilateral jelly like, velvety
or white lesion, vascularised but not wing shaped
unlike pterigium. (2) limbal dermoid (congenital
rounded white lesion) (3) pannus secondary to
blepharitis, ocular rosacea, trachoma, phlycten,
atopy).
• Treatment is with topical vasoconstrictors, mild
topical steroids, or topical NSAID.
2 Corneal Diseases
1. Band keratopathy
a. Decreased vision, FB sensation, often asymptomatic
b. Anterior corneal plaque of calcium at level of
Bowman’s membrane with Swiss cheese appearance.
c. Commonly associated with JRA, interstitial keratitis,
corneal edema, long-standing glaucoma; often
associated with hypercalcemia, gout, renal failure.
d. Treatment is with artificial tear drops/ointment,
removal of calcium in slitlamp by application of 3%
EDTA under LA followed by cycloplegic eyedrop and
antibiotic ointment and pressure patch for 24 hours.
2. Corneal ulcer
• Mild to severe ocular pain, red eye, discharge,
decreased vision
• Circumcorneal congestion, stromal edema around
ulcer, folds in Descemet’s membrane, hypopion;
posterior synechiae and glaucoma in severe cases.
• Most common organisms are bacteria (mostly pneu-
mococcus), fungi (feathery borders with satellite
lesions); acanthamoeba , HSV, atypical mycobacteria
• Sterile ulcers are seen in collagen vascular disease,
vernal catarrh, vitamin A deficiency, staphylococcal
hypersensitivity.
• Treatment of bacterial ulcer is with (1) cycloplegic, (2)
topical antibiotic—tobramycin/gentamicin alter-
nating with cefazolin/vancomycin eyedrops every
hour, (3) subconjunctival gentamicin 20-40 mg/
cefazolin 100 mg/vancomycin 25 mg, (4) oral
fluoroquinolone, (5) eye shield (not patch), (6) pain
willers, (7) for atypical mycobacteria—amikacin eye-
drop/kanamycin/cefoxitin eyedrop.
3. Fungal keratitis
• Causative agent can be (1) non-filamentous fungi
(candida species) or (2) filamentous fungi (aspergil-
lous, fusariam).
Corneal Diseases 9
• Cycloplegic drops (scopolamine 0.25% tid)

• Natamycin 5% eyedrop every hour
• Amphotericin B-0.15% for candida, miconazole 0.1%
or clotrimazole 1% for asperigillus; oral itraconazole
200 mg PO daily since it has highest corneal
penetration among antifungals.
4. Acanthamoeba conjunctivitis
• Think of it in contact lens users, swimming; no
response to antivirals and antibiotics,severe pain
disproportionate to ulcer; sterile bacterial culture;
little discharge.
• Culture on non-nutrient agar with E.coli overlay
• Consider corneal biopsy if staining and culture are
negative
• Treatment is with (1) cycloplegic and NSAID eye-
drops, (2) propamidine isethionate 0.1% eyedrop +
polyhexamethyl biguanide 0.02% eyedrop in combi-
nation with oral itraconazole 200 mg PO daily and
Neosporin eyedrop.
5. HSV keratitis
• May be seen as SPK, satellite keratitis, dendritic
keratitis, geographic ulcer, branching lesion with
club shaped terminal.
• Decreased corneal sensation; conjunctival follicles
and eyelid/ skin vesicles may be present.
• May present as corneal stromal disease, i.e (1) disci-
form keratitis without necrosis and neovasculari-
zation, (2) necrotising interstitial keratitis with
necrosis, neovascularisation, ↑ IOP and iritis may be
present in both.
• Uveitis and retinitis are rare but can occur with
severe stromal involvement.
• Dendritic ulcers also occur in HZV, corneal erosion,
contact lens use, acanthamoeba infection (pseudo-
dendritic ulcer in last two).
• Scraping for intranuclear eosinophilic inclusions
• Trifluorothymidine 1% drops 9 times daily or
vidarabine 3% oint 5 times daily along with cyclo-
plegic eyedrop and oral acyclovir 400 mg PO 5 times
daily (oral acyclovir does not prevent stromal
keratitis/iritis)
• Topical steroids (prednisolone acetate 1%) in stromal
keratitis often combined with oral steroids (provided
there is no epithelial defect) but oral antivirals are

of no use.
• Oral antivirals (acyclovir, valacyclovir, famciclovir)
are of help in viral iritis along with aqueous sup-
pressants for ↑ IOP.
• Topical antivirals can cause papillary or follicular
conjunctivitis
• Severe stromal disease may need corneal transplant.
6. Superficial punctate keratitis (SPK)
• Symptoms are pain, photophobia, red eye, FB
sensation
• Pinpoint corneal epithelial defects in fluorescent
stain
• Watery to mucoid discharge, conjunctival injection.
• SPK is non-specific; most commonly seen with dry
eye syndrome, blepharitis, trauma, exposure kerato-
pathy, photokeratopathy, entropion/ ectropion,
trichiasis, etc.
• Treatment is with cycloplegic eyedrop, artificial tear
antibiotic eyedrop/ointment, and removal of the
cause
7. Filamentary keratopathy
• Photophobia, moderate eye pain, red eye, FB
sensation
• Short strands of epithelial cells staining with
fluoroscein
• Dry eye syndrome is most common cause, often
associated with neurotrophic keratopathy, chronic
bullous keratopathy, superior limbic keratoconjunc-
tivitis
• Treatment is removal of cause, artificial tear, debride-
ment of filament under anesthesia, 10% acetyl
cystine or 5% NaCl eyedrops.
8. Exposure keratopathy
• Red eye, burning, FB sensation, conjunctival injec-
tion.
• Inadequate blinking or closure of eyelids lead to
corneal drying and epithelial defects.
• May follow facial nerve palsy, eyelid deformity,
proptosis, floppy eyelid syndrome.
• Treatment is with correction of underlying disorder,
artificial tear, lubricating ointments; surgical
correction (for ectropion, proptosis).
Corneal Diseases 11
9. Neurotrophic keratopathy
• Red eye, FB sensation, swollen eyelids.
• Loss of corneal sensations, epithelial defects in
fluoroscein stain
• Follows HSV, stroke, trigeminal palsy, acoustic
neuroma
• Treatment is with artificial tear and ointment;
cycloplegic drops, antibiotic drops, tarsorrhaphy
10. Recurrent corneal erosion
• Recurrent ocular pain, photophobia, tearing at the
time of awakening or during sleep.
• Localized roughening of corneal epithelium or
corneal abrasion
• May follow anterior corneal dystrophy, stromal
corneal dystrophy (lattice, granular, macular
dystrophies)
• Previous corneal abrasion
• Treatment of acute episode is with cycloplegic drop,
antibiotic ointments; once healing is complete
artificial tears and ointment
• Unresponsive erosions may need anterior stromal
puncture (if outside visual axis), debridement with
diamond burr, excimer laser ablation of superficial
stroma.
11. Thermal/UV keratopathy
• Red eye, tearing, photophobia, moderate to severe
pain, blurred vision
• Confluent punctate epithelial defects
• Treatment is with cycloplegic eyedrops, antibiotic eye
ointment.
12. Thygen’s superficial punctate keratopathy
• Bilateral, chronic course with remissions and
exacerbations
• Photophobia, FB sensation, tearing
• Coarse punctate corneal epithelial opacities
• No, conjunctival injection, corneal edema, or anterior
chamber reaction
• Treatment is with artificial tear (drop/ointment) mild
topical steroid (fluorometholone- 0.1%).
13. Interstitial keratitis
• Pain, tearing, photophobia, corneal stromal edema
and vascularization, anterior chamber reaction.
• Common to congenital syphilis, less common in

acquired syphilis, TB, Cogan‘s syndrome, systemic
vasculitis, leprosy, HSV.
• Treatment is with cycloplegics, topical steroids and
treatment of underlying disease.
14. Peripheral corneal thinning
• Pain, photophobia, often asymptomatic
• Besides thinning there may be sterile infiltrate or
ulcer
• Occurs in (1) collagen vascular diseases (2) Terrien’s
marginal degeneration (usually bilateral, quiet
anterior chamber). (3) Mooren’s ulcer (idiopathic
painful corneal thinning (4) pellucid marginal
degeneration (painless, bilateral) (5) furrow degene-
ration (6) dellen (7) staphylococcal hypersensitivity
(8) dry eye syndrome (9) neuropathic keratopathy
(10) sclerokeratitis (11) vernal keratoconjunctivitis
• Treatment is removal of cause, antibiotic oint/drops,
ocular lubricants, systemic steroids, immunosup-
pressants (topical steroids and interferon for
Mooren’s ulcer).
• Lamellar keratoplasty when thinning is extreme.
15. Dellen
• Usually asymptomatic, irritation, FB sensation
• Corneal thinning usually at limbus, with adjacent
elevation
• No, anterior chamber reaction
• Lubricating oint/ artificial tear, antibiotic ointments
16. Staphylococcal hypersensitivity
• Acute photophobia, red eye, mild pain, itching
• Bilateral peripheral corneal stromal infiltration with
clear space between infiltrates and limbus; quiet
anterior chamber.
• Blepharitis, SPK, phlyctenule (wedge shaped raised
sterile infiltrate near limbus), corneal revasculari-
zation in contralateral eye may be present.
• Treatment is with warm compress, erythromycin
bacitracin oint, prednisolone acetate (0.125%) drops;
long-term systemic antibiotic prophylaxis for
recurrent disease.
17. Keratoconus
• Progressive decreased vision, usually beginning in
adolescence
Corneal Diseases 13
• Slowly progressive irregular astigmatism, resulting

from paracentral thinning and bulging of cornea,
Vogt’s stria, irregular corneal retinoscopic reflex, egg
shaped mires in keratometry; inferior steepening on
corneal topographic evaluation
• Fleischer’s ring (epithelial iron deposit at base of
cone)
• Bulging of lower eyelid when looking downward
(Munson’s sign), superficial corneal scarring
• Acute corneal hydrops can present with red eye,
pain, photophobia and tearing.
• Associated with MVP, atopic disease, chronic eye
rubbing
• Pellucid marginal degeneration and keratoglobus are
to be excluded where corneal transplant has higher
failure rate
• Treatment is with glass (mild case), gas permeable
rigid contact lens (moderate case) or keratoplasty
• Acute hydrops needs cycloplegics, NaCl ointment
and often pressure patch.
18. Corneal dystrophies
• Bilateral, inherited, progressive corneal disease, non-
inflammatory, no corneal vascularisation, no assoc-
iated systemic disease.
a. Anterior corneal dystrophy
i. Anterior basement membrane dystrophy (map-dot-
fingerprint dystrophy)—With pain and photo-
phobia on awakening.
ii. Miesmann’s dystrophy—Tiny diffuse epithelial
vesicles, more so in palpebral fissure
iii. Reis Buckler’s dystrophy—Gray reticular opacity
in central cornea with painful recurrent erosions
May require superficial keratectomy or excimer laser
keratectomy when there is significant visual loss or
recurrent pain and photophobia
b. Corneal stromal dystrophy
i. Lattice dystrophy—Refractile branching lines, re-
current erosions, tend to recur after PTK and
corneal transplant
ii. Granular dystrophy—Anterior stromal deposits in
central cornea, recurs after PTK or corneal trans-
plant
iii. Macular dystrophy—Gray white stromal deposits

with ill-defined edges, significant visual loss,
cured by corneal transplant.
iv. Central crystalline dystrophy—Fine yellow white
central stromal crystals, associated hyperlipidemia,
rarely affect vision
c. Corneal endothelial dystrophy
i. Fuch’s dystrophy
• After 50 years of age, glare and blurred vision,
bilateral but asymmetric, corneal guttate and
stromal edema.
• Folds in Descemet’s membrane, fine pigment
dusting on endothelium
• Be differentiated from aphakic bullous keratopathy,
posterior polymorphous dystrophy, iridocorneal
endothelial syndrome.
• Treatment is with NaCl eyedrops, dehydration of
cornea by warm air from blower, IOP reduction if
raised and corneal transplant.
ii. Posterior polymorphous dystrophy—Changes at
the level of Descemet’s membrane, with vesicles,
iris abnormalities common and glaucoma may
occur.
iii. Congenital hereditary endothelial dystrophy—
Bilateral corneal edema, no corneal guttata or
raised IOP, can be AD or AR.
19. Wilson’s disease
• No ocular complaints; greenish-brown band in cor-
neal periphery, at the level of Descemet’s membrane
(Kayser-Fleischer ring); anterior and posterior sub-
capsular copper deposit producing sun flower
cataract.
• Typically no visual/ocular complaint
• Exclude other causes—Primary biliary cirrhosis,
CAH, multiple myeloma; arcus senilis (corneal
stromal lipid deposit)
20. Photorefractive keratectomy
It is removal of corneal epithelium and partial ablation
of anterior corneal stroma using excimer laser to correct
refractive error.
It can lead to progression of refractive error, severe
glare and monocular diplopia, non-healing epithelial
defects, irregular astigmatism.
Corneal Diseases 15
21. Laser in situ keratomileusis (LASIK)

In LASIK a partial thickness corneal flap is raised using
a microkeratome and the underlying stroma is ablated
using excimer laser. The corneal flap is repositioned over
the stroma without suture. Usually employed to correct
refractive error.
Can be followed by progression of refractive error,
irregular astigmatism, diplopia, glare, halos, painful dry
eyes. It is indicated for those above 18 years wearing
glasses or contact lenses for at least 2 years and have
a thick cornea. Myopia upto -12D, astigmatism of 6D
and hypermetropia upto + 6D can be corrected by LASIK
surgery.
22. Radial keratotomy
This is flattening of cornea to correct myopia by putting
deep incisions on cornea in a radial fashion using
diamond knife. Astigmatic keratotomy is a similar
procedure in which arcuate or tangential incisions are
made to correct astigmatism. Myopia upto 6D can be
corrected with it.
3 Diseases of Eyelids
and Orbit
1. Chalazion/hordeolum
• Eyelid lump, swelling, pain, tenderness, erythema.
• Blocked meibomian orifice, may be associated with
blepharitis/acne rosacea.
• Should be differentiated from (1) sebaceous gland
carcinoma (recurrent calazion in aged, loss of
eyelashes) (2) pyogenic granuloma
• Treatment is topical antibiotic, warm compress, exci-
sion and curettage or local triamcinolone injection
2. Ectropion
• Outward turning of eyelid margin, associated SPK
and conjunctival injection, thickening.
• Etiology includes aging, 7th cranial palsy, cicatricial,
allergic.
• Treatment is that of exposure keratopathy and if need
be surgical correction.
3. Entropion
• Ocular irritation, FB sensation, tearing, red eye
• Inward turning of eyelid margin, SPK, conjunctival
injection
• Treatment is with antibiotic ointment for SPK and
surgical correction
4. Trichiasis
• Misdirected eyelashes rubbing against globe causing
SPK, tearing, red eye and FB sensation.
• Can be idiopathic or due to chronic blepharitis
• Treatment is with epilation, antibiotics for SPK and
blepharitis; electrolysis/cryotherapy/surgery are
reserved for resistant cases.
5. Districhiasis
Aberrant second row of eyelashes emanates from
meibomian gland opening, either congenital or due to
blepharitis.
Diseases of Eyelids and Orbit 17
6. Floppy eyelid syndrome

• Easily reversible upper eyelid, chronically red,
irritated eye often worst on awakening, mild mucus
discharge.
• Soft rubbery superior tarsal plate, SPK, often have
keratoconus.
• Symptoms are due to spontaneous eversion of eyelid
during sleep allowing superior palpebral conjunc-
tiva to rub against pillow, bed sheet.
• Treatment is with antibiotic oint, eyelid tightening
surgery.
7. Blepharospasm
• Always bilateral, uncontrolled blinking, twitching,
decreased vision.
• Disappears during sleep
• Though idiopathic, can be due to FB, trichiasis,
blepharitis, dry eye.
• Exclude (1) hemi facial spasm (does not disappear
during sleep, entire side of face contracts, MRI be
done to rule out CP angle tumor compressing
7th nerve (2) Tourette’s syndrome (3) tic douloureux
(4) tardiva dyskinesia (5) eyelid myokemia
• Treatment is with botulinum toxin A injection, or
surgical excision of orbicularis muscle into eyelid.
8. Canaliculitis
• Most common infecting agent is Actinomyces israelli
followed by fusobacteria, candida, aspergillus HSV.
• Tearing or discharge, red eye, red pouting punctum.
• Remove concretion from canaliculus if any, irrigate
with penicillin 1 lac units/ml or 1% iodine , if fungus
detected on smear nystatin irrigation.
9. Dacryocystitis
• Erythematous tender swelling on nasal aspect,
mucoid or mucopurulent discharge from punctum
when pressure is applied over lacrimal sac.
• Pain, tenderness, swelling over lacrimal sac, tearing,
discharge
• May be related to nasolacrimal duct obstruction,
diverticulum of lacrimal sac, trauma. Responsible
organisms are staphylococci, streptococci and diph-
theroids.
• Consider CT scan of orbit and PNS in atypical or

severe cases that donot respond/worsen with
appropriate antibiotics.
• Treatment is with augmentin or cefaclor/cefuroxime,
topical antibiotics, warm compress; dacryocysto-
rhinostomy in chronic dacryocystitis.
10. Dacryoadenitis
• Erythema, swelling and tenderness over outer one
third of upper eyelid, with tearing/discharge.
• Ipsilateral preauricular lymphadenopathy.
• Commonly involved pathogen are staphylococci,
gonococci and streptococci.
• Differentiate it from orbital pseudotumor, malignant
lacrimal gland tumor.
• When concomitant parotid enlargement—think of
sarcoidosis, tuberculosis, lymphoma, syphilis.
• Treatment is as far dacryocystitis.
11. Preseptal cellulitis.
• Tenderness, redness of the eyelid, iritation.
• No pain on eye movement, no restriction of extra-
ocular motility.
• Staphylococci and streptococci are the etiologic
agents but H. influenzae be considered in children.
• Treatment is with augmentin/ erythromycin for 10
days; severe infection be treated with ceftriaxone and
vancomycin.
12. Tumors of eyelid
Benign Seborheic keratosis, hordeolum, chalazion,
keratoacanthoma, cysts (epidermal, inclu-
sion, sebaceous, sudoriferous), mulluscum
contagiosum, xanthelsma, squamous papil-
loma, actinic keratosis.
Malignant (i) Basal cell carcinoma (most common) can
be nodular, morpheaform (firm, flat)
(ii) Squamous cell carcinoma
(iii) Sebaceous gland carcinoma arising from
meibomian gland, often multifocal.
13. Orbital inflammatory pseudotumor
• Can be acute, recurrent or chronic; diplopia, pain
decreased vision, often asymptomatic proptosis.
• Usually unilateral, CT scan shows thickened

posterior sclera, thickening of extraocular muscles,
orbital fat/lacrimal gland involvement.
• Uveitis, ↑ IOP, conjunctival chemosis, weak corneal
reflex.
• Mostly idiopathic, but collagen disease be excluded
• Oral prednisolone or low dose radiation therapy
brings relief.
14. Orbital cellulitis
• Red eye, pain, blurred vision, double vision, head-
ache
• Proptosis, chemosis, restricted ocular motility,
painful eye movements.
• Retinal venous congestion, optic disc edema, CT may
show ethmoid/other sinusitis.
• Can be also complication of orbital trauma/ surgery,
bacteremia
• Staphylococci, streptococci, H. influenzae are most
common agents but bacteroids and gram –ve rods
may be involved (following trauma).
• Treatment is with ceftriaxone 100 mg/kg/day (mxm-
4 gm) in 2 divided doses IV + vancomycin 40 mg/
kg/day (mxm—2 gm) IV in 2 doses.
• Patients allergic to cephalosporins can have
vancomycin + clindamycin 300 mg IV 6 hrly or
gentamicin 5 mg/kg. Change over to oral
augmentin once there is improvement to
complete 14 day of therapy.
• When no improvement—think of orbital abscess (CT
scan is diagnostic, meningitis and cavernous sinus
thrombosis.
15. Orbital tumors in children
• Dermoid and epidermoid cysts—best defined in CT
scan
• Capillary haemangioma—proptosis increased during
crying, contrast enhancing irregular mass in CT.
• Rhabdomyosarcoma—rapid progression, bone des-
truction in CT.
• Lymphangioma—slowly progressive, non-encapsu-
lated irregular mass in CT.
• Juvenile pilocystic astrocytoma—decreased vision,
afferent pupillary defect, optic atrophy, fusiform
enlargement of optic nerve in CT.
• Leukemia—(granulocytic sarcoma) may precede

bone marrow or blood signs of leukemia. CT shows
irregular mass with bone erosion and extension to
temporal fossa.
• Metastatic neuroblastoma—proptosis, echymosis,
poorly defined mass with bone destruction.
• Plexiform neurofibroma—ptosis, facial asymmetry,
irregular soft tissue mass in CT.
• Teratoma—severe unilateral proptosis at birth with
visual loss from ↑ IOP, optic atrophy, CT shows
multi loculated mass.
16. Orbital tumor in adults.
• Prominent eye, double vision, pain, decreased
vision, often asymptomatic.
• Palpable mass, limited ocular mobility, edematous
disc.
• Mostly metastatic—from breast (most common), lung,
GI tract (prostate), enophthalmos may be seen with
schirrous carcinoma, CT shows poorly defined
diffuse tumor.
• Other etiologies include (1) cavernous haemangioma
(MRI most diagnostic) (3) mucocele (CT shows
extension from ethmoid/frontal sinus (3) optic nerve
sheath meningioma (slowly progressive visual loss,
disc edema) (4) neurilemoma (progressive painless
proptosis), (5) localized neurofibroma (well defined
mass in CT, (6) fibrous histiocytoma (resembles
haemangiopericytoma), (7) lymphoid tumors—slow
onset and progression, less responsive to steroid, CT
shows irregular mass conforming to shape of orbit.
17. Chronic dacryoadenitis
• Persistent or progressive swelling on outer one-third
of upper eyelid, with proptosis and displacement of
globe.
• Exclude (1) sarcoidosis (bilateral, ↑ ACE level), (2)
orbital inflammatory pseudotumor, (3) pleomorphic
adenoma, (4) dermoid, (5) lymphoid tumor (CT
shows irregular lesion conforming to globe and lacri-
mal fossa without bony erosion), (6) adenoid cystic
carcinoma (acute onset of pain and proptosis, ptosis,
motility disturbances, (7) pleomorphic adeno-
carcinoma (elderly, rapid progression, pain), (8)
lacrimal gland cyst (floctuating mass).
• Benign mixed tumors and dermoids not to be

biopsied since rupture leads to severe inflammatory
reactions. They should be completely excised without
rupturing capsule/pseudocapsule.
4 Ocular Tumors
1. Conjunctival amelanotic tumors

i. Limbal dermoid—Usually located in inferotemporal
quardant of limbus, may involve the cornea; solid,
fairly well circumscribed, often hair coming out
from surface, often associated with vertebral
anomalies, The cornea/ sclera underlying dermoid
may be very thin and globe may be ruptured while
its removal.
ii. Dermolipoma: Occur on bulbar conjunctiva tem-
porally, yellow white solid tomor; removal be
avoided because of extension to orbit.
iii. Pyogenic granuloma—Benign, deep red, peduncu-
lated mass, occurring at site of prior surgery,
chalazion or trauma; responds to topical steroid-
antibiotic combination.
iv. Lymphangioma—Diffuse multiloculated cystic
mass, haemorrhage into it may produce chocolate
cyst, may enlarge with upper respiratory infection,
do not regress like capillary haemangioma,
difficult to remove in one sitting.
v. Papilloma
Viral—Multiple pedunculated or sessile lesions in
children, tendency for spontaneous resolution,
recur after removal
Nonviral—Single, commonly near limbus, often
precancerous thus demanding complete excisional
biopsy.
In dark coloured individuals papillomas may
appear pigmented, hence mistaken for malignant
melanoma.
vi. Kaposi’s sarcoma—Red or purple malignant
subconjunctival nodule in AIDS patients.
vii. Conjunctival carcinoma in situ/dysplasia—Leuko-
plakic or gray white gelatinous lesion at limbus,
may have papillomatous fern like appearance,
Ocular Tumors 23
unilateral and unifocal. Need meticulous excision

and dissection of adjacent sclera and cornea.
viii. Lymphoid tumors—Light pink to salmon coloured
lesion in young, appearing in bulbar conjunctiva
and fornix, biopsy is diagnostic; benign reactive
lymphoid hyperplasia is treated with steroid
drops/cryo but lymphoma needs complete
excision.
ix. Amyloid—Smooth waxy yellow masses in lower
fornix, biopsy is definitive
x. Sebaceous gland carcinoma—Elderly patient with
refractory unilateral blepharoconjunctivitis be
screened for it. Involvement of palpebral conjunc-
tiva is common.
2. Melanotic lesions
i. Ocular melanocytosis—An episcleral lesion over
which conjunctiva is freely mobile; lesion is
unilateral, blue gray, with ipsilateral darker iris
and choroids, can predispose to malignant mela-
noma of uveal tract, orbit and brain.
ii. Acquired melanosis—Flat brown patches of
pigmentation in middle aged, malignant transfor-
mation likely if elevation and ↑ vascularity occur.
Biopsy and cryotherapy may be required
iii. Nevus—Occurs at puberty within the palpebral
fissure on the bulbar conjunctiva, presence of small
cyst within the lesion, close follow-up required.
iv. Malignant melanoma—Middle aged or elderly
patient, nodular brown vascularized mass, often
associated with ciliary body melanoma. Excisional
biopsy be performed unless intraocular or obital
involvement is present that demands exenteration.
3. Malignant melanoma (MM) of iris
• May occur as a localized or diffuse pigmented or
non-pigmented lesion, common to inferior half of iris
with prominent feeder vessel; secondary glaucoma
may be present, so also focal iris nodules; spon-
taneous hyphema may occur.
Tumors of iris pigment epithelium are usually
black in contrast to melanoma which are amelanotic
to brown. Localized lesion be differentiated from
(1) metastasis (rapid growth, multiple, pseudohypo-
pion) (2) leiomyoma (transparent) (3) iris cyst (4)
inflammatory granuloma (sarcoid, TB). Diffuse

lesions may be mistaken for (1) congenital iris
heterochromia (smooth iris, non-progressive,
glaucoma) (2) Fuch’s heterochromic iridocyclitis
(asymmetry of iris colour, unilateral) (3) iris nevus
syndrome (corneal edema, iris atrophy, iris nodules,
glaucoma) (4) haemosiderosis.
• Close follow-up is required; surgical resection is
indicated if growth is documented, tumor interferes
with vision or produces intractable glaucoma
• Diffuse iris MM with secondary glaucoma need
enucleation
4. Malignant melanoma (MM) of choroids
• Decreased vision, visual field defect, floaters, light
flash, pain but often asymptomatic.
• Gray-green to brown or yellow choroidal mass with
retinal detachment, height > 2 mm, orange pigment
over lesion or mushroom shape with blood vessels
on its dome
• Diffuse choroidal MM can appear as thickened
choroids without a distinct mass
• Carefully differentiate it from pigmented lesions like
(1) congenital hypertrophy of retinal pigment
epithelium (2) reactive hyperplasia of retinal
pigmentary epithelium (3) melanocytoma of optic
nerve (4) choroidal detachment (5) peripheral
disciform degeneration (yellow to red mass with
exudates and haemorrhage) (6) age related disciform
macular degeneration (subretinal blood may stimu-
late melanoma).
Non-pigmented lesions to be differentiated
include (1) choroidal haematoma (red orange, never
mushroom shaped) (2) metastatic carcinoma (↑CEA)
(3) choroidal osteoma (yellow-orange, close to optic
disc, pseudopodia like projection from margin in
women, US shows calcified mass) (4) posterior
scleritis (pain, proptosis, T sign in US).
• Treatment depends upon tumor characteristic, status
of other eye and age. Photocoagulation, thermo-
therapy, radiotherapy, local resection/enucleation
are the options.
5 Glaucoma
1. Primary open angle glaucoma (POAG)

Usually asymptomatic till late when true tunnel vision
develops; patient with early symptom may complain
that parts of a page are missing.
• IOP > 22 mmHg in 60% cases
• Open anterior chamber angle on gonioscopy.
• Optic nerve appearance (a) notching in the rim (b)
acquired pit of the optic nerve (c) drance
haemorrhage (d) nerve fiber layer defect (e) cup/disc
ratio asymmetry >0.2 (f) bayoneting of vessels as they
exit the nerve.
• Should be differentiated from (1) ocular hypertension
(2) secondary open angle glaucoma (3) secondary
angle closure glaucoma (4) chronic angle closure
glaucoma (5) optic atrophy (6) congenital optic nerve
defect and (7) optic nerve drusens.
• Atypical cases like (a) colour vision loss (b)
decreased visual acuity out of proportion to cupping
or field loss (c) unilateral progression despite equal
IOP in both eyes (d) IOP < 21 mmHg (e) visual field
defects greater than cupping (f) optic nerve pallor out
of proportion to cupping (g) visual field patterns not
typical of glaucoma (hemianopic defect, enlarged
blind spot) need neurological avaluation with CT/
MRI, serology for syphilis , ANA, and cardiovascular
evaluation.
• Treatment is individualized because not all the three
elements of pressure, optic nerve damage and visual
field loss are present in every patient. Consideration
be given to the amount of damage already present,
rate of damage progression, and patient’s life
expectancy. IOP should be reduced by 30-40% to halt
damage to optic nerve.
• Treatment options are (1) argon laser trabeculoplasty
(ALT) (2) trabeculectomy (3) medications. Other
treatments modalities are (a) tube shunt procedures

(b) laser cyclophotocoagulation of ciliary body (c)
cyclocryotherapy (d) cyclodialysis, specially reser-
ved for those not responding to ALT, medication and
trabeculoplasty.
I. Beta blockers—timolol 0.25 and 0.5% qid or bid,
metipranolol 0.3% bid, cartelol 1% bid, betaxolol
0.25-0.5%, barring the last others may aggravate
asthma, COPD, CHF, depression, myasthenia and
all are likely to blunt hypoglycemia in diabetics.
II Alfa 2 receptor agonists—brimonidine 0.2%, tid,
apraclonidine, 0.5% tid, can be used in conjunction
with beta blockers.
III Carbonic anhydrase inhibitors – dorzolamide 2%,
brinzolamide 1% tid-bid, can be used with beta
blockers.
IV Prostaglandin agonists—lanatoprost 0.005%, but
contraindicated in patients of active uveitis.
V Miotics—pilocarpine—0.5-1% initially, gradually
increase to 4% but not tolerated by patients < 40
years because of accommodation spasm. Miotics
are contraindicated in patients with retinal holes,
high myopics and aphakes. Pilocarpine ocular
insert replaced every week is useful in young
patients. Longer acting echothiophate iodide is
preferred for aphakic or pseudoaphakic glaucoma
patients.
VI Sympathomimetics—dipivefrin—0.1% bid or epi-
nephrine 0.5-2% bid can be used but are inferior.
VII Systemic carbonic anhydrase inhibitors—metha-
zolamide 25-50 mg PO or acetazolamide 125-250
mg PO bid, can cause hypokalemia and be avoided
in patients allergic to sulfa, renal stone disease.
Ocular hypertension
Clinical signs
I Asymptomatic rise in IOP > 22 mm Hg
II Normal anterior chamber angle on gonioscopy.
III Normal optic nerve and visual field.
Differential diagnosis
• Primary open angle glaucoma
Glaucoma 27
• Secondary open angle glaucoma (lens induced,

inflammatory, exfoliative, pigmentary, steroid indu-
ced, angle recession, developmental anterior segment
abnormalities, trauma, iridocorneal endothelial
syndrome).
• Chronic angle closure glaucoma (findings of primary
open angle glaucoma except presence peripheral
anterior synechiae in gonioscopy.
Treatment
• IOP < 27 mm Hg, no optic nerve damage, no visual
field defect—no treatment, only close observation.
• IOP > 27 mm Hg—medications as for open angle
glaucoma.
2. Angle recession glaucoma

• Usually asymptomatic until late, unilateral, history
of trauma.
• Gonioscopy shows uneven iris insertion with an
area of torn or absent iris processes and posteriorly
recessed iris to reveal a widened ciliary band.
• The scleral spur may appear abnormally white on
gonioscopy because of the recessed angle.
• Treatment is similar as for primary angle closure
glaucoma except that pilocarpine may increase IOP
by reducing uveoscleral flow and trabeculoplasty is
ineffective.
3. Inflammatory open angle glaucoma

• Pain, photophobia, decreased vision, often minimal
symptoms
• Aqueous flare, white blood cells in aqueous
• Miotic pupil, peripheral anterior synechiae, ciliary
flash, keratic precipitates.
• Etiologies include uveitis( anterior, posterior, both),
trauma, intraocular surgery.
• Should be differentiated from (1) glaucomatocyclitic
crisis (2) angle closure glaucoma (3) pigmentary
glaucoma (4) neovascular glaucoma and (5) Fuch’s
heterochromic iridocyclitis.
• Treatment is with (a) topical steroid, depending upon
severity of anterior chamber cellular reaction (b)
cycloplegics (c) beta blockers and other topical
agents as for POAG. However miotics and prostag-
landin agonists are contraindicated in inflammatory

glaucoma. Mannitol infusion 1-2 gm/kg IV over/1
hour may be required when IOP rise is severe and
even filtering surgery with adjunctive antifibrotic
therapy may indicated.
4. Pigmentary glaucoma
• Episodes of blurred vision, eye pain, coloured halos.
• Common to young myopic males, usually bilateral
but asymmetric
• ↑ homogeneous trabecular meshwork pigments,
with characteristic mid peripheral spoke like iris
transillumination defects
• Vertical pigment band on corneal endothelium
(Krukenberg’s spindle), pigment deposition on
equatorial lens surface
• Other features of ↑ IOP—i.e. cupping, visual field
defect.
• To be differentiated from (1) exfoliative glaucoma (tra-
becular meshwork pigmentation is black, less homo-
geneous, more prominent inferiorly. A Sampolesi’s
line at 6 O’clock is characteristic) (2) inflammatory
open angle glaucoma (3) iris melanoma (raised
pigmented iris lesion).
• Antiglaucoma medications except miotics be
prescribed, miotics (pilocarpine) can cause retinal
detachment in these myopic patients. Argon laser
trabeculoplasty is very effective in young patients in
contrast to POAG. Filtration procedure when all
above methods fail but young myopics are at risk of
developing hypotonic maculopathy.
5. Exfoliative glaucoma
• Usually asymptomatic in early stages.
• A systemic disease where white flaky material is
deposited on pupillary margin, iris, ciliary epithe-
lium and trabecular meshwork
• Peripupillary iris transillumination defect, anterior
lens capsular changes, irregular black pigment depo-
sition on trabecular meshwork more so inferiorly,
pigments anterior to Schwalbe’s line (Sampolesi’s
line), bilateral but asymmetric.
• Treatment is as for POAG but IOP is highly unstable
and glaucoma may progress rapidly to cause optic
nerve damage.
Glaucoma 29
6. Phacolytic glaucoma
• Acute onset of glaucoma with pain, photophobia
diminished vision due to leakage of lens material
from cataract through intact lens capsule causing
trabecular meshwork out-flow obstruction.
• Corneal edema, anterior chamber flare and cells,
pseudohypopion, severe conjunctival injection.
• Should be differentiated from (1) inflammatory glau-
coma (2) glaucomatocyclitic crisis (3) acute angle
closure glaucoma (4) lens-particle glaucoma (5)
endophthalmitis (6) ghost cell glaucoma (7) trau-
matic glaucoma, etc.
• Treatment is as for POAG with medication including
topical steroids and IV mannitol, cataract removal
is usually performed within 24-36 hours of IOP
control.
7. Lens particle glaucoma

• It is due to obstruction of aqueous out flow channel
by lens material liberated by trauma or surgery.
• Patients have pain, blurred vision, photophobia and
tearing
• White fluffy pieces of lens material are seen in
anterior chamber along with other features of
increased IOP
• Treatment is with antiglaucoma medication, topical
steroid drops and IV mannitol.
8. Steroid glaucoma
• Rise in IOP occurs 2-4 weeks after starting topical
steroid; also can follow oral or inhalation or derma-
tologic steroid use.
• IOP increase is due to reduced outflow through
pigmented trabecular meshwork.
• Steroids be tapered and low concentration/low
potency ones be used.
• Antiglaucoma medications be used as for POAG.
• When a patient received steroids for ocular inflam-
mation and develops ↑ IOP—it is difficult to know
if it is inflammatory or steroid induced glaucoma.
In such patients steroid dose be first increased to
control inflammation and if glaucoma persists it is
due to steroids.
9. Neovascular glaucoma
• Glaucoma is caused by a fibrovascular membrane
overgrowing the anterior chamber angle structures.
The membrane subsequently contracts causing
peripheral anterior synechiae and secondary angle
closure glaucoma. The genesis of fibrovascular mem-
brane is ischaemia due to (1) diabetic retinopathy (2)
CRAO (3) CRVO (4) carotid occlusive disease (5)
chronic retinal detachment, chronic uveitis, etc.
• Treatment is with cycloplegic and topical steroid
drops along with other topical agents but not pilo-
carpine, alongwith cryoablation for neovascularisa-
tion, goniophotocoagulation and glaucoma filtration
surgery.
• The pain in neovascular glaucoma is not primarily
a function of IOP, hence reducing IOP may not be
needed if the goal is only pain control. In eyes
without useful vision only topical steroids and
cycloplegics are sufficient. Beta blockers, retrobulbar
alcohol injection or enucleation may be adopted for
pain.
10. Ididocorneal endothelial syndrome.
• It is due to abnormal corneal endothelial layer which
grows over anterior chamber angle and then
contracts to cause angle closure and glaucoma.
• Patient is typically young or middle aged, has
irregular iris, unilateral pain and blurred vision.
• Corneal endothelium has fine hammered metal
appearance, irregular peripheral anterior synechiae,
deep central anterior chamber.
• Iris changes—atrophy, thinning and pigmented
nodules
• Corneal edema occasionally
• Should be distinguished from (1) posterior polymor-
phous dystrophy (bilateral, endothelial vesicles or
bandlike lesions) (2) Fuch’s endothelial dystrophy
(bilateral corneal edema, endothelial guttata).
• Antiglaucomatous medications as for POAG
• Hypertonic saline topical/oint to reduce corneal
edema
• Filtering procedure when medical therapy fails to
control IOP
• Corneal transplant if corneal edema is chronic in
presence of good IOP control.
Glaucoma 31
11. Postoperative glaucoma

IOP may rise following cataract extraction due to
retained viscoelastic, hyphema, pupillary block, pigment
dispersion and inflammation. The rise is < 30 mmHg
and remains for weeks which most normal eyes tolerate.
However, eyes with optic nerve damage need anti-
glaucoma medications. When inflammation is marked
steroid drops and NSAID drops be instilled.
Pupillary block within 2 weeks of surgery is due to
blood, fibrin, hyphaema, malignant glaucoma (aqueous
misdirection), suprachoroidal bleed, vitreous plugs, etc.
Treatment of pupillary block is YAG laser peripheral
iridectomy (two or more) immediately. If cornea is hazy
and eye is inflamed then antiglaucoma medications
along with topical steroids be generously used to reduce
the IOP followed by YAG laser iridectomy and filtration
procedure.
Uveitis glaucoma hyphaema syndrome (UGHS) is
usually due to irritation from a malpositioned anterior
or posterior chamber IOL, often with a vitreous wick.
Such patients need cycloplegics, topical steroids and
other antiglaucoma medications along with reposition-
ing, replacement or removal of the IOL.
Ghost cell glaucoma occurs when degenerated RBCs
pass from vitreous into anterior chamber and obstruct
the trabecular meshwork, usually 4 weeks after vitreous
haemorrhage. Antiglaucoma medication and anterior
chamber irrigation bring relief.
12. Malignant glaucoma
It is due to aqueous misdirection that fills the vitreous
displacing it forwards, pushing the ciliary processes,
thus causing angle closure and glaucoma. The anterior
chamber is shallow, and there is no iris bombe. This
often occurs after surgical treatment of angle closure
glaucoma, or surgery in a patient of shallow anterior
chamber without patent peripheral iridectomy.
Treatment is with immediate peripheral iridectomy
with cycloplegics and antiglaucoma medication, if un
successful YAG laser treatment of ciliary process , core
vitrectomy and reformation of anterior chamber,
vitrectomy, etc. may be done.
13. Acute angle closure glaucoma (ACG)

• Common predispositions are narrow anterior
chamber angle recess, anterior insertion of iris root,
common to Asians, often precipitated by topical
mydriatics, systemic anticholinergics/antihista-
minics/antipsychotics; use of accommodation (near
work) or dim illumination.
• Severe pain, blurred vision, coloured halos around
lights, frontal headache, nausea and vomiting.
• Shallow anterior chamber in both eyes, corneal
microcystic edema, ↑ IOP, conjunctival injection,
mid-dilated pupil.
• Must be differentiated from secondary angle closure
glaucomas (1) neovascular glaucoma—abnormal
misdirected blood vessels along the pupillary
margin, or trabecular mesh work (2) mechanical
closure of the angle secondary to anterior displace-
ment of lens-iris diaphragm (lens displacement,
choroid detachment, choroid swelling after extensive
retinal surgery, posterior segment tumor, aqueous
misdirection syndrome. (3) peripheral anterior
synechae.
• Treatment depends upon severity and duration of
attack. Severe permanent damage may occur within
hours. Hence when ↑ IOP reduces visual acuity
significantly-immediate reduction with IV manitol,
IV acetazolamide and topical antiglaucoma medi-
cations including topical steroids be given. Of course
in aphakic or pseudoaphakic pupillary block or
mechanical closure of angle pilocarpine should not
be used.
• If IOP does not decrease within 2-3 hours or vision
deteriorates laser peripheral iridectomy be perfor-
med. If corneal edema prevents use of laser, surgical
iridectomy be done. The untreated eye caries 40-80%
chance of developing acute angle closure in 5-10
years, hence peripheral iridectomy (PI) be done
prophylactically.
When IOP still remains high after PI, trabeculectomy
be done. In mechanical angle closure laser gonio-
plasty be done to open the angle.
• Acute angle closure glaucoma is highly inheritable,
50% of relatives are expected to have it and hence
be warned. When IOP decreases with therapy,
Glaucoma 33
appearance of cornea worsens. Despite PI if repeated

attacks of ACG develop, plateau iris syndrome be
suspected. ACG can be seen without rise in IOP and
be suspected in a patient with pain and reduced
visual acuity in presence of (1) edematous thick
cornea (2) markedly asymmetric pressure in both eyes
(3) shallow anterior chamber in both eyes.
14. Plateau iris
• The peripheral iris can bunch up in anterior cham-
ber angle and obstruct aqueous outflow. Anterior
chamber depth is normal centrally. Mydriatics can
precipitate angle closure glaucoma in them but
tropicamide is safe. If patient has acute ACG
treatment is with topical antiglaucoma medications
and PI. If ineffective laser iridoplasty is the answer.
15. Congenital glaucoma
• In most patients it is idiopathic but may be due to
Lowe’s syndrome (oculocerbrorenal syndrome),
aniridia, rubella, (glaucoma, cataract, salt pepper
chorioretinopathy, hearing and cardiac defects),
developmental anterior segment anomalies.
• Photophobia, tearing, enlarged often hazy cornea in
the affected infant.
• Usually bilateral, enlarged globe, increase cup: disc
ratio, corneal edema
• Linear tears in Descemet’s membrane (Haab’s stria).
• Should be differentiated from (i) congenital megalo-
cornea ( corneal horizontal diameter > 13 mm) with
normal IOP and cup disc ratio (ii) congenital here-
ditary endothelial dysprophy (bilateral corneal
edema with normal corneal diameter) mucopoly
saccharidosis (cloudy cornea).
• Treatment is medical (topical betablocker and carbo-
nic anhydrase inhibitor) or surgical – i.e (i) gonio-
tomy, trabeculotomy (opening canal of Schlemm to
anterior chamber) or trabeculectomy. Miotics are not
effective and medial therapy provides only
temporary relief.
• Ketamine increases IOP while halothane reduces
IOP.
6 Uveitis
1. Anterior uveitis (iritis/iridocyclitis)

• Pain, red eye, photophobia, tearing, ↓ vision, often
recurrent episodes.
• Cells and aqueous flare in anterior chamber.
• Fine keratic precipitates (KP) on corneal endothe-
lium in non-granulomatous form and large mutton
fat KP/ Busacca’s nodules on iris in granulomatous
form.
• Other signs include cells in anterior vitreous,
posterior synechiae, low IOP, ciliary flush, fibrinous
hypopion in severe cases, cystoid macular edema if
chronic and occasionally cataract.
Etiology
Acute non-granulamatous—Idiopathic, trauma, ankylo-
sing spondylitis, IBD, Reiter’s, glaucomatocyclitic crisis,
postoperative, uveitis—glaucoma—hyphema syndrome,
Behcet’s, anterior segment ischaemia, viral (mumps,
influenza, adenovirus), drugs (sulfa, rifabutin, cidofovir,
etc. chlamydia/rickettsia).
Chronic granulomatous—Sarcoidosis, syphilis, tubercu-
losis
Chronic non-granulomatous—Juvenile rheumatoid arth-
ritis, Fuch’s herterochromic iridocyclitis.
Treatment
• Cycloplegics—Cyclopentolate 1%, 2%, scopolamine
0.25%
• Topical steroids—Prednisolone acetate—1%
• Periocular repository steroids—Methylprednisolone 40-
80 mg, subtendon.
• Antiglaucomatous medications if there is associated
glaucoma.
• Treatment of primary cause.
Uveitis 35
2. Posterior uveitis
• Blurred vision, floaters, occasionally pain, redness
and photophobia
• White blood cells and opacities in vitreous, retinal
and choroidal infiltrates, edema, vascular sheathing.
• Retinal haemorrhage or exudates, disc swelling,
features of anterior segment inflammation may be
present.
• Glaucoma, cataract, choroidal neovascularization or
retinal detachment may develop.
• Common etiological factors include (1) toxoplasmosis
(fuzzy yellow white retinal lesion) (2) sarcoidosis
(white yellow motton-fat exudates in retina and
vitreous, sheathing around retinal vein, white nodu-
les in vitreous and retina) (3) syphilis (4) pars
planitis (bilateral vitritis in young patient with snow
ball exudates over ora serrata and pars plana) (5)
CMV, candida, etc. in AIDS.
• Less common causes include (1) acute posterior
multifocal placoid pigment epitheliopathy (AMPPE)
(2) acute retinal necrosis (3) Krill’s disease (acute
retinal pigment epithelitis) (4) Behcet’s disease (5)
Bird shot retinochoroidopathy. (6) embolic (septic)
retinitis (7) serpiginous choroidopathy (8) toxocaria-
sis (9) tuberculosis (10) Whipple’s disease.
• Should be differentiated from (1) reticulum cells sar-
coma with retinal infiltration (2) malignant mela-
noma (3) retinitis pigmentosa (4) rheumatogenous
retinal detachment (5) posterior scleritis (6) asteroid
hyalosis.
• Treatment is according to etiology. Toxoplasmosis is
treated, with pyrimethamine 200 mg orally loading
followed by 25 mg PO twice daily with folinic acid
10 mg orally twice weekly combined with sulfadia–
zine 2 gm loading, then 1 gm qid; clindamycin 450-
600 mg qid can replace sulfa; atovaquone is equally
effective. Oral steroids can be added. Anterior seg-
ment inflammation is treated with cycloplegics and
topical steroids. The above treatment stands good for
immunocompromised with ocular toxoplasmosis
but in immunocompetent patients mild peripheral
retinochoroiditis does not need antitoxoplasma treat-
ment except for topical cycloplegics and steroids.
Ocular sarcoidosis needs cycloplegics, topical

and oral steroids (periocular steroids also)
Parsplanitis does not need treatment unless
vision is grossly low due to cystoid macular edema
or vitreous opacities when topical steroid or
periocular repository steroid or oral steroid may be
warranted. Pan vitrectomy and cryotherapy are
reserved for special cases.
3. Acute retinal necrosis
• Blurred vision, ocular pain, photophobia.
• Multiple white opaque patches of thickened retina,
bilateral in one-third.
• Vitreous and anterior chamber reactions, ↑ IOP, optic
disc edema, rheumatogenous retinal detachment in
two-third.
• HIV, CMV, toxoplasma are potent risk factors.
• Treatment is with acyclovir IV, then orally, anti-
platelet therapy (aspirin), anticoagulants (heparin),
laser photocoagulation, pars plana vitrectomy and
optic nerve sheath decompression surgery.
4. Reticuluar cell sarcoma (large cell lymphoma)
• Painless bilateral decrease in vision, usually no
history of uveitis.
• Large amount of vitreous cells and debris in older
patients.
• Yellow white chorioretinal or subretinal pigment,
epithelial infiltrate, retinal edema/haemorrhages.
5. Postoperative uveitis
• Postoperative inflammation is typically mild to
moderate, usually resolving within 6 weeks
• It can be severe immediately after surgery as infec-
tious endophthalmitis, phacoanaphylactic endoph-
thalmitis or aseptic endophthalmitis.
• Persistent infection (beyond 6 weeks) is due to too
rapid tapering of steroid drops/non-compliance,
UGH syndrome, sympathetic ophthalmia, infection
with Propioni Bacterium Acne, in growth of conjunc-
tival/corneal tissue.
• Patients complain sudden onset of progressive
decrease of vision, redness and increasing eye pain.
• Examination reveals intense flare and cells in ante-
rior chamber and vitreous and reduced red reflex.
Uveitis 37
• Delayed onset of endophthalmitis can be due to

fungi (aspergillus > candida), Propionobacterium acne
and may need specific therapy after vitrectomy, i.e.
topical natamycin 5% and IV amphotericin B or oral
flucytosine.
• Traumatic endophthalmitis occurs due to staph.
epidermidis, streptococci and often mixed organism.
They may have proptosis, high fever and corneal
abscess. CT scan and US are essential to exclude
retention of intraocular FB. Systemic antibiotic
(gentamicin) along with intravitreal antibiotic are
the answers combined with pars plana vitrectomy.
Steroids should not be used till fungi are excluded.
• Endogenous bacterial endophthalmitis is caused by
Bacillus cereus, Streptococci, N. meningitides, S. aureus,
etc. Iris microabscess, absent fundus red reflex, reti-
nal inflammatory infiltrate, corneal edema are
common. Panophthalmitis with proptosis and res-
tricted ocular motility may develop. IV drug abusers
who are predisposed to Bacillus cerius infection are
treated with aminoglycoside, for other infections
suitable broadspectrum antibiotic is given. Topical
steroids are used depending upon degree of anterior
segment inflammation; intravitreal antibiotic and
vitrectomy may be required.
• Phacoanaphylactic endophthalmitis is a sterile auto-
immune inflammatory reaction to exposed lens
protein. It occurs after surgical, traumatic or
spontaneous disruption of lens capsule. The anterior
segment inflammation is more with hypopion and
mutton fat keratic precipitates. IOP may be raised;
pain, photophobia, red eye and decreased vision are
usual. Topical and subconjunctival steroids and
even systemic steroids be prescribed liberally and
after inflammation subsides residual lens material
and capsule be removed.
7. Sympathetic ophthalmia
It follows penetrating injury to one eye or surgical pro-
cedure in one eye. The other eye has pain, photophobia,
decreased vision. These features occur within 1 year in
90% cases. The traumatized eye also develops such
features. Bilateral severe anterior chamber reactions,
mutton fat keratic precipitates, Dalen-Fuch’s nodules on
retina, and thickening of uveal tract are usual. Nodular

infiltration of iris, neovascularisation of iris, exudative
vetinal detachment, papillitis can be seen.
• The earliest sign may be loss of accommodation.
• Enucleation of a blind traumatized eye before
sympathetic reaction develops in best. If sympathetic
ophthalmia develops enucleation still may be
beneficial.
• Inflammation is controlled with steroids, the dose
depending upon severity of inflammation. When
steroid is ineffective or contraindicated, methotrexate
or cyclosporin may be tried.
7 Retinal Diseases
1. Central retinal artery occlusion.

• It is due to embolism (from heart, carotids),
thrombosis, giant cell arteritis or collagen vassular
disease, hypercoagulation disorders.
• Symptoms are unilateral painless, sudden visual
loss
• Whitening of retina in the posterior pole and a
cherry red spot in center of macula
• Marked afferent pupillary defect, segmentation of the
blood column in arterioles, cilioretinal artery,
sparing of the foveola is evident.
• When visual acuity, light perception are less,
strongly suspect ophthalmic artery occlusion.
• Exclude other causes of cherry red spots like Tay-
Sach’s or other storage diseases (present in early life,
usually bilateral).
• Diagnosis confirmed by fluorescein angiogram, ERG
or both
• Treatment is by immediate ocular massage, anterior
chamber paracentesis and measures to reduce IOP.
• When giant cell arteritis is suspected from very high
ESR, high dose systemic steroid be started.
• Carotid Doppler evaluation and cardiac evaluation
with Echo and Holter are also warranted.
• Branch retinal artery occlusion (BRAO) can occur
due to similar causes as CRAO.
• Visual loss is of partial visual field, with whitening
and edema of affected retina with appearance of
cotton wool spots.
• When BRAO is accompanied by optic nerve edema
or retinitis serologic testing be done to rule out
catscratch disease (Bortonella henselale), syphilis,
toxoplasmosis.
• No ocular therapy is of proven value. Ocular
massage and anterior chamber paracentesis may
dislodge a cholesterol embolus (bright refractile

crystal at bifurcation).
2. Central retinal vein occlusion (CRVO)
• CRVO can be (1) ischaemic >10 cotton-wool spots,
extensive retinal haemorrhage, (2) non-ischaemic—
mild fundus changes, no afferent pupillary defect,
better visual acuity.
• Etiologic factors include (1) atherosclesosis (2) hyper-
tension (3) glaucoma (4) optic disc disease (5) hyper-
coagulation state (6) retrobulbar external compres-
sion (7) optic disc edema.
• Patient has painless visual loss, disc edema and
haemorrhages, neovascularization of the optic disc,
retina and iris.
• Radiation retinopathy and diabetic retinopathy need
exclusion
• It is important to distinguish ischemic from non-
ischemic CRVO. Presence of relative afferent
pupillary defect, visual field constriction and poor
visual acuity speak of ischemic CRVO.
• Treatment is that of underlying disorder, aspirin 325
mg PO daily, reduction of IOP if raised, photocoagu-
lation if neovascularization is present.
3. Branch retinal vein occlusion (BRVO)
• Diseases of adjacent arterial wall (usually due to
hypertension, arteriosclerosis, diabetes) compress
the venous wall at crossing point to cause BRVO.
• Superficial haemorrhages, cotton wool spots, retinal
edema, dilated and tortuous veins, retinal neovas-
cularisation are the findings.
• Treatment is that of underlying disease, photocoagu-
lation may be needed if there is retinal neovasculari-
sation, or chronic macular edema.
4. Amaurosis fugax
• It is monoocular visual loss lasting for seconds to
minutes due to vascular insufficiency or embolism
to retinal artery from carotids, aorta or heart.
• Other features of ocular ischemic syndrome (dilated
veins, dot-blot haemorrhage, neovascularization of
iris, retina) may be evident.
• Exclude carotid/ heart disease, stop smoking
• Aspirin prophylaxis
Retinal Diseases 41
5. Central serous chorioretinopathy

• Usually idiopathic, age group 25-50 years.
Exogenous/endogenous cortisol may have a role in
causation.
• Blurred or dim vision, objects appear distorted and
miniature in size, colours appear washed out,
central scotoma, usually unilateral.
• Retinal detachment at macula without blood / lipid
exudates, the margins of detachment are sloping and
merge gradually into the surrounding retina.
• Should be differentiated from age related macular
degeneration, rhegmatogenous RD (a hole in retina
can be seen), pigmental epithelial detachment
(margin very distinct), choroidal tumor .
• Treatment (laser photocogulation) is only needed when
(1) spontaneous recovery is delayed to beyond 6 months
(2) recurrence of the condition in an eye that sustained
a permanent deficit from previous episode.
6. Optic pit
• Isolated pits are asymptomatic, small round depres-
sion, usually hypopigmented in the nerve tissue of
optic disc. Majority are temporal but one-third are
central.
• May develop localized retinal detachment, exten-
ding from disc to macula.
• Acquired pits (pseudo pit) some times seen in
patients of low tension glaucoma or primary open
angle glaucoma
• Isolated pits need no treatment, when associated
with serous retinal detachment laser photocoagu-
lation is required.
7. Age related macular degeneration (ARMD)
• Can be exudative or non-exudative; always occur
beyond 50 years.
• Non-exudative form—gradual loss of central vision,
macular drusen, retinal pigment epithelial atrophy,
bilateral confluent retinal and choriocapillaries
atrophy. No treatment available but antioxidants may
be tried.
• Exudative form – distorsion of straight lines or
edges, rapid onset of visual loss. Choroidal neovas-
cular membrane (CNVM), subretinal haemorrhages
exudates, disciform scar.
• Advanced age, high myopia, systemic hypertension,

smoking are the risk factors for both the forms.
• Diseases associated with CNVM are ocular histo-
plasmosis syndrome, angioid streaks, high myopia,
traumatic choroidal rupture, inflammatory chorio-
retinal lesions.
• Fluorescein angiogrpahy be performed immediately
when CNVM is suspected and photocoagulation be
done. Argon green and krypton red laser are equally
good but krypton red is preferred for juxtafoveal
CNVM.
8. Angioid streaks
• Half the cases are associated with systemic diseases
like pseudoxanthoma elasticum, Paget’s disease,
sickle cell disease, Ehlers-Danlos syndrome and half
are idiopathic.
• Usually asymptomatic but vision may decrease due
to CNVM.
• Bilateral reddish-brown or gray bands deep in retina
radiating in spoke line pattern from optic disc; peau-
d-orange appearance of fundus , retinal pigmentary
changes in macula.
• Should be distinguished from myopic chorioretinal
degeneration and choroidal rupture.
• Careful examination of macula with slit lamp and
Hruby 60-90 D fundus contact lens can show
CNVM, else fluorescein angiogram be done.
• Treatment is with laser photocoagulation
9. High myopia
• Myopic crescent around fundus separated from
fundus by a pigmented line; tilting of optic disc,
macular pigmentary abnormalities, Fuch’s
hyperpigmented spot in macula, myopia in excess
of 6 D and axial length > 26 mm.
• Temporal optic disc pallor, posterior staphyloma,
peripheral retinal thinning, lattice degeneration,
choroidal sclerosis and atrophy; CNVM and retinal
detachment may occur.
• Should be differentiated from ARMD, ocular histo-
plasmosis, toxoplasmosis and gyrate atrophy
• Symptomatic retinal breaks be treated with photo-
coagulation, cryo or scleral buckling surgery, CNVM
be treated with photocoagulation.
Retinal Diseases 43
10. Ocular histoplasmosis syndrome

• Classic triad: (1) histo spots, i.e. yellow—white
punched out round spots deep in retina (2) CNVM
(3) atrophy or scarring adjacent to optic disc.
• Should be differentiated from ARMD, high myopia.
• Antifungal treatment not helpful, laser photocoagu-
lation of CNVM be done.
11. Cystoid macular edema
• It occurs in diabetic retinopathy, following ocular
surgery including laser, CRVO, uveitis, retinitis
pigmentosa, Eale’s disease, Coat’s disease (retinal
telangiectasis), ARMD and pseudocystoid macular
edema (no leakage in FA as in nicotinic acid
maculopathy)
• Decreased vision; blurring or irregular foveal light
reflex, thickening with intraretinal cysts in fovea.
• Loss of choroidal vascular pattern underlying
macula, vitreous cells
• FA shows early leakage of dye out of perifoveal
capillaries (flower petal/spoke wheel pattern).
• Treatment is with topical NSAID (ketorolac), topical/
systemic steroids, acetazolamide PO can be added.
12. Macular Hole
• May be caused by trauma, cystoid macular edema,
epiretinal traction on retina, can be partial thickness
or whole thickness.
• Decreased vision, distorted vision.
• Round red spot in the center of macula ; small yellow
precipitates within the hole.
• In selected cases vitrectomy may be beneficial
13. Epiretinal membrane
• Though mostly idiopathic can be due to rhegmato-
genous retinal detachment, after retinal cryo/ photo-
coagulation, trauma, uveitis, diabetic retinopathy,
retinal vascular disease.
• Decreased or distorted vision or both; fine glistening
membrane to thick gray-white membrane present on
macular area.
• Retinal folds radiating out from membrane, displace-
ment or straightening of retinal vessels, macular
edema.
• Treatment is that of underlying disorder, surgical pee-
ling is required when vision is seriously hampered.
14. Retinal breaks

• Predisposing factors are lattice degeneration, high
myopia, aphakia, pseudoaphakia, vitreoretinal tufts,
age related retinoschisis.
• Acute retinal break presents with flashes of light,
floaters and blurred vision, chronic retinal break is
usually asymptomatic.
• Associated findings include pigment cells in anterior
vitreous, vitreous haemorrhage, retinal flaps. In
chronic retinal break a ring of pigmentation around
the break.
• Treatment is with laser, cryo, scleral buckling for
acute symptomatic break, asymptomatic break of >
1.5 mm/in aphakic/pseudoaphakic eye.
15. Retinal detachment (RD)
• Can be of three types: rhegmatogenous, exudative
and traction types. In all the forms there is elevation
of retina.
• Flashes of light, floater or curtain or shadow moving
the field of vision, visual loss in rhegmatogenous
RD, minimal to severe visual loss or visual field
defect in exudative form and tractional forms.
• Associated signs—pigmented cells in anterior
vitreous, vitreous haemorrhage, posterior vitreous
detachment, low IOP, clear subretinal fluid that does
not shift with body position, corrugated appearance
of the detachment—all to rhegmatogenous RD.
• Traction leading to RD results from proliferative
retinopathy (diabetes, sickle cell anaemia, retino-
pathy of prematurity), etc.
• All forms of RD be distinguished from retinoschisis,
(age related and juvenile)
• Patients with acute RRD or TRD that threatens fovea
be given bed rest and surgical repair be performed
immediately.
• For ERD, treatment of underlying condition leads to
resolution of detachment.
16. Retinoschisis
It is splitting of retina and is of two forms (i) X-linked
recessive (ii) age-related. In the former there is cystoid
retinal changes with radiating retinal folds from fovea.
In latter retinal splitting is bilateral, occurs at the level
of outer plexiform layer with sheathing of retinal vessels.
Retinal Diseases 45
Both the forms are either asymptomatic or have

decreased vision. Retinal detachment may occur in both
and needs treatment.
17. Choroidal detachment
It can be serous or haemorrhagic and can also be post-
operative or traumatic. Patients are either asymptomatic
or have decreased vision. Pain occurs when the
choroidal detachments are touching and red eye occurs
in haemorrhagic form. The smooth bullous orange,
brown elevation of retina and choroids can be seen. IOP
is low in serous form with shallow anterior chamber but
IOP is raised in haemorrhagic form with cells and
aqueous flare in anterior chamber.
General treatment is with cycloplegics, and topical
steroids. Surgical drainage of suprachoroidal fluid may
be done if anterior chamber depth continues to remain
low. In haemorrhagic form anterior vitrectomy may be
required.
18. Vitreous haemorrhage
• Vitreous haemorrhage occurs in diabetic retinopathy,
retinal vein occlusion, vitreous detachment, ARMD,
trauma, sickle cell disease, intraocular tumour,
subarachnoid bleed, Eale’s disease, etc.
• Patients have sudden painless loss of vision or
sudden appearance of black spots with flashing
lights.
• When bleeding is significant, the red fundus reflex
may be absent
• It should be differentiated from vitritis and RD.
• Since retinal break is very often associated, it should
be excluded by ultrasound.
• Vitrectomy be performed when there is RD, neo-
vascularization of iris, ghost cell glaucoma, chronic
vitreous haemorrhage or bilateral involvement.
19. Retinitis pigmentosa
• Can be AD, AR and sex-linked recessive.
• Patients have difficulty in night vision, and loss of
peripheral vision
• Clumps of pigment dispersed throughout retina in
perivascular pattern, ring scotoma, atrophy of retinal
pigment epithelium, arterial narrowing.
• Hereditary retinal degeneration also occurs in beta-

lipoproteinemia, Refsum’s disease and Kearn’s Sayre
syndrome
• Pseudoretinitis pigmentosa occurs in phenothiazine
toxicity, syphilis, congenital rubella.
• Night blindness also occurs in gyrate atrophy,
choroidoremia, vitamin A deficiency, congenital
stationery night blindness (paradoxic pupillary
response).
• No treatment is known.
20. Choroidoremia
It is X-linked recessive manifesting as night blindness
in males of 4-30 years followed by loss of peripheral
vision. Women who are otherwise asymptomatic have
salt pepper fundus. The choroidal pigment is dispersed
throughout sparing the macula ending up in total
loss of retinal pigment epithelium and choroidal
atrophy.
• ERG and fluorescein angingraphy are diagnostic
• No effective treatment is known.
21. Gyrate atrophy
It is autosomal recessive. There are sharply defined areas
of choreoretinal atrophy separated from each other by
thin margins of pigment. Ornithine levels are markedly
increased in body fluids. Common other findings are
high myopia, posterior subcapsular cataract, optic disc
pallor and narrowing of vessels. Night blindness and
decreased vision are the principal complaints.
• Arginine restricted diet and B6 supplement may
help.
22. Cone dystrophies
• Inheritance is sporadic, AR, AD and even X-linked.
Symptoms are slowly progressive bilateral visual
loss, photophobia and poor colour vision. Vision is
worse during day than night.
• In early disease only ERG is abnormal. In late
disease there is bull’s eye macular appearance in FA
and atrophy of RPE.
• Nystagmus, temporal pallor of optic disc, pigment
clumping in macular area can be seen.
• There is no proven treatment but miotic drops during
day may improve vision and reduce photophobia.
Retinal Diseases 47
23. Stargardt’s disease

• An autosomal disease presenting with bilateral
decrease in vision starting in childhood.
• A relatively normal appearing fundus except for
heavily pigmented RPE/yellow–white fleck like
deposits at RPE or atrophic macular degeneration.
(beaten metal appearance, pigment clumping).
• FA shows silent choroids or midnight fundus due
to increased lipofuscin in the RPE cells.
• No treatment is known.
24. Drugs and retina
• High dose phenothiazines cause retinal depigmen-
tation, oedema, pigment clumping and depressed or
extinguished ERG. Blurred vision, brownish vision
and difficulty in night vision are usual.
• With chlorpromazine there is an additional abnor-
mal pigmentation of eyelid, cornea, conjunctiva,
anterior lens capsule, cataract (anterior and posterior
subcapsular).
• In chloroquine toxicity there is loss of foveal reflex
with bull’s eye macula (total chloroquin commula-
tive dose > 300 gm) and once ocular toxicity
develops—drug withdrawal does not affect it.
25. Best’s disease
It is autosomal dominant. Patients are asymptomatic or
have decreased vision, usually bilaterally. Yellow round
subretinal lesions likened to egg yolk in fovea are
characteristic but with normal ERG but abnormal EOG.
The lesions may degenerate and macular-choroidal
neovascularization, haemorrhage and scarring may
occur mimicking age related macular degeneration. No
form of treatment is known.
8 Cataract
Opaqueness of lens or its capsule is called cataract.

Cataract can be due to senility, ocular trauma, toxic
agent, (steroids, antipsychotics), radiation, uveitis,
degenerative ocular disease (retinitis pigmentosa), intra-
ocular tumor (ciliary body malignant melanoma), sys-
temic disease (diabetes, hypocalemia, Wilson’s disease,
myotonic dystrophy, atopy, Down’s syndrome).
Types of Cataract
a. Nuclear—yellow or brown discoloration of central
part of lens on slit lamp examination. Typically blurs
distance vision more than near vision.
b. Cortical—radial or spoke like opacities in the lens
periphery that expand to involve anterior and poste-
rior lens. Often asymptomatic, until the changes
develop centrally.
c. Posterior subcapsular—opacities appear near posterior
aspect of the lens, forming a plaque, best seen in
retroillumination. Glare and reading difficulty are
common; may be associated with ocular inflam-
mation, trauma, diabetes, steroid or radiation.
Occurs in people < 50 years of age.
• Symptoms are slowly progressive visual loss, glare
while driving at night, reduced color perception, the
symptoms depend upon location and density of the
lens opacity.
• Retina appears indistinct on fundoscopy, dilated red
reflex is dim on retinoscopy. The patient may be
found to be more myopic than previously noted
(second sight).
• Besides investigation to know of the etiology (i) a
dilated slit lamp examination by using direct and
retro illumination (ii) B scan ultrasound to see for
posterior segment pathology and (iii) potential
acuitymeter or laser inferometry to estimate the visual
potential are mandatory.
Cataract 49
• Near vision is often the most accurate manner of

evaluating macular function if the cataract is not too
dense.
• Indications of cataract surgery include (i) improve-
ment of visual disability, (ii) treatment of lens related
glaucoma/uveitis, (iii) to facilitate management of
ocular disease (to monitor or treat diabetic retino-
pathy/glaucoma).
• Patients who refuse surgery, a trial of mydriasis with
scopolamine 0.25% daily may be used.
1. Congenital cataract
• Though mostly idiopathic, can be familial (AD) and
due to galactosemia.
• Persistent hyperplastic primary vitreous, rubella
(salt pepper chorioretinitis), Lowe’s syndrome, hypo-
calcemia, hypoparathyroidism, etc.
• Presentation is with white fundus reflex, absent red
pupillary reflex, and often nystagmus, strabismus.
• Types of congenital cataract can be: (i) polar (opacity
of the lens capsule and adjacent anterior/posterior
pole), (ii) zonular or lamellar (onion skin like alter-
nating clear and white cortical lamella), (iii) nuclear,
(iv) posterior lenticonus (most common cause of non-
traumatic acquired cataract).
• Cataract extraction be expeditiously done to prevent
amblyopia; after cataract extraction, amblyopia be
treated in all below 9 to 11 years. Unilateral cataracts
that are not large enough to obscure visual axis may
still result in amblyopia.
2. Lens subluxation/dislocation
• Trauma is the most common cause. When more than
25 per cent of zonular fibers are ruptured dislocation
occurs. Other responsible factors are: Marfan’s syn-
drome, (superiorly and temporally) homocystinuria
(inferiorly and nasally), Weill-Marchesani syndrome,
high myopia, hypermature cataract, syphilis, Ehler’s
Danlos syndrome, Crouzon’s syndrome, etc.
• Patient has decreased vision, double vision (mono-
ocular diplopia), iridodonesis.
• Some have marked astigmatism, cataract, glaucoma,
acquired high myopia, asymmetry of anterior
chamber depth.
• Lens can dislocate to anterior chamber or into

vitreous. In anterior chamber dislocation the lens can
be repositioned with head manipulation. It may be
necessary to indent the cornea after topical
anaesthesia. After repositioning pupil is constricted
with pilocarpine with peripheral iridectomy.
• If dislocated into vitreous, lens capsule is broken, eye
is inflamed—the lens be extracted but when lens
capsule is intact, and patient is asymptomatic-only
observation suffices.
• In subluxation with high uncorrectable astigmatism
or monocular diplopia—surgical removal of lens is
required.
3. Albinism
• Albinism can be ocular or oculocutaneous (hair, skin
and eye). Ocular albinism is X-linked recessive,
patients have decreased vision and photophobia;
nystagmus, iris transillumination defects, visible
choroidal vasculature, pink reflex though an
undilated pupil are the other findings. The only
reliable ocular finding present in all patients is foveal
hypoplasia.
Patients of albinism often have associated platelet
dysfunction or white blood cell dysfunction, thus
predisposing to easy bruise and infection.
• Albinism with strabismus rarely achieve binocularity
after strabismus surgery and also do poorly after
retinal detachment repair because of nystagmus and
inherently weak retinal pigment epithelium.
• There is no effective treatment for albinism but tinted
glass use reduces photophobia.
4. Leukocoria
A white pupillary reflex is called leukocoria. It can be
due to (i) retinoblastoma, (ii) toxocariasis, (iii) Coat’s
disease, (4) persistent hyperplastic primary vitreous, (v)
congenital cataract, (vi) retinal astrocytoma, (vii)
retinopathy of prematurity, (viii) myelinated nerve fiber,
(ix) retinochoroidal coloboma, (x) incontinenti pigmenti
(xi) retinal detachment, (12) familial exudative vitreo-
retinopathy.
Retinoblastoma appears as a white nodular mass
extending into vitreous (endophytic), as a mass lesion
underlying retinal detachment (exophytic) or as a
Cataract 51
diffusely spreading lesion simulating uveitis. Iris

neovascularisation is common. Pseudohypopion and
vitreous seeding may occur. May often be bilateral and
multifocal. Enucleation, irradiation, photocoagulation,
cryotherapy, chemoreduction, chemotherapy are
employed for local disease and systemic chemotherapy
for metastatic disease.
Toxocariasis may appear as a localized, white
elevated granuloma in the retina or as diffuse endopht-
halmitis. Traction, retinal detachment and vitreous
bands are usual. Anterior chamber aspirate yields
eosinophils. Treatment is with steroids. The nematode
if visible can be killed by laser. Vitrectomy is employed
for vitreal traction bands.
Coat’s disease is a retinal vascular anomaly resulting
in small multifocal outpouching of retinal vessels asso-
ciated with yellow intraretinal and subretinal exudates.
The exudative retinal detachment may account for
leukocoria. Boys in first two decades of life are affected.
Laser photocoagulation and /or cryotherapy of leaking
vessels are required.
Persistent hyperplastic primary vitreous (PHPV) is a
fibroglial and vascular proliferation in the vitreous.
Associated findings include glaucoma, cataract, fibro-
vasular membrane behind the lens and retinal
detachment. Treatment is of cataract extraction, vitreal
membrane excision.
Condition of aphakic eyes
• Hypermetropic
• Loss of accommodation
• Astigmatism due to corneal scar
• Retinal image of aphakic eye is 25% larger after
correction
• ↓ visual field
• Prismatic effect due to thick glasses
Clinical investigations in squint
• Cover test
• Hirschberg test
• Prism vergence test
• Madox rod and wing test
• Hess screen test
• Diplopia goggles
• Major amblyoscope
• After image test
9 Retinopathy of
Prematurity
It occurs in children born < 32 weeks gestation with

birth weight < 1250 gm, especially those receiving
supplemental oxygen. There is extraretinal fibrovascular
proliferation with retinal detachment (leukocoria)
bilaterally.
• Poor pupillary dilatation to mydriatics.
• In older children poor visual acuity, strabismus,
lattice vitreoretinal degeneration and retinal
detachment.
Stages of Disease
Stage I
• Flat demarcation line separating vascular posterior
retina from avascular peripheral retina.
Stage II
• Ridged demarcation line
Stage III
• Ridged demarcation line with extraretinal fibro-
vascular proliferation.
Stage IV
A Extrafoveal retinal detachment
B Subtotal retinal detachment involving macula
Stage V
• Total retinal detachment
Plus Disease
Engorged veins and tortuous arteries in posterior pole.
Treatment
Stage I & II No treatment
Stage III Laser photocoagulation or cryotherapy
Stage IV, V Surgical repair of retinal detachment
10 Pupil
1. Anisocoria
• Abnormal pupil is constricted—iritis, Horner’s
syndrome, long-standing Adie’s pupil.
• Abnormal pupil in dilated—iris rupture, Adie’s tonic
pupil, third nerve palsy.
2. Argyl Robertson pupil
• Small irregular pupils, reacting poorly to light but
constrict normally during accommodation; vision is
normal.
• Do not dilate well with myedriatics.
• Usually due to tertiary syphilis
• Other causes of light near dissociation be excluded
like (i) bilateral optic neuropathy (ii) Adie’s tonic
pupil (iii) Perinaud’s syndrome.
3. Adie’s tonic pupil
• Irregularly dilated pupils, no reaction to light, slow
constriction to convergence and slow radilatation.
Typically unilateral at first; supersensitive to
cholinergics normal dilatation with mydriatics.
• Deep tendon reflexes often absent (Adie’s syndrome)
• Mostly idiopathic but can follow orbital trauma
diabetes, autonomic neuropathy, Guillain-Barre
syndrome.
4. Convergence insufficiency (CI)
• Often idiopathic, but can follow illness, uveitis,
trauma,
• Inability to maintain fusion; hence eye discomfort
headache, blurred vision after near work, common
to teenagers and young adults.
• Should be differentiated from accommodative
insufficiency (AI) in which symptoms develop after
20-40 minutes of reading, patients have normal
fusional capacities. When 4D base in prism is placed
in front of eye while reading, the print blurs in AI
but becomes clearer in CI. Patients of AI benefit from

reading glasses but not patients of CI.
• Treatment is with near point exercises, e.g. pencil
push ups and with base-out prism or combination
of both. Those who do not improve with near point
exercises may improve with reading glasses with
base in prism.
5. Accommodative spasm
• Accommodative spasm is involuntary. It may occur
after prolonged reading/near work. Patient has
bilateral blurring of distant vision, headache and
eyestrain. Spasm of near reflex is associated with
excess accommodation, excess convergence and
miosis. Myopia after cycloplegic refraction is very
less incomparison to myopia without cycloplegic.
• It can also be manifestation of iridocyclitis and pseu-
domyopia (diabetes, forward displacement of lens).
• Treatment is with correction of refractive error, and
lens for near reading.
6. Hypotony syndrome
• It can be postsurgical, post-traumatic, ocular ischae-
mic syndromes, uveitis, systemic dehydration,
uremia, diabetes, etc.
• Diminished vision, IOP < 6 mmHg, corneal edema,
aqueous cells and flare, retinal edema, chorioretinal
folds, choroidal detachment, shallow anterior
chamber, appearance of optic disc swelling.
• Treatment is according to etiology.
11
Differential Diagnosis
of Ocular Symptoms
and Signs
1. Decreased vision
Transient (lasting upto 24 hours) amaurosis fugax
(embolism/low flow) as in vertebrobasilar insufficiency
(bilateral), TIA (unilateral), migraine, giant cell arteritis,
ischaemic optic neuropathy.
Persistent (lasting beyond 24 hours)
a. Sudden and painless—retinal artery/vein occlusion,
ischemic optic neuropathy, retinal detachment,
vitreous haemorrhage, optic neuritis (painful eye
movement), occipital infarction.
b. Gradual painless loss—cataract, glaucoma, retinal
disease
c. Painful loss—acute congestive glaucoma, uveitis,
corneal hydrops (keratoconus).
2. Distorted vision
Refractive error, macular disease, corneal irregularity,
cataract, migraine, retinal detachment.
3. Double vision
Monocular: Refractive error, corneal opacity/irregularity,
cataract, lens dislocation, RD, macular disease, malin-
gering.
Binocular:
Intermittent—Myasthenia gravis
Constant: Isolated III,IV,VI, disease, thyroid eye disease,
superior orbital fissure syndrome, postocular surgery.
INO, orbital trauma, vertebrobasilar insufficiency.
4. Flashes of light
Retinal break, RD, posterior vitreous detachment,
occipital lobe disease, retinitis
5. Halos around light
Cataract, acute congestive glaucoma, corneal edema due
to endothelial dystrophy, bullous keratopathy, digitalis/
chloroquine.
6. Night blindness
Refractive error (myopia), advanced glaucoma, retinitis
pigmentosa, drugs (phenothiazines, chloroquine),
vitamin A deficiency, gyrate atrophy, choroideremia.
7. Photophobia
Corneal disease, anterior uveitis, abinism, aniridia,
retrobulbar neuritis.
8. Spots in front of eyes
Migraine, posterior uveitis, vitreous haemorrhage,
posterior vitreous detachment, RD, corneal opacity.
9. Hypopion
Corneal ulcer, endophthalmitis, severe iritis, IOL
reaction, intraocular tumor necrosis (retinoblastoma).
10. Corneal crystals
Schnyder’s crystalline dystrophy, multiple myeloma,
cystinosis, gout, uremia, hypergammaglobulinemia,
drugs (indomethacin, chloroquine), infectious crystalline
keratopathy.
11. Corneal edema
Congenital: Congenital glaucoma, congenital hereditary
endothelial dystrophy, posterior polymophous dystro-
phy.
Acquired: Bullous keratopathy, Fuchs’ endothelial dys-
trophy, acute congestive glaucoma, acute keratoconus,
HSV, PPMD, iridocorneal endothelial syndrome.
12. Enlarged corneal nerves
MEN IIb, keratoconus, keratitis, neurofibromatosis,
Refsum’s syndrome. Leprosy, Fuch’s endothelial
dystrophy.
13. Membranous conjunctivitis
Streptococcal, pneumococcal, diphtheria, HSV, adeno-
virus.
14. Opaque cornea in infancy
Congenital glaucoma, endothelial/stromal dystrophy,
PPMD, mucopolysaccharidoses, interstitial keratitis,
corneal dermoid, sclerocornea.
15. Pannus
Trachoma, phlycten, staphylococcal hypersensitivity,
vernal keratoconjunctivitis, HSV.
Differential Diagnosis 57
16. Pigmentation of conjunctiva

Nevus, melanoma, Addison’s disease, pregnancy,
radiation, chlorpromazine.
17. Whorl like opacity in corneal epithelium
Amiodarone, chloroquine, phenothiazine,
indomethacin.
18. Ptosis
Congenital, myasthenia gravis, Horner’s syndrome,
third nerve palsy, chronic external progressive ophthal-
moplegia, prolonged topical steroid use.
19. Bull’s eye macular lesion
ARMD, cone dystrophy, chloroquine retinopathy.
20. Choroidal folds
Choroidal tumor, thyroid orbitopathy, orbital inflam-
matory pseudotumor, hypotony, RD, papilledema.
21. Choroidal neovascularization
ARMD, high myopia, angioid streaks, Drusen of optic
nerve head, histoplasmosis.
22. Cotton wool spots
Retinopathy, AIDS, hypertension, collagen vascular
disease, retinal artery/vein occlusion, anaemia, leuke-
mia, lymphoma.
23. Macular exudates
Diabetes, hypertension, Coat’s disease, retinal vein
occlusion, papilledema.
24. Decrease vision with normal fundus
Retrobulbar optic neuritis, Stargardt’s disease, alcohol/
tobacco amblyopia.
25. Retinal neovascularization
Diabetes, CRVO, sickle retinopathy, sarcoidosis, retino-
pathy of prematurity, Eale’s disease.
26. Roth spots (haemorrhages with white centers)
Leukemia, septic chorioretinitis, diabetes, sickle cell
disease, SLE.
27. Sheathing of retinal veins (Periphlebitis)
Syphilis, sarcoidosis, pars planitis, sickle cell disease,
tuberculosis, multiple sclerosis, Eale’s disease, Behcet’s
disease, fungal/AIDS retinitis.
28. Optic atrophy

Glaucoma, CRAO/CRVO, ischaemic optic neuropathy,
optic neuritis, chronic papilledema, compression of optic
nerve, syphilis, retinitis pigmentosa, Leber’s optic atrophy.
29. Paradoxic pupillary reaction (dilating in light,
constricting in darkness)
Congenital night blindness, cone dystrophy, optic
neuritis.
30. Extraocular muscle thickening in CT
Thyroid orbitopathy, orbital inflammatory pseudotumor,
carotid cavernous fistula, cavernous haemangioma,
rhabdomyosarcoma (children).
31. Shallow anterior chamber
Pupillary block, glaucoma, syprachoroidal haemor-
rhage, malignant glaucoma (all with ↑ IOP), choroidal
detachment (↓ IOP).
32. Progressive hypermetropia
Orbital tumor, central serous chorioretinopathy,
posterior scleritis, hypoglycemia.
33. Progressive myopia
Cataract, diabetes, staphyloma
34. Altitudinal field defects
Ischemic optic neuropathy, glaucoma, optic nerve
coloboma.
35. Arcuate scotoma
Glaucoma, ischemic optic neuropathy, drusens, high
myopia.
36. Binasal field defects
Glaucoma, retinitis pigmentosa.
37. Bitemporal hemianopia
Chiasmal lesion, tilted optic discs.
38. Enlarged blind spot
Papilledema, glaucoma, optic nerve drusens, optic nerve
coloboma, medulllated nerve fibers.
39. Central scotoma
Macular disease, optic neuritis, ischemic optic neuro-
pathy, optic atrophy.
Differential Diagnosis 59
40. Vitreous opacities

Asteroid hyalosis, haemorrhage, vitritis, snow ball
opacities of pars planitis/sarcoidosis, vitreous dege-
neration.
12 Ocular Trauma
1. Chemical burns
Includes alkalies (cements, plasters, detergents), acids,
solvents. This is an emergency. Eyes need copious irri-
gation with saline/ringer lactate for atleast 30 minutes
or till neutral pH is achieved. Patient might have
sustained corneal burn which may be mild to moderate
or severe. In mild form there is SPK or superficial
epithelial loss with conjunctival chemosis, eyelid edema,
anterior chamber reaction. Patient be given topical
cycloplegics, topical antibiotic, and analgesics. In severe
burn cornea becomes opaque with no view of AC, iris
or lens, ↑ IOP and often local necrotic retinopathy. Such
patients need hospitalization, removal of corneal necro-
tic tissue and topical cycloplegics—antibiotic, steroids
along with antiglaucoma medication. Lysis of conjunc-
tival adhesions be done. Collagenase inhibitor, e.g.
acetylcystine 10-20%, cyanoacrylate tissue adhesive or
even corneal transplant may be required when cornea
is very thinned out or perforates.
2. Corneal abrasion
• Patients have sharp pain, photophobia, foreign body
sensation,
• There are conjunctival injection, lid swelling and
mild anterior chamber reaction.
• Fluorescein stains the epithelial defects
• Treatment is with antibiotic and cycloplegic oint-
ments, topical NSAIDS for pain control. When
corneal infiltrate is seen, culture is mandatory before
selecting antibiotics.
3. Hyphaema
Blood in anterior chamber is called hyphaema. The
blood may present as a clot, as layering or both. It may
be black or red, microhyphaema is visible with slit lamp.
The suspended RBC may give haziness to anterior
Ocular Trauma 61
chamber. Poor outcome is predicted when there is (1)

markedly reduced visual acuity (2) ↑ IOP uncontrollable
by medication (3) recent aspirin/ NSAID use (5) delayed
presentation.
Treatment is bed rest, head elevation, cycloplegics,
antiglaucoma medications (only beta blockers are safe
in hyphaema with sickle cell trait/disease). Aminocap-
roic acid upto 30 gm daily may be given in hospitalized
patient to contain bleeding. If there is no rebleed by 2
days aminocaproic acid dose is reduced by one half but
once fibrinolysis starts IOP is increased.
• Surgical evacuation of hyphaema may be indicated
when there is (1) corneal stromal blood staining (2)
significant visual deterioration (3) total filling of AC
with blood (4) persistent clot in angle for 7 days (5)
persistently raised IOP (> 50 mmHg for 5 days or
>35 mmHg for 7 days).
• Steroid drops if traumatic uveitis is superadded.
• All patients be closely followed up for angle
recession glaucoma.
• Spontaneous hyphaema occurs when there is
neovascularization of iris or AC angle as in diabetes,
ocular ischaemic syndrome, chronic uveitis.
• Postsurgical and microhyphaema are usually self
limited. Patients should avoid aspirin and NSAID.
4. Commotio retinae
This is confluent area of retinal whitening with undis-
turbed retinal vessels following ocular trauma. Patient
may be asymptomatic or has decreased vision. No treat-
ment is required as it clears but it should be differen-
tiated from retinal detachment and branch retinal artery
occlusion.
5. Choroidal rupture
There is yellow or white crescent-shaped subretinal
streak, usually concentric to optic disc. It may not appear
for several days to weeks after trauma. Patient is asymp-
tomatic or has decreased vision; choroidal neovascular
membrane (CNVM) may develop late. Fluorescein angio-
graphy can delineate CNVM and choroidal rupture.
CNVM can also be seen by slit lamp biomicroscopy with
either fundus contact or 60/90 D lens. CNVM needs
laser coagulation.
6. Orbital blow out fracture

Patient has pain, particularly on attempted vertical eye
movement, local tenderness, binocular double vision,
crepitus on nose blowing, restricted eye movement,
subcutaneous-subconjunctival emphysema, hypesthesia
on ipsilateral cheek and upper lip (infraorbital nerve);
palpable irregularity of orbital rim, eyelid edema, ecchy-
mosis, and hypesthesia in the distribution, supratro-
chlear or supraorbital nerve (ipsilateral forehead),
ptosis, point tenderness.
• CT scan is a must to delineate the fracture
• Treatment is (1) ice pack to orbit (2) broad spectrum
oral antibiotic (3) nasal decongestants (4) advice not
to blow nose (5) surgical repair at 7-14 days after
trauma if diplopia persists, endophthalmos is
unacceptable or fracture is large or has displacement.
7. Retrobulbar haemorrhage
• Patients complain of decreased vision, have
subconjunctival haemorrhage and proptosis.
• IOP is raised and ocular mobility is restricted, vision
is threatened from central retinal artery occlusion,
choroidal ruputure.
• Treatment is (1) immediate reduction of IOP with
mannitol infusion and other antiglaucoma measure
(2) lateral canthotomy and cantholysis (3) orbital
decompression if optic nerve is compromised, colour
vision is lost or visual acuity decreases.
8. Intraocular foreign body
• Clues to intraocular FB are microcystic edema of
cornea, iris transillumination defect, irregular pupil,
iritis/uveitis, ↓IOP, vitreous haemorrhage, lens dislo-
cation, etc. Long-standing iron containing FB may
cause corneal endothelial/epithelial deposit, ante-
rior subcapsular cataract, optic atrophy.
• Carbon, glass, lead, rubber, silver, stone are inert but
iron, copper, produce severe inflammation, nickel
and aluminium mild inflammation
• US and CT scan better delineate the FB
• Cycloplegics and broad spectrum antibiotics are
must; surgical removal is indicated when FB lies in
visual axis, causes severe or recurrent inflammation
or retinal metallosis (on ERG follow-up).
Ocular Trauma 63
9. Traumatic optic neuropathy

• Patient has decreased vision, decreased colour
vision and field defect
• Initially optic disc is normal but there is afferent
pupillary defect
• Shearing injury from blunt trauma, compression of
nerve by bone/blood, perineural edema are respon-
sible.
• CT and US be done to document fracture and FB
• Treatment is broad spectrum antibiotics, IV methyl
prednisolone and endoscopic canal decompression.
13 Diagnostic Test in
Ophthalmology
1. Scintigraphy like 99m-Tc is used for lacrimal

drainage physiology.
2. 67 Gallium scan is for extraocular sarcoid
granuloma.
3. MRI is for orbit, neuroophthalmic pathways, CNS,
ocular muscles.
4. Fluorescein agiography for imaging of retinal,
choroidal, optic disc and iris vasculature, suspected
retinal hypoxia/neovascularisation, choroidal neo-
vascularization (ARMD, ocular histoplasmosis,
angioid streaks).
5. Indocyanine angiography better delineates choroidal
vasculature than retinal vessels.
6. Ocular US following trauma (scleral rupture, intra-
ocular FB, intraocular tumor, retinal detachment,
choroidal detachment, optic disc druscens/colo-
boma.
7. US bimicroscopy—excellent for defining anterior
chamber angle, ciliary body, corneoscleral—limbal
pathology, iris pathology, suspected cyclodialysis.
8. Orbital Doppler—for superior ophthalmic vein
thrombosis, orbital varix, AV malformation, caver-
nous sinus fistulae.
Short Cases
Case No.1
A 60-year-old man complains of gradual diminution of

distant vision over past 5 years. He has discarded his
presbyopic glasses too. Torch light examination reveals
gray shadow from the pupil and distant vision 6/36 in
both eyes.
What is your diagnosis?

Senile immature cortical cataract.
Characteristics of cortical cataract
• The lesion is wedge shaped with apex towards
center, involves anterior, posterior and equatorial
cortex
• Uniocular polyopia is a prominent complaint
• Vision is poor in dim light
• The opacity appears black against red of reflex of
retina.
What are types of senile cataract?
• Subcapsular cataract
• Cortical cataract
• Nuclear cataract.
Pathogenesis of nuclear cataract
• Sclerosis of lens nucleus with aging
• These changes begin centrally and spread peri-
pherally
• There is accumulation of yellow brown pigment-
urochrome, an oxidation product aromatic amino-
acids of lipids. Thin pigment absorbs its complimen-
tary colours blue light with relatively excess percep-
tion of red and green.
• The refractive index of lens is increased resulting in
myopia.
Characteristics of subcapsular cataract
• The opacities appear as brown granules or cysts in
subcapsular region
• Patients with posterior subcapular cataract feel
discomfort with glare and sunlight and their near
vision is disturbed more than distant vision.
Causes of non-senile cataract
• Traumatic cataract from penetrating injury, infrared
radiation (glass blowers) or ionizing radiation
• Drugs like corticosteroids, chlorpromazine, amioda-

rone
• Metabolic disorders like diabetes mellitus, galacto-
semia, hypocalcemia, Wilsons’s disease, Fabry’s
disease
• Maternal infections during pregnancy like rubella,
CMV, toxoplasmosis
• Hereditary like Down’s syndrome,
• Dermatogenic like congenital icthyosis, psoriasis
(skin and lens both are of ectodermal origin)
Types of Congenital cataract
• Anterior capsular cataract often associated with
persistent pupillary membranes
• Posterior capsular cataract due to persistent hyloid
artery
• Nuclear cataract confined to embryonic nucleus
• Lamellar cataract
• Sutural cataract (X-linked inheritance).
Complications of cortical cataract during maturation
• Phacolytic glaucoma (macrophage response to lens
protein)
• Phacoanaphylaxis (granulomatous uveitis)
• Phacomorphic glaucoma (closed angle glaucoma
due to intumuscence of lens)
• Pseudoexfoliation with deposition of gray material
on lens capsule, basement membrane of ciliary body
and iris with open angle glaucoma
Characteristics of diabetic cataract
• Usually anterior or posterior capsule involved
• Snow flake like opacities
• Fluctuating power of correction related to changes
in blood sugar control.
Indications for lens extraction in cataract
• Grossly diminished vision hampering easy living
• Complicated cataract.
Types of intraocular lenses
• Anterior chamber lens
• Iris supported lens
• Capsular fixated lens
• Posterior chamber lens.
Short Cases 69
Role of ultrasound in lens implantation

To calculate the power of the lens to be implanted one
need to calculate the corneal power with help of keratome-
ter and axial length of eyeball with US scan. Ultrasound
helps to assess any disease of posterior segment too.
How to assess posterior segment of eye in a cataract
patient
• Electroretinography
• Electro-oculography
• Visual evoked response
• Ultrasound
Contraindications for intraocular lens implantation
• Patient with one eye
• Patient of diabetic retinopathy
• Corneal dystrophy/degeneration
• Case of chronic uveitis
• Galucoma.
Complications of intraocular lens implant
• Vitreous loss
• Corneal edema and decompensation
• Uveitis
• Retinal detachment
• Dislocation of lens.
Problems with spectacle correction after lens
extraction
• There is 30% magnification of the objects seen
• Objects seem close to body
• Spherical aberration causes distortion of object
• The field of vision is limited by the size of lens.
Disadvantages of intraocular lens
• Judgement of distance is disturbed
• Colour perception is altered
• Posterior capsular opacity developing as a late
complication of extracapsular extraction. It can be
managed by neodymium laser capsulotomy.
Types of cataract extraction
• Extracapsular extraction where anterior capsule is
cut and removed. The posterior capsule is left intact
that prevents vitreous loss and helps for better
anchorage and placement of lens implant.
• Intracapsular extraction where the lens is removed
enblock. Vitreous prolapse is a danger.
What is phacoemulsification and its advantages?

Phacoemulsification is less traumatising and removes
the nucleus and cortical matter of the lens by aspiration
leaving behind the posterior capsule intact. The corneal
incision for inserion of canula is too small to cause any
corneal flattening at a later date. No, postoperative res-
triction of activity is needed after phacoemulsification.
What is couching?
Couching is a crude roadside surgery to improve vision
in cataract patients. The lens is dislocated from its
attachment so that some light rays are able to reach
retina with improvement in vision. Tremulousness of
iris points towards dislocation of lens. Few patients
loose vision due to vitreous degeneration and bleeding.
Common complications of cataract surgery
Complications during surgery Postoperative complications
Hyphaema Prolonged orbicularis paresis
Lens capsule rupture Delayed formations of AC
Dislocated lens Detachment of choroid
Vitreous loss Distortion of the pupil
Expulsive haemorrhage Iris prolapse
Delayed healing
Infection
Epithelial in growth to A/C
Complicated glaucoma
Rential detachment
Iridocyclitis, endophthalmitis
Sympathetic ophthalmitis
Delayed complications
• Corneal oedema
• Striate keratitis
• Corneal dystrophy
• Spastic entropion
• Astigmatism
• Macular oedema & degeneration.
Causes of diminution of vision
Sudden loss Gradual loss
Methyl alcohol Senile cataract
Multiple sclerosis Chronic simple glaucoma
Rentinal detachment Chronic iridocyclitis
Macular bleed Senile macular degeneration
Central retinal artery thrombosis Primary optic atrophy
Retinopathies
Short Cases 71
Signs of aphakia
• Jet black pupils
• Iridodonesis
• Deep anterior chamber.
Causes of iridodonesis
• Aphakia
• Posterior dislocation of lens
• Hypermature cataract
• Buphthalmos.
Complications of hypermature cataract
• Phacoanaphylactic iritis
• Glaucoma
• Subluxation of lens.
Case No.2
A 20-year-old patient has presented with pain in the left

eye, lacrimation and photophobia of 7 days duration.
Examination reveals marked circumciliary congestion
and opaque spots on the cornea.

A case of keratitis
Causative agents of keratitis
• Bacterial—gonococcus, meningococcus, corynebac-
terium diphtheriae, pseudomonas, staphylococci.
• Fungi
• Herpes simplex and zoster
• Ultraviolet/radiation.
What is interstitial keratitis?
It is the inflammation of stroma of cornea without
primary involvement of epthelium or endothelium. It is
associated with congenital syphilis, tuberculosis and
Cogan’s syndrome (interstitial keratitis with acute
tinnitus, vertigo and deafness).
Clinical features of bacterial keratitis
• Symptoms of corneal involvement like pain, lacri-
mation, photophobia, circumciliary congestion,
blepharospasm
• Keratic precipitates, hypopion
• Positive flurescein staining
• Associated signs like iritis, aqueous flare, posterior
synechae
• Bacterial ulcer due to staphylococci tends to be oval,
yellow-white, while that due to pseudomonas is
regular with sharp margin and opaque surrounding
stroma (in staph keratitis the stroma is relatively
clear).
Clinical features of herpes keratitis
• HSV1 keratitis is acquired by kiss, following steroid
use (topical & systemic), exposure to extreme heat,
cold and wind.
• Watery discharge with follicles on conjunctiva
• Preauricular lymphadenopathy
• Fine epithelial punctate keratitis often progessing to
disciform keratitis and subepithelial infiltration
Short Cases 73
• Diminished corneal sensation

• Healing leaves thin nebular corneal opacity
(bacterial ulcers heal with thick corneal opacity)
• H. zoster keratitis is due to involvement of nasociliary
branch of first division of trigeminal
• Mild epithelial puntuate kratitis is usual followed
by thin nebular scar. Only severe cases have stromal
keratitis leaving behind a thick scar.
• Associated skin vesicles often progressing to cranial
nerve palsy, postherepetic neuralgia, optic atrophy.
What are keratometry and pachometry?
Keratometry helps to define corneal curvature, i.e. its
radius in vertical and horizontal meridians are mea-
sured. Pachometer helps to measure corneal thickness,
a prerequisite for corneal transplant and radial kerato-
tomy. The central corneal thickness ranges between 0.49-
0.56 mm. Reading above 0.6 mm. suggests endothelial
disease.
What are the methods for clinical examination of
cornea?
• Torch and binocular loupe
• Slit lamp examination by diffuse illumination,
sclerotic scatter, focal illumination, retroillumination,
specular reflection
• Keratometry and pachometry (optical and ultrasonic)
• Specular microscopy
• Fluorescein staining
• Testing for corneal sensation.
What are the layers in cornea?
Corneal layers from exterior to interior are:
• Epithelium
• Bowman’s membrane
• Substantia propria
• Descemets’ membrane
• Endothelium.
How cornea is nourished?
Cornea is avascular and hence allows uniform passage
of light into eye. It is dependent for its nourishment upon
diffusion of tissue fluid from vessels at its periphery and
material from aqueous humor.
What are optical chracteristics of cornea?

The anterior surface of cornea can be regarded as
spherical with a radius of curvatue of about 8 mm.
Cornea has same refractive index as that of aqueous and
vitreous. The anterior and posterior focal distances of
cornea are 15 mm. and 24 mm. respectively.
Treatment modalities for keratitis
• Atropine eyedrops or atropine eye oinment to prevent
posterior synechia and to provide relief from pain
due to ciliary spasm
• Antibiotic drops like gentamycin, cefalexin, tobra-
mycin and ciprofloxacin for bacterial conjunctivitis
• Subconjuctival antibiotic injection
• Natamycin or nystatin eyedrop in fungal keratitis
• Acyclovir 3% ointment, trifluoridine 1% drops,
adenine arabinocide 3% ointment, idoxuridine 0.5%
ointment or 0.1% drops for viral keratitis
• Optical iridectomy or corneal transplant if the scar
left after healing disturbs vision.
What are the types of corneal opacity?
Nebula (very thin )
Macula (dense)
Leucoma (very dense).
Complications of keratitis
• Corneal perforation, iris prolapse, anterior
staphyloma, intraocular bleed, anterior synechia
• Anterior capsular cataract
• Purulent iridocyclitis often leading to endoph-
thalmitis
• Corneal opacity
• Secondary glaucoma.
Types of non-infective corneal ulcers
• Mooren’s ulcer, the rare superficial corneal degene-
ration of elderly persons
• Central ulcer in marasmic children
• Keratomalacia of vitamin A deficiency
• Atheromatous ulcer in old, dense leucoma
• Neuro-paralytic keratitis
What is phlyctenular keratitis?
It is a form of superficial keratitis with localized
lymphocytic infiltration of cornea at its periphery. It is
due to allergy to bacterial proteins, commonly tubercular.
Short Cases 75
The phlycten may progress towards center of cornea

with superficial ulceration, but always carries a bunch
of blood vessels with it.
What are the causes of punctate keratitis?
• Epidemic keratoconjunctivitis
• Pharyngoconjunctival fever
• Herpes Simplex and vaccinia
• Thygeson’s superficial punctate keratitis of unknown
etiology.
What are degenerative conditions of cornea?
Corneal degenerations are conveniently divided into
three categories: primary degenerations, secondary dege-
nerations and infiltrations associated with metabolic
disturbances.
• Arcus senilis is lipoid infiltrations of old people
involving corneal margin
• Hereditary corneal dystrophy in young involving
central portion of cornea bilaterally
• Fuch’s endothelial corneal dystrophy of old females
• Salzman’s nodular dystrophy
• Band keratopathy common to blind shrunken eyes
due to defective nutrition and exposure as following
chronic uveitis, glaucoma, hypercalcemia
• Stromal dystrophy (lattice, granular and macular).
What is keratoconus?
Keratoconus is a non-inflammatory ectatic condition of
cornea, usually familial, manifesting at puberty with
gradual loss of vision, photophobia and mono-ocular
diplopia. Patients have high myopic irregular astigma-
tism, that responds to contact lens or better keratoplasty.
The disease may be associated with retinitis pigmentosa,
Down’s syndrome, Marfan’s syndrome, etc.
Indications for lamellar keratoplasty
• Indolent corneal ulcer
• Superficial opacity
• Lattice dystrophy.
Indications for penetrating keratoplasty
• Keratoconus
• Stromal dystrophies, endothelial dystrophy
• Dense corneal opacity
• Fungal ulcers (deep)
• Interstitial keratitis.
Complications of penetrating keratoplasty

• Iris prolapse
• Astigmatism
• Glaucoma
• Cystoid macular edema
• Recurrent disease in the graft as in dystrophies
Short Cases 77
Case No.3
A 40-year-old male has presented with severe agonizing

pain in and around the eyes with marked ciliary and
conjunctival congestion, intense headache. Examination
reveals corneal edema, shallow anterior chamber, fixed
pupils and marked diminution of vision.
What do you think of this case?

A case of acute congestive glaucoma (primary angle
closure glaucoma).
How will you classify glaucoma?
• Primary open angle glaucoma
• Primary angle closure glaucoma
• Congenital glaucoma
• Low tension glaucoma
• Secondary glaucoma
• Glaucoma associated with congenital anomalies.
Ophalmoscopic findings in glaucoma
• Cupping of disc with concentric enlargement
• Splinters or flame shaped haemorrhage at disc margin
• Notching of the cup rim and pallor of the disc
• Cup disc ratio greater than 0.3
• Full retinal veins, often with looping near the disc.
Slit lamp examination findings in glaucoma
• Corneal epithelial edema
• Pigmentation of corneal endothelium
• Shallow anterior chamber
• Keratic precipitates
• Cells in aqueous humor
• Rubeosis
• Iris atrophy.
Role of tonometry in glaucoma
Tonometry records the intraocular pressure and is
helpful in diagnosis and follow-up of patients with glau-
coma. Tonometry is basically of two types: indentation
tonometry and aplanation tonometry. The latter type is more
accurate as its reading is not affected by scleral rigidity.
Normal intraocular pressure is between 15-20 mm. Hg.
A diurnal variation in intraocular pressure greater than
20 mm. Hg. is diagnostic of glaucoma.
Role of gonioscopy in glaucoma

The aim of gonioscopy is to visualize the angle of ante-
rior chamber and assess its width. Shaffer grading of
chamber is based on gonioscopic findings. In grade I,
only Schwabe’s line is visible in gonioscopy, while in
grade II, trabecular network is visible in addition. In grade
III, scleral spur is also visible, while in grade IV, all the
above structures including ciliary body is visible. Grade
I has highest risk of closed angle glaucoma, while grade
II has moderate risk. Grade III & IV are open angles.
Provocative tests for diagnosis of glaucoma
• Dark room test
• Prone test
• Prone dark room test
The test is positive if intraocular pressure rises by
more than 8-10 mm Hg. in dark or prone position. Such
cases are patients of latent or intermittent glaucoma.
They may give history of seeing halos with haziness of
vision at times.
Predisposing factors for glaucoma
• Positive family history
• Diabetes mellitus
• High myopia
• Steroid use
• Uveitis
• Hyphema
• Dislocation/subluxation of lens
• Glomus capsulare
• Venous obstruction
• Intraocular tumor.
What is buphthalmos?
Buphthalmos is simple obstructive glaucoma due to
failure of development of filtering tissue at angle of
anterior chamber or persistence of embryonic tissue that
blocks the angle of anterior chamber. Boys are affected
more commonly than girls. The globe enlarges and there
is deep cupping. The cornea is forced forward to assume
a globular shape and anterior chamber is deep. Axial
myopia due to enlarging globe is usual. Long-standing
cases may have gross deterioration of vision. Common
associations are neuro-fibromatosis and Sturge-Weber
syndrome.
Treatment is by trabeculotomy or goniotomy.
Short Cases 79
What is low tension glaucoma?

In low tension glaucoma, the angle is open, intraocular
pressure is normal, but there is cupping of disc and
visual field loss. These patients only need careful follow-
up.
What is glaucomatocyclitic crisis?
It is characterized by sudden and rapid rise in
intraocular pressure with mild anterior uveitis. There
is no pain, but patient sees halos around bright light.
Treatment is usually medical.
Treatment of acute congestive glaucoma (primary
angle closure glaucoma)
• IV mannitol rapid infusion
• Inj. fortwin, buprenorphine
• Two percent pilocarpine eyedrops
• 8 mg. dexamethasone IV followed by oral predni-
solone to control uveal reaction
• Diamox 250 mg. every six hours
• Once patient is stable, gonioscopy is to be done to
assess the angle. Iridectomy is advised if angle is
open 50% but filtration surgery is indicated, where
angle is blocked by more than 50%.
What is treatment for open angle glaucoma?
• Timolol 0.25% to be instilled twice daily; increased
to 0.5% daily.
• If tension still uncontrolled, add propine eyedrops
twice daily (a pro drug of adrenaline)
• If both above drugs fail add pilocarpine and carbonic
anhydrase inhibitor
• Filtration surgery.
What is surgical therapy of glaucoma?
• Laser iridectomy in acute angle closure glaucoma
• Argon laser trabeculoplasty to open inter trabecular
spaces
• Filtration surgery, i.e. thermosclerostomy or trabecu-
lectomy along with peripheral iridectomy.
Differential diagnosis of acute primary angle closure
glaucoma
• Acute anterior uveitis
• Glaucomatocyclitic crisis
• Phacolytic glaucoma
• Neovascular glaucoma.
Glaucomatous cupping is to be differentiated from

• Physiologic cupping
• Coloboma of optic disc
• Anterior ischaemic optic neuropathy
• Chiasmal lesions
• High myopic fundus.
Causes of rubeosis iridis
• Diabetes mellitus
• Central retinal vein thrombosis
• Eale’s disease
• Old retinal detachment
Short Cases 81
Case No.4
A patient has presented with irritation and watering

from the eyes and mucopurulent discharge. Examination
reveals chemosis, conjunctival infection with normal
cornea and vision.
What is the diagnosis?

Acute mucopurulent conjunctivitis.
What are the varieties of infective conjunctivitis?
1. Acute conjunctivitis—serous, catarrhal, mucopurulent,
purulent, membranous
2. Subacute/chronic conjunctivitis—simple chronic conjun-
ctivitis, angular conjunctivitis, follicular conjunctivitis.
Differential diagnosis of follicular conjunctivitis
Acute Follicular Conjunctivitis
• Trachoma in exacerbation
• Adenoviral conjunctivitis
• Acute haemorrhagic conjunctivitis
• Perinaud’s oculoglandular fever
Chronic Follicular Conjunctivitis
• Inclusion conjunctivitis
• Trachoma
• Angular conjunctivitis
• Molluscum contagiosum conjunctivitis
• Toxic reaction to topical drugs like pilocarpine,
neomycin, atropine.
What is trachoma and its evolution?
Trachoma is caused by serotype A,B and C of Chlamydia
trachomatis. It is one of the leading causes of preventable
blindness in the world.
The evolution of the disease is in 4 stages
• Stage of lymphoid hyperplasia
• Stage of florid inflammation
• Stage of scarring
• Stage of deformities.
Conjunctival and corneal signs in trachoma
• The diagonostic lesion in conjunctivitis is follicle,
that appears as multiple, discrete, elevated nodules
on upper tarsal conjunctiva. The follicles heal by scar
formation, usually star shaped.
• Corneal lesion is of superficial keratitis and pannus.

Pannus develops as a lymphoid infiltration with
vascularisation of cornea, initially limited to upper
limbus, but subsequently involving entire cornea.
The pannus may resolve completely leaving cornea
clear, apart from the fine obliterated vessels, provided
treatment is given early. Once Bowman’s membrane
is destroyed with extension of infection to substantia
propria, permanent opacity is inevitable.
• Herbert’s pits are small depressions in limbocorneal
junction, the result of healing of follicles at limbus.
Complications and sequelae of trachoma
• Trichiasis
• Entropion
• Xerosis
• Corneal opacity
• Trachomatous ptosis
What is inclusion conjunctivitis?
Inclusion conjunctivitis is due to Chlamydia trachomatis
of serotype D to K. It occurs in infants born to mothers
with trachomatous infection of birth passage or in adults
with venereal contact, transmitted from genitals by finger
contact. In them conjunctivitis manifests one week after
sexual exposure, often associated with non-specific
urethritis/cervicitis. Another common mode of infection
is through water of swimming pools responsible for
local epidemics.
It manifests with acute bilateral mucopurulent con-
junctivitis with follicles first appearing in lower fornix,
preauricular lymphadenitis and superficial epithelial
keratitis. Local application of tetracycline ointment and
systemic doxycycline for 2 weeks cures this benign
disease.
What is adenoviral kerato conjunctivitis?
Ten out of thirty-one serotypes of adenoviruses are
known to produce keratoconjunctivitis, principally in
two forms: pharyngoconjunctival fever and epidemic
keratoconjunctivitis. Virus types 3 and 7 are responsible
for former and types 8 and 19 for the latter. Both the
forms are highly contagious with preauricular lympha-
denitis, watery discharge and slow resolution without
sequelae.
Short Cases 83
What is allergic conjunctivitis?

Allergic conjunctivitis may be of the following forms
• Acute or chronic allergic conjunctivitis
• Spring catarrh
• Phlyctenular keratoconjunctivitis
• Giant papillary conjunctivitis
• Stevens-Johnson syndrome
Spring conjunctivitis is IgE mediated and is common
to atopic individuals. It is recurrent and bilateral disease
that may be of palpebral or bulbar forms with papillary
hypertrophy (cobble-stone appearance), ropy, sticky
conjunctival discharge, and perilimbal white spots
(Tranta’s dots).
Treatment of allergic conjunctivitis/spring catarrh
• Topical steroid
• Sodium chromoglycate 2%
• Flurbiprofen eyedrops
• Vasoconstrictors, antihistamines.
Clinical chracteristics of phlyctenulosis
Phlyctenular keratoconjunctivitis is a delayed response
to microbial proteins, commonly of tubercle bacillus or
staphylococcus. Patients present with photophobia,
lacrimation, blepharospasm. Conjunctival phlycten
appears as a small red elevated nodule, while corneal
nodule is gray-white, mainly at limbus, often with
ulceration and scar formation.
What is Stevens-Johnson syndrome?
It is a mucocutaneous vesicobullous disease due to
hypersensitiveness to sulphonamides, bacterial and
viral proteins. Haemorrhage into the vesicles is charac-
teristic. Besides skin lesions, there is mucopurulent
conjunctivitis, corneal involvement and often visual
loss. Treatment is with steroids, and immunosup-
ressants.
What is entropion?
Entropion is inturning of lid margin leading to irritation
of cornea by eyelashes. Entropion can be congenital,
spastic, senile, or cicatricial.
Case No. 5
A 30-year-old male who has been having itching and

redness of eyes for the past 2 years is noticing overflow
of tears all the time. Examination reveals eversion of lid
margin and conjunctival infection.

A case of epiphora following chronic conjunctivitis and
ectropion.
Causes of epiphora
• Atresia, misplacement, eversion or occlusion of
punctum
• Atresia, stenosis, inflammation of canaliculi
• Chronic inflammation in lacrimal sac
• Congential occlusion of nasolacrimal duct
• Hypertrophied inferior turbinate, deviated nasal
septum, nasal allergy and chronic rhinitis.
What is dacryocystitis and dacryoadenitis?
Inflammation of lacrimal sac is called dacryocystitis,
while inflammation of lacrimal gland is called
dacryoadenitis.
Composition of tear film

• External lipid layer
• Middle aqueous layer
• Internal mucus layer.
The lipid layer is formed by lipids from meibomian
glands, while mucus is contributed by secretion from
conjunctival goblet cells. The normal brea-up time for
tear is 15-35 seconds. Fluorescein does not stain mucus.
What is Schirmer’s test?
This test is helpful in assessing the rate of tear
production. It is performed by measuring the amount of
wetting of a special filter paper, which is 5 mm wide
35 mm long.
What is Rose Bengal test?
Rose Bengal has affinity for devitalized epithelial cells
and mucosa. Thus, it is helpful in detecting mild cases
of keratoconjunctivitis sicca.
Short Cases 85
Biochemical tests in dry eye syndrome

• Lysozyme assay
• Tear osmolality
• Conjunctival biopsy for goblet cell population.
Causes of dry eye syndrome
1. Hypofunction of lacrimal gland
• Sjogren’s syndrome
• Sarcoidosis
• Leukemia, lymphoma
2. Mucin deficiency
• Avitaminosis A
• Conjunctival scarring following trachoma, irra-
diation
3 Miscellaneous
• Deficient blinking
• Diuretics, sympatholytics.
What is Sjogren’s syndrome?
It is a triad of
• Rheumatoid arthritis
• Keratoconjunctivitis sicca
• Xerostomia
Management of dacryocystitis
• Culture of exluding pus from punctum and
institution of suitable antibiotics
• Dacryocystorhinostomy
Treatment of epiphora in infants
Congential obstruction of nasolacrimal duct is the
common cause of epiphora in infants. Lacrimal probing
is ideal surgery for them, preferably around 3 months
of age. If punctum is absent or stenosed, operative
intervention is mandatory.
Treatment of dry eye syndrome
• Tear substitutes like methyl cellulose eyedrops
• Acetyl cysteine 5% eyedrop, mucolytic for patient of
Sjogren’s syndrome.
• Advice to the patient to avoid heat, wind and strong
light.
Clinical classification of dacryocystitis
• Dacryocystitis neonatorum
• Acute dacryocystitis
• Chronic dacryocystitis
• Chronic dacryocystitis with functional block

• Chronic dacryocystitis with fistula
• Chronic dacryocystitis with encysted lacrimal sac
• Chronic dacryocystitis with atrophic sac
• Chronic dacryocystitis with pseudosac.
Investigations advisable in a case of dacryocystitis
• Regurgitation test
• Syringing of lacrimal passage
• Radioactive tracer
• Dacryocystography
• X-ray PNS and orbit.
What is pterygium?
It is a degenerative condition of subconjunctival tissues
which proliferate as vascularized granulation tissue to
invade the cornea. The lesion is triangular with apex
on cornea and small opacities of cornea lying around
the apex.
What is pinguecula?
It is an yellow triangular patch on bulbar conjunctiva
due to hyaline infiltration and elastotic degeneration of
submucous tissue. A ptreygium frequently follows
pinguecula.
Treatment modality of pterygium
Pterygium is best left alone, unless it is disfiguring or
is invading cornea. When it invades cornea, resection
followed by lamellar corneal graft is warranted. The
apex of pterygium can be destroyed by diathermy/laser
to halt its progress.
Common tumor of conjunctiva and its treatment
Demoid, the yellow tumor arises from outer corneal
margin and adjoining tissue. It contains sebaceous
glands with hairs to cause irritation. It should be
removed followed by lamellar corneal graft to the site
of attachment.
Short Cases 87
Case No.6
A 20-year-old female has been complaining of pain in

the eyes, photophobia, lacrimation and dim vision.
Examination reveals irregular pupil with muddy iris.

A case of uveitis
Classification of uveitis
1. Anatomical classification
• anterior uveitis
• posterior uveitis
2. Clinical classification
• acute uveitis
• chronic uveitis
3. Etiological classification
• exogenous uveitis
• endogenous uveitis
4 Pathological classification
• granulomatous uveitis
• non-granulomatous uveitis
What are keratic precipitates?
Keratic precipitates are cellular exudates from inflamed
iris and ciliary body. Small keratic precipitaes are
characteristic of Fuch’s uveitis and herpes zoster.
Medium size keratic precipitates are seen in acute and
chronic anterior uveitis, while large size precipitates
indicate granulomatous uveitis. Fresh precipitates are
round and white, while old ones are shrunken and
pigmented.
Significance of iris nodules

Presence of nodules usually indicates granulomatous
uveitis. Nodules at pupillary border are known as
Koeppe Nodules, while those on anterior surface of iris
are called Busacca Nodules.
What is rubeosis iridis?
Rubeosis iridis is a condition of neovascularization of
iris. It is seen in chronic anterior uveitis and in Fuch’s
uveitis. It can encroach on the angle of anterior chamber
producing glaucoma.
What is Fuch’s uveitis?

It is a chronic non-granulomatous anterior uveitis of
gradual onset. It is unilateral and affects young adults.
Symptoms are minimal in the form of vitreous floaters,
dim vision and often progress to cataract formation and
glaucoma. Short term steroid is indicated to control acute
symptoms.
What is sympathetic uveitis?
It is bilateral granulomatous uveitis, occurring after
penetrating injury involving the uveal tract or following
intraocular surgery. The eye suffering the trauma is
called exciting eye and the other eye as sympathizing
eye. The time interval between injury and inflammation
in the fellow eye is 2 weeks.
Histopathologic features in sympathizing eye
• Epithelioid cell, lymphocyte and giant cell
infiltration of uveal tract
• Isolated nests of epithelioid cells present in pigment
epithelium, known as Dalen-Fuch’s Nodule
• Phagocytosis of pigment cells by epitheloid cells but
not macrophages, as occur in other forms of uveitis.
Features of posterior uveitis
• Main symptoms are floaters in front of eye
• A positive scotoma in early stage
• Vitreous opacity
• Features of choriditis in the form of whitish-yellow
patch with surrounding pigment cells and criss-
crossing retinal vessels.
Differential diagnosis of granulomatous uveitis
• Ankylosing spondylitis
• Behcet’s syndrome
• Reiter’s syndrome
• Sarcoidosis
• Syphilis
• Tuberculosis and leprosy
• Toxoplasmosis
• Toxocariasis
• Onchocerciasis
• Fuch’s uveitis
• Sympathetic uveitis.
Short Cases 89
Clinical features of leprotic uveitis

• Conjunctivitis, episcleritis and scleritis
• Uveitis, can be acute or chronic
• Slit lamp examination shows, the iris pearls at
pupillary margin, nodular lesions leading to iris
atrophy and formation of holes in iris.
Ocular lesions of sarcoidosis
• Sarcoid plaque on the skin of eyelid
• Granulomatous infiltration of lacrimal gland with
xerosis
• Episcleritis
• Acute iridocyclitis or chronic iridocyclitis with
Koeppe and Busacca nodules on iris, with mutton
fat keratic precipitates
• Retinal periphlebitis and periphlebitic nodules with
venous occlusion
• Choroiditis, vitreous haze and retinal granulomas.
Role of HLA testing in uveitis
HLA B27 Ankylosing spondylitis, Reiter’s syndrome
HLA B5 Behcet’s syndrome
HLA B22 Vogtl-Koyanagi-Harada disease
HLA Bw54 Glaucomatocyclitic crisis.
Treatment strategy of uveitis
• Steroids—Topical, periocular injection or systemic
• Cycloplegics
• Immunosuppresants—Chlorambucil and cyclophos-
phamide
• Enucleation of injured eye in sympathetic uveitis
may prevent development of uveitis in non-injured
eye
• Treatment of complications like glaucoma, cataract,
synechae, vitreal opacity.
Types of keratic precipitates
• Fine
• Mutton fat (in granulomatous conditions)
• Tapfol KP (Fuch’s heterochromatic cyclitis)
Causes of unilateral iridocyclitis
• Traumatic
• Herpes zoster
• Fuch’s heterochromatic cyclitis
• Retinal detachment
• Juxta capillary choroiditis.
Characteristics of Argyl Robertson pupil

• Loss of light reflex (both direct and consensual)
• Presence of accommodation reflex
• Miosis
• Irregular pupil
• No dilatation with atropine
• Bilateral
• Pupilllary light reaction loss is not proportional to
visual loss.
Characteristics of Horner’s Syndrome
• Miosis
• Enophthalmos
• Narrow palpebral fissure
• Absence of sweating on affected side of face
• Pupil does not dilate on pinching platysma.
Short Cases 91
Case No. 7
A 20-year-old college-going boy complains of gradually

weakening distant vision. He has headache on watching
television or on near work. Examination reveals narrow
palpebral fissure and prominent eyes.
What is your presumptive diagnosis?

A case of myopic disorder.
Predisposing factors for myopia
• Racial (Japanese)
• Myopic parents
• Toxemia, rubella, toxoplasma in pregnancy
• Debilitating illness in childhood
• Poor lighting
Types of myopia
• Corneal (curvature myopia)
• Lenticular (index myopia)
• Axial
• Developmental
Ophthalmoscopic findings in myopia
• Crescent at the disc with a large cup
• Posterior staphyloma
• Hyper pigmentation at macula, with Fuch’s spots.
Chorioretinal changes in the form of haemorrhage,
focal degeneration
• Liquified vitreous with floaters.
Gonioscopic findings in myopia
Anterior chamber is deep in cases of pathologic myopia
of more than 6 diopters. The presence of anterior
insertion of iris or iris processes or pigmentation in the
angle indicates tendency for glaucoma and demands
provocative tests and regular check-up for glaucoma.
What is posterior staphyloma?
Backward bulging of globe is called posterior staphy-
loma. The edges of this bulge can be visible by indirect
ophthalmoscopy as a crescentic shadow, 2-3 disc dia-
meters to the temporal side of disc and concentric with
it and associated change in course of retinal vessels.
Characteristics of axial myopia
• Hereditary and progressive degeneration of eye.
• Common to women of Jewish and Japanese race

• Posterior pole and surrounding retina form staphy-
loma
• Anterior chamber is deep and eyeballs prominent
• Pupils are sluggish in reaction
• Apparent convergent squint due to negative angle
kappa
• Scotoma may be present, both central and peripheral
• Chorio-retino–macular atrophy.
What is index myopia?
Here, myopia is due to decreased refractive index of lens
cortex as in diabetes or sclerosis of lens in incipient
cataract.
Systemic disorders associated with myopia
• Albinism
• Monogolism
• Marfan’s syndrome
• Ehler-Danlos syndrome
• Homocystinuria
• Laurence-Moon Biedl sydrome.
Ocular diseases associated with myopia
• Nyctalopia, retinitis pigmentosa
• Microphthalmos
• Keratoconus
• Ectopia lentis
• Choriodemia
Treatment approaches in myopia
• Spectacle correction
• Contact lens
• Low vision aids
• Corneal correction
• Anterior chamber lens
• Lensectomy
• Scleral resection
Operations on cornea for correction of myopia
• Radial keratotomy
• Keratomileusis
• Epikeratophakia
• Intrastromal implants.
Factors influencing results of keratotomy
• Radial keratotomy in myopia up to 6 diopters gives
better results, with minimal chances of under or over
Short Cases 93
correction
• Results are better in patients of higher age group
• Higher the corneal curvature, better is the result
• A thin cornea gives smaller correction than a thick
cornea
• A cornea of greater diameter enhances correction,
because of greater length of incision
• A 4 incision radial keratotomy is good for low
myopia, while 8 incision is good for myopia upto
10 Diopters
• A deep incision gives better correction with less
number of incisions.
Side effects and complications of radial keratotomy
• Perforation
• Over/under correction
• Induced astigmatism
• Glare, photophobia, lacrimation
• Fluctuating vision, return of myopia after few years.
Complications of myopia
• Chorio-retinal degeneration
• Posterior staphyloma
• Glaucoma.
Case No.8
Mother has presented her child of 3 years for yellow-

white reflex from pupils and poor vision.
What is the probable diagnosis?

Retinoblastoma
Differential diagnosis of yellow-white reflex from pupil
• Retinoblastoma
• Congenital cataract
• Pseudoglioma (Coat’s syndrome, parasitic endoph-
thalmitis, fundus coloboma, retrolental fibroplasia,
old vitreous haemorrhage)
Clinical features of retinoblastoma
• Bilateral disease in one-third
• White reflex from pupil
• Buphthalmos and proptosis in later stages
• Vitreous haemorrhage, retinal detachment.
Investigations in retinoblastoma
• Bone free X-ray of globe for any calcification
• B scan ultrasonography
• CT scan of orbit for involvement of optic nerve
• Aqueous humor paracentesis for enzyme assay and
cytology
• ELISA test to exclude toxocariasis
• Fine needle aspiration biopsy to confirm diagnosis
Treatment of retinoblastoma
• Enucleation with a long piece of optic nerve
• Radiotherapy with an external beam or cobalt 60
• Photocoagulation with xenon arc for small posterior
tumors not involving optic nerve
• Cryo application for small peripheral tumors.
• Systemic chemotherapy if there is metastasis
• Histopathology of tumor showing rosettes bears
good prognosis (8% mortality). Undifferentiated
tumor may have mortality upto 40%.
What is Coat’s syndrome?
It is a non familial, unilateral disease common to infants
and children, primarily girls. It is a severe form of retinal
telangiectasia, with dilated and tortuous vessels, intra
and subretinal haemorrhages often leading to retinal
Short Cases 95
detachment, cataract, rubeosis iridis, glaucoma and

phthisis bulbi. Early Cryo or photocoagulations may
arrest progress of disease and restore vision.
What is persistent primary hyperplastic vitreous?
It is characterized by funnel shaped grey or pink
retrolental mass, with patent or occluded hyaloid artery.
The mass is vascular and is prone for repeated haemor-
rhages, often-causing cataract, and glaucoma.
What is retrolental fibroplasia?
Otherwise known as retinopathy of prematurity, it
affects premature babies given high concentration of
oxygen. The retrolental membrane forms sometimes after
birth bilaterally to give white reflex from pupil. There
is peripheral neovascularization, vitreous haemorrhage,
and retinal detachment.
What is Von Hippel-Lindau disease?
It is association of multiple retinal capillary haeman-
gioma with haemangioblastoma of cerebellum and
medulla oblongata and cystic diseases of liver, kidney,
ovary, and lungs. The retinal lesions are multiple, small
or large orange red tumors supplied by large tortuous
vessels with retinal exudates and often detachment.
Cryo or photocoagulation may save vision
Symptoms of vitreous disease
• Floaters and flashes
• Visual loss
Vitreous pathology resulting in vitreous opacity
• Synchysis and syneresis
• Asteroid hyalosis
• Vitreous haemorrhage
• Vitreous detachment
• Hyperplastic primary vitreous.
Causes of vitreous degeneration
• Senility
• Myopia
• Retinitis pigmentosa
• Trauma-direct, thermal
• Systemic connective tissue disorders like Marfan’s
syndrome, homocystinuria, Ehler’s-Danlo’s syn-
drome
• Choroiditis, pars planitis.
Etiology of vitreous haemorrhage

• Trauma
• Proliferative retinopathy accompanying diabetes,
Eale’s disease, sickle cell disease.
• Leukemia, anemia
• Dysproteinemia.
Effects and course of vitreous haemorrhage
Retrovitreous haemorrhage is located between the retina
and the detached posterior hyaloid membrane, around
paramacular area. The blood remains fluid with boat
shape in upright position. Resorption of blood is quick
and complete, if it is small. Intravitreal haemorrhage
readily clots along vitreal fibres and form finger like
projections from the site of bleeding to vitreous cavity.
Resorption is slow and incomplete with prolonged
visual loss.
Indications for vitrectomy
• Vitreous bleed
• Vitreous opacity
• Pupillary membrane
• Ocular trauma
• Vitreous loss during ocular surgery
• Traction detachment of retina.
Short Cases 97
Case No.9
A 50-year-old male, suffering from diabetes mellitus for

past 15 years is now complaining of photopsia, small
spots and floaters in the fields of vision. Since the past
2 days, he is having visual loss in left eye with
appearance of a curtain.

A case of diabetic retinopathy with retinal detachment
on left side.
Types of diabetic retinopathy
• Background retinopathy
• Preproliferative retinopathy
• Proliferative retinopathy
• Diabetic maculopathy.
Role of fluorescein angiography in diagnosis
Fluorescein angiography shows areas of leakage and
non-perfusion. Abnormal angiographic findings inc-
lude hyperfluorescence, hypofluorescence, retrofluores-
cence, florescein leakage, fluorescein staining and
fluorescein pooling.
Clinical features of background retinopathy
• Microaneurysm
• Dot and blot haemorrhages in middle layers of retina
• Flame shaped haemorrhages along course of retinal
nerve fibres
• Hard exudates appearing as yellow waxy circinate
spots of varying sizes.
Features of preproliferative retinopathy
• Cotton wool exudates due to retinal venous
infarction
• Dilated, tortuous beaded retinal veins
• Narrowed retinal arteries.
Features of proliferative retinopathy
• Neovascularization in vitreo retinal space in the
areas of perfused retina
• Vitreous detachment due to growing fibrovascular
tissue
• Vitreal haemorrhage and degeneration of vitreous.
Treatment modalities for proliferative retinopathy

1. Photocoagulations with xenon arc, argon laser or
turntable dye laser/krypton laser
2. Strict control of diabetes
3. To avoid physical strain that may lead to
haemorrhage
4. Pars plana vitrectomy to save vision and prevent
detachment.
Indications of laser surgery in eye disorders
• Xenon arc photocoagulation of lid haemangioma
• Argon laser therapy for pterygium, corneal
vascularization, disruption of corneal nylon suture.
• Laser iridectomy and keratotomy
• Laser goniotomy for glaucoma
• Photocoagulation of retinal neovascularization,
retinal holes and leaks
• Laser destruction of small retinoblastoma (upto 4
disc diameters) and small choroidal melanomas.
Diagnosis of retinal detachment
• Indirect ophthalmoscopy and direct ophthalmoscopy
• Ultrasonography
• Electroretinogram.
Causes of retinal detachment
• Vitreoretinal break
• Peripheral retinal degeneration like
• lattice degeneration
• snail track degeneration
• diffuse chorioretinal atrophy.
Differential diagnosis of retinal detachment
• Acquired retinoschisis
• Choroidal detachment
• Solid detachment due to choroidal tumor
• Vitreous haemorrhage
• Retinal artery occlusion.
Predisposing factors for retinal detachment
• High myopia
• Aphakia
• Family history of retinal detachment
• Systemic diseases like Marfan’s, Ehler-Danlos
• Physical trauma
• Physical stress and strain like jumping, lifting
heavyweight.
Short Cases 99
Surgical treatment of retinal detachment

• Scleral buckling—radial, segmental, circumferential
or encircling
• Drainage of subretinal fluid
• Intra-vitreal injection of air (pneumatic retinopexy),
silicon oil
• Cryotherapy or photocoagulation.
Classification of hypertensive retinopathy
Grade 1 Mild narrowing of arterioles
Grade II Anteriovenous nicking
Grade III Cotton wool spots, haemorrhages, retinal
edema
Grade IV All above plus papilledema.
Case No.10
A 25-year-old female has presented with sudden onset

of visual loss in right eye. Pupillary reaction is sluggish
and ill-sustained. Fundoscopic examination reveals a
hyperemic disc with blurred margins and full
physiological cup.

A case of papillitis, probably due to multiple sclerosis.
How papillitis differs from papilledema?
Papillitis Papilledema
Gross visual loss Enlarged blind spot
Normal retinal veins Retinal veins engorged
Pupillary contraction ill-sustained Pupillary reaction normal
Pain on moving the eye Eye movements painless
Normal retinal angiogram Leakage of fluorescein
What is retrobulbar neuritis?

In retrobulbar neuritis, fundus is normal, but there is
visual loss and afferent pupillary defect and marked loss
of colour perception. The lesion is behind the globe,
commonly a tumor of optic nerve or compressive lesion.
Causes of sudden loss of vision
• Central retinal artery occlusion
• Amaurosis fugax
• Anterior ischaemic optic neuropathy
• Optic neuritis
Predisposing/causative factors for optic neuritis
1. Demyelinating disorders
2. Postviral (measles, mumps, zoster, influenza)
3. Autoimmune disorders
4. Spread of infection from meninges, paranasal sinus
or orbital tissue.
5. Toxic (methyl alcohol, tobacco and drugs).
What is anterior ischaemic optic neuropathy?
• It is due to occlusion of posterior ciliary vessels that
supply anterior portion of optic disc.
• There is latitudinal sudden visual loss with disk
swelling
• It commonly follows giant cell arteritis or systemic
hypertension
• Treatment is with high dose steroids.
Short Cases 101
What is ‘amaurosis fugax’?

Amaurosis fugax or fleeting blindness is due to retinal
emboli from ipsilateral carotid disease. The visual loss
is usually described as a curtain passing vertically
across the visual field, with complete monocular
blindness lasting for a few minutes. Treatment is that of
carotid lesion, i.e. end arterectomy for high-grade
stenosis and antiplatelet drugs for low grade stenosis.
Cardiac emboli, if suspected need treatment of
endocarditis.
Characteristic findings of optic nerve lesion
• Marked loss of central vision, with reduced visual
acuity
• Pain in the eye on movement of the globe
• Sluggish or ill sustained pupillary reaction
• Marked loss of colour vision. Dim vision with
normal colour vision speaks against optic nerve
lesion
• Light brightness sensitivity is reduced in the affected
eye so that bright thing also appear dim.
Drugs incriminated in optic neuritis
• Quinine
• Ethambutol, INH, thiacetasone
• Oral contraceptives
• Chloramphenicol
• Lead, arsenic, thallium.
What is Leber’s optic neuropathy?
• It is a hereditary disorder affecting healthy young
males
• Progressive loss of vision to blindness over periods
of time
• Absolute centrocecal scotoma
• Pupillary reaction to light is normal despite servere
visual loss
• Initially there is papillitis, finally ending in optic
atrophy.
What is tobacco amblyopia?
• Visual loss is gradual and progressive
• Peripheral vision is normal, but there is centrocecal
scotoma, more for red target.
• Amblyopia is due to degeneration of ganglion cell
layers of retina or involvement of papilomacular
bundle
• Abstinence from smoking and alcohol, vitamin

B1-B12 supplement are helpful to arrest or reverse the
disease.
What is optic atrophy?
Optic atrophy is the end result of chronic papilledema,
papillitis and retrobulbar neuritis. It can be primary
(tabes)or follows toxic or ischaemic retinopathy, chronic
glaucoma, etc. Hereditary optic atrophy is either Leber
type or Behr’s type.
How to differentiate primary optic atrophy from
secondary one
In primary form optic disc is pale, with clear margins
and reduced number of retinal veins, while in the
secondary form as due to chronic papilledema, the disc
margin is obscured.
Relation of brain tumor to optic atrophy
Brain tumor can produce primary optic atrophy by
compressing the optic nerve or chaisma or secondary
optic atrophy from papilledema by increased intra-
cranial pressure.
What is consecutive atrophy?
It means optic atrophy with coexistent retinal and cho-
roidal disease. The disc is yellow, waxy in appearance,
with indistinct edges and markedly contracted vessels.

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Short Notes and

Short Notes and Short Cases in Ophthalmology

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

First Edition: 2003

Publishing Director: RK Yadav

Typeset at JPBMP typesetting unit

Eyes are the precious gifts of God. Eye diseases have to

• Complications include corneal opacity, trichiasis,

• Chronic course with exacerbation and remission

• Cycloplegic drops (scopolamine 0.25% tid)

there is no epithelial defect) but oral antivirals are

• Common to congenital syphilis, less common in

• Slowly progressive irregular astigmatism, resulting

iii. Macular dystrophy—Gray white stromal deposits

21. Laser in situ keratomileusis (LASIK)

6. Floppy eyelid syndrome

• Consider CT scan of orbit and PNS in atypical or

• Usually unilateral, CT scan shows thickened

• Leukemia—(granulocytic sarcoma) may precede

• Benign mixed tumors and dermoids not to be

1. Conjunctival amelanotic tumors

unilateral and unifocal. Need meticulous excision

inflammatory granuloma (sarcoid, TB). Diffuse

1. Primary open angle glaucoma (POAG)

treatments modalities are (a) tube shunt procedures

• Secondary open angle glaucoma (lens induced,

2. Angle recession glaucoma

3. Inflammatory open angle glaucoma

landin agonists are contraindicated in inflammatory

7. Lens particle glaucoma

11. Postoperative glaucoma

13. Acute angle closure glaucoma (ACG)

appearance of cornea worsens. Despite PI if repeated

1. Anterior uveitis (iritis/iridocyclitis)

Ocular sarcoidosis needs cycloplegics, topical

• Delayed onset of endophthalmitis can be due to

retina, and thickening of uveal tract are usual. Nodular

1. Central retinal artery occlusion.

dislodge a cholesterol embolus (bright refractile

5. Central serous chorioretinopathy

• Advanced age, high myopia, systemic hypertension,

10. Ocular histoplasmosis syndrome

14. Retinal breaks

Both the forms are either asymptomatic or have

• Hereditary retinal degeneration also occurs in beta-

23. Stargardt’s disease

Opaqueness of lens or its capsule is called cataract.

• Near vision is often the most accurate manner of

• Lens can dislocate to anterior chamber or into

diffusely spreading lesion simulating uveitis. Iris

It occurs in children born < 32 weeks gestation with

but becomes clearer in CI. Patients of AI benefit from

16. Pigmentation of conjunctiva

28. Optic atrophy

40. Vitreous opacities

chamber. Poor outcome is predicted when there is (1)

6. Orbital blow out fracture

9. Traumatic optic neuropathy

1. Scintigraphy like 99m-Tc is used for lacrimal

A 60-year-old man complains of gradual diminution of

What is your diagnosis?

• Drugs like corticosteroids, chlorpromazine, amioda-

Role of ultrasound in lens implantation