Jaypee Gold Standard Mini Atlas Series®

CLINICAL
OPHTHALMOLOGY

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 Jaypee Gold Standard Mini Atlas Series®

CLINICAL
OPHTHALMOLOGY

Samar K Basak MD DNB FRCS

Disha Eye Hospitals and Research Centre
Barrackpore, Kolkata
West Bengal, India
E-mail: basak_sk@[Link]

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Jaypee Gold Standard Mini Atlas®: Clinical Ophthalmology

© 2009, Jaypee Brothers Medical Publishers
All rights reserved. No part of this publication and Photo CD-Rom should be reproduced, stored in a retrieval system, or transmitted
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First Edition: 2009

ISBN : 978-81-8448-606-3

Typeset at JPBMP typesetting unit

Printed at
 Dedicated to
Sohini Basak (Chotto Mamu)
for her
constant inspiration
 Preface

The world of Ophthalmology has an ever-widening horizon.

After success of the Atlas on Clinical Ophthalmology, I happily
present to you—the Mini Atlas. It is compact and portable version
of the original book with some new photographs. It will hopefully
aid all comprehensive ophthalmologists and postgraduate
trainees by serving as a ready reference during busy clinical
schedules. This book will also helpful for undergraduate students
along with their regular textbook.
I take this opportunity to thank my colleagues and friends
for their constant encouragement. My gratitude extends to my
beloved wife Dr. Bani and my children Soham and Sohini. Finally,
a big thanks to my publisher and his technical team for realizing
the vision I had for this book.

Samar K Basak
February, 2009
 Contents

1. Diseases of the Eyelids ............................................... 1

2. Diseases of the Conjunctiva ..................................... 21
3. Diseases of the Cornea and Sclera ..........................47
4. Anterior Chamber and Pupillary Abnormalities ..99
5. Diseases of the Uvea .............................................. 121
6. Diseases of the Lens ............................................... 151
7. Glaucomas ............................................................... 177
8. Diseases of the Vitreous and Retina .................... 201
9. Diseases of the Optic Nerve .................................. 277
10. Diseases of the Orbit .............................................. 299
11. Diseases of the Lacrimal Apparatus .................... 319
12. Motility Disturbances and Squint ........................ 327
13. Ocular Injuries ......................................................... 347

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

 CLINICAL OPHTHALMOLOGY

COLOBOMA OF THE EYELID

(FIG. 1.1)
A notch or defect of the lid
margin. Unilateral or bilateral;
upper or lower. In upper lid: at
the junction of middle and inner
1/3 and in lower lid at middle
and outer 1/3 junction. Fig. 1.1: Lid coloboma
Treatment: Urgent plastic repair
at a very early age to prevent
exposure keratitis.

BLEPHAROPHIMOSIS
SYNDROME (FIG. 1.2)
Autosomal dominant. Consists
of bilateral narrowing of palpe-
bral apertures, telecanthus,
inverse epicanthus folds, lateral
ectropion and moderate to
severe ptosis.
Treatment: Plastic reconstruc- Fig. 1.2: Blepharophimosis
tion of the eyelids, along with syndrome
bilateral brow suspension for
ptosis.

–2–
 DISEASES OF THE EYELIDS

TRICHIASIS (FIG. 1.3)

Inward misdirection of eyelash
(es) which irritate the cornea
and/or conjunctiva. When asso-
ciated with entropion - called
pseudo-trichiasis.
Treatment: Temporarily by
epilation; Permanently by elec-
trolysis, cryotherapy, or argon Fig. 1.3: Trichiasis
laser cilia ablation. If more cilia
are involved: operative pro-
cedure as entropion.

LASH IN THE PUNCTUM

(FIG. 1.4)
An uncommon phenomenon
which may cause a pricking
sensation on blinking. Mostly
seen in the lower punctum.
Treatment: Simple removal of
the offending eyelash.
Fig. 1.4: Eyelash in lower
punctum

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 CLINICAL OPHTHALMOLOGY

CONGENITAL ENTROPION
(FIG. 1.5)
Rare, may be associated with
micro- or anophthalmos. Some-
times associated with epi-
blepharon. Medial 1/3 is
commonly involved.
Treatment: Excess skin may be
removed with resection of Fig. 1.5: Congenital entropion—
tarsus. right lower lid

INVOLUTIONAL (SENILE)
ENTROPION (FIG. 1.6)
Most common and affects the
lower lid only. Caused by
horizontal lid laxity and over-
riding of preseptal part of
orbicularis.
Treatment: Weis’s procedure,
horizontal lid shortening, tuck-
ing of inferior lid retractors, etc. Fig. 1.6: Senile entropion—
lower lid

–4–
 DISEASES OF THE EYELIDS

INVOLUTIONAL (SENILE)
ECTROPION (FIG. 1.7)
Age-related condition which
affects the lower lid. Due to
excessive horizontal eyelid
length with weakness of the
preseptal orbicularis. Laxity of
medial canthal tendon is mar-
ked.
Fig. 1.7: Senile ectropion—left
Treatment: Medial conjunctivo- lower lid
plasty, Bick’s procedure, hori-
zontal lid shortening, etc.

CICATRICIAL ECTROPION
(FIG. 1.8)
Contracture of the skin and
underlying tissues of the lower
eyelid or rarely upper lid.
Caused by chemical or thermal
burn, and lacerated injury.
Treatment: excision of the scar
with a skin graft and lengthen- Fig. 1.8: Cicatricial ectropion—
ing of vertical shortening by chemical injury
Z-plasty.

–5–
 CLINICAL OPHTHALMOLOGY

CONTACT DERMATITIS
(FIGS 1.9A AND B)
Unilateral or bilateral condition,
caused by sensitivity to topical
medication, hair dyes, cos-
metics, etc. edema, erythema,
vesiculation, and later on crus-
ting.
Treatment: Withdrawal of the Fig. 1.9A: Bilateral contact
irritants, oral antihistaminics dermatitis—atropine induced
and/or antibiotic-steroids drops
and ointment.

Fig. 1.9B: Left-sided contact

dermatitis

–6–
 DISEASES OF THE EYELIDS

BLEPHARITIS
(FIGS 1.10A AND B)
Subacute or chronic inflam-
mation of the eyelids. Mostly in
children and usually bilateral.
Associated with seborrhea
(dandruff) of the scalp.
Squamous blepharitis: Hypere-
mia of the lid margins, white
dandruff-like scales on the lid Fig. 1.10A: Squamous blepharitis
margins, falling of eyelashes
(madarosis), thickening of lid
margins (tylosis).
Ulcerative blepharitis: Soreness
of the lid margins, loss of
eyelashes, and yellow crust at
the root with matting; small
ulcers at the base of crust. May
cause marginal keratitis.
Fig. 1.10B: Ulcerative blepharitis
Traetment: Lid hygiene (lid
scrub), massage, antibiotic-
steroid ointment, systemic
tetracycline/doxycycline, treat-
ment of dandruffs, etc.

–7–
 CLINICAL OPHTHALMOLOGY

MEIBOMITIS
(FIGS 1.11A AND B)
Chronic infection of the mei-
bomian glands. Occurs in the
middle age. White, frothy secre-
tion on the eyelid margins and
at the canthi (seborrhea). Vertical
yellowish streaks shining
through the conjunctiva; bloc-
ked meibomian ducts, thick Fig. 1.11A: Meibomian seborrhea
secretion on expression (‘tooth
paste sign’).
Treatment: Hot compress, tarsal
(vertical lid) massage, steroid-
antibiotic ointment, systemic
doxycycline, etc.

Fig. 1.11B: Meibomitis—tooth

paste sign

–8–
 DISEASES OF THE EYELIDS

PRESEPTAL CELLULITIS
(FIG. 1.12)
Unilateral erythema and edema
with tenderness involving the
upper eyelid. May lead to lid
abscess. But without any prop-
tosis and normal ocular moti-
lity.
Treatment: Systemic antibiotics,
analgesics, hot compress and Fig. 1.12: External hordeolum
topical antibiotics. with preseptal cellulitis

EXTERNAL HORDEOLUM
(STYE) (FIG. 1.13)
Acute suppurative inflamma-
tion of the eyelash follicle. Lid
margin swelling and may be
associated with preseptal cellu-
litis. A whitish, round, raised pus
point at eyelash root.
Treatment: Hot compress, Fig. 1.13: External hordeolum
systemic analgesics, topical (stye)
antibiotics, epilation of the
offending eyelash.

–9–
 CLINICAL OPHTHALMOLOGY

INTERNAL HORDEOLUM
(FIG. 1.14)
Unilateral acute infection of the
meibomian gland. Tender, dif-
fuse, inflamed swelling within
the tarsal plate. Swelling is away
from the lid margin. Pus-point
is away from the eyelash root.
May be associated with presep-
tal cellulitis. Fig. 1.14: Internal hordeolum

Treatment: Treatment of acute

infection followed by incision
and curettage of the chalazion.

CHALAZION (FIG. 1.15)

Chronic non-specific inflamma-
tory granuloma of the meibo-
mian gland. Painless nodular lid
swelling away from the margin.
Tarsal conjunctiva is velvety red
and slightly elevated. May be
single or multiple.
Fig. 1.15: Chalazion lower lid
Treatment: Steroid-antibiotic
ointment for small chalazion
and incision and curettage’for the
large one.

–10–
 DISEASES OF THE EYELIDS

CONGENITAL PTOSIS
(FIGS 1.16A TO C)
Unilateral or bilateral with vary-
ing severity—mild, moderate
or severe. May be simple or with
other anomalies like ‘jaw-win-
king phenomenon’.
Treatment: Depends on seve-
rity, early intervention is requi-
red in severe ptosis to prevent
amblyopia. B

C
Fig. 1.16A: Right-sided ptosis Figs 1.16B and C: Marcus-Gunn
phenomena

–11–
 CLINICAL OPHTHALMOLOGY

SENILE (APONEUROTIC)
PTOSIS (FIG. 1.17)
Common unilateral or bilateral
ptosis caused by defect in
levator aponeurosis. Good
levator function. Absent or high
upper-lid crease, thinning of
upper-lid above the tarsal plate,
deep upper supratarsal sulcus.
Treatment: Surgical correction Fig. 1.17: Bilateral senile ptosis
in severe cases.

OTHER ACQUIRED PTOSIS or prostigmin in myasthenia: a

(FIGS 1.18A AND B) positive test means dramatic
improvement of ptosis.
In Third nerve palsy, or Horner’s
syndrome, or due to Myasthenia Other causes: Ocular myo-
gravis. I/V injection of tensilon pathy, traumatic or mechanical.

Fig. 1.18A: Myasthenia gravis Fig. 1.18B: Myasthenia gravis

(before prostigmin test) (after prostigmin test)

–12–
 DISEASES OF THE EYELIDS

LAGOPHTHALMOS
(FIGS 1.19A AND B)
Inadequate closure of upper
eyelid. Associated ectropion of
lower eyelid. Dryness of lower
conjunctiva and cornea. May
cause exposure keratitis and
frank corneal ulceration.
Fig. 1.19A: Lagophthalmos
Treatment: Artificial tears, lid
taping, tarsorrhaphy and lid-
load operation.

Fig. 1.19B: Lagophthalmos—

healed exposure keratitis

–13–
 CLINICAL OPHTHALMOLOGY

SYMBLEPHARON
(FIGS 1.20A AND B)
Adhesion of lid with the globe as
a result of adhesion between
bulbar and palpebral conjunctiva.
May be anterior, posterior or
total. May be in the form of small
band or frank broad adhesion. A
Causes: Chemical burn, trauma,
thermal burn, ocular pemphi-
goid, Stevens Johnson syn-
drome, etc.
Treatment: Radical excision of
the scar tissue along with disea-
sed conjunctiva and conjunc-
tival autograft. Prevention by
sweeping a glass rod and sym- B
blepharon ring. Fig. 1.20A and B: Symblepharon

PHTHIRIASIS
PALPEBRARUM (FIG. 1.21)
Infestation of eyelashes and lid
margin with crab louse
“phthirus pubis” and its ova,
called nits. Typically affects
children and young female.
Treatment: Pilocarpine-soaked
cotton applied for few minutes Fig. 1.21: Phthiriasis palpebrum

–14–
 DISEASES OF THE EYELIDS

then the lice can be easily remo-

ved or trimming of lashes.
Simultaneous treatment for body
louse infestation.

CAPILLARY HEMANGIOMA
(FIG. 1.22)
Develops soon after birth, and
then grows for 6 month to 1
year. Irregular, raised, bright
red lesion. It blanches on pres-
sure and may swell on crying.
Treatment: Hypertonic saline/
corticosteroids injection and Fig. 1.22: Capillary (strawberry)
laser therapy. hemangioma

PORT-WINE STAIN (FIG. 1.23)

Congenital bilateral or unilateral
lesion. Sharply demarcated red
to purple patch along the 1st
and 2nd divisions of Vth nerve.
Lesion does not blanch on
pressure.
Larger lesion may be asso-
ciated with Sturge-Weber syn-
drome (choroidal hemangioma
with glaucoma, and heman- Fig. 1.23: Port wine stain—
gioma of leptomeninges). Sturge-Weber’s syndrome

–15–
 CLINICAL OPHTHALMOLOGY

MOLLUSCUM
CONTAGIOSUM (FIG. 1.24)
Single or multiple yellowish-
white umbilicated lesions. In
immunodeficiency conditions
(as in AIDS), it may be more
severe and confluent, often in
other parts of body. Associated
with keratitis or follicular con-
junctivitis. Fig. 1.24: Molluscum
contagiosum
Treatment: Investigations for
immune deficiency states; che-
mical cautery in some cases.

EXTERNAL ANGULAR
DERMOID (FIG. 1.25)
Present since early infancy.
Smooth, subcutaneous, firm,
slow growing swelling most
frequently located just below
the lateral eyebrow. May be
associated with bony defect.
Treatment: Excision of the mass, Fig. 1.25: External angular
internal extension should be dermoid
dissected carefully.

–16–
 DISEASES OF THE EYELIDS

BASAL CELL CARCINOMA

(RODENT ULCER)
(FIG. 1.26)
Most common malignant lid
tumor. Lower lid is more
commonly involved, near the
inner canthus. Edges are raised
(rolled out edges) and indura-
ted. Ulcer spreads very slowly.
It does not metastasize to Fig. 1.26: Basal cell carcinoma of
lymph nodes. lower lid

Treatment: Large surgical

excision, radiotherapy.

SQUAMOUS CELL
CARCINOMA (FIG. 1.27)
Second most common lid malig-
nancy. Appears as a nodular or
ulcerative lesion, or a papilloma.
Growth rate is faster than basal
cell carcinoma. It metastasizes
into the regional lymph nodes.
Treatment: Radical surgery Fig. 1.27: Squamous cell
carcinoma
with lid reconstruction.

–17–
 CLINICAL OPHTHALMOLOGY

MEIBOMIAN GLAND
CARCINOMA
(FIGS 1.28A AND B)
Appears as a discrete, yellow,
firm nodule which is sometimes
incorrectly diagnosed as
‘recurrent chalazion’. Wide-
spread metastasis is common
with large tumor.
Treatment: Radical excision Fig. 1.28A: Meibomian carcinoma—
mimicking a chalazion
with reconstruction of the
involved lid. Prognosis is poor.

Fig. 1.28B: Meibomian

carcinoma—after everting the lid

–18–
 DISEASES OF THE EYELIDS

XANTHELESMA (FIG. 1.29)

Raised, yellow plaques, most
commonly at the inner part of
upper lids. Often symmetrical
and grow slowly, eventually it
may spread all four lids, may
be associated with familial
hypercholesterolemia, produce
only a cosmetic defect. Fig. 1.29: Xanthelesma—
all four lids
Treatment: cosmetic surgery,
recurrence may occur.

BAGGY EYELIDS (FIG. 1.30)

Usually bilateral, age-related
condition. Due to orbital fat
herniation through the
weakened orbital septum.
Initially, fat-pockets herniate
into the medial aspect of the
upper lid, then through the
Fig. 1.30: Baggy eyelids
lower lids.
Treatment: Cosmetic surgery,
but a recurrence is common.

–19–
 CLINICAL OPHTHALMOLOGY

DERMATOCHALASIS
(FIG. 1.31)
Usually bilateral, loss of skin
elasticity, prolapse of the orbital
fat mainly in uppernasal region,
lower lid also involved with
bagginess.
Treatment: Cosmetic surgery, Fig. 1.31: Dermatochalasis
but recurrence is common.

KERATIC HORN (FIG. 1.32)

A rare benign condition, hyper-
keratotic horn-like lesion which
protrudes from the skin sur-
face.
Treatment: Excision if necessary.

Fig. 1.32: Keratic horn

–20–
 CLINICAL OPHTHALMOLOGY

SUBCONJUNCTIVAL
HEMORRHAGE
(FIGS 2.1A AND B)
Rupture of a conjunctival blood
vessel causes a bright red, shar-
ply delineated area surrounded
by the normal appearing con-
junctiva. Usually unilateral, but
it may be bilateral when Fig. 2.1A: Subconjunctival
precipitated by some straining hemorrhage
factor.
Treatment: Only assurance and
astringents eyedrops.

Fig. 2.1B: Bilateral subconjunctival

hemorrhage—whooping cough

–22–
 DISEASES OF THE CONJUNCTIVA

FOLLICLES (FIG. 2.2)

Round swellings, 0.5-2 mm in
diameter. Each follicle is encir-
cled by tiny blood vessels.
Mostly seen in palpebral and
fornicial conjunctiva. Seen in
acute follicular conjunctivitis,
trachoma, or may be drug-
induced. Fig. 2.2: Conjunctival follicle

PAPILLAE (FIGS 2.3A TO E)

Hyperplasia of normal system
of vascularization invaded by
inflammatory cells. They are
hyperemic flat-topped eleva-
tions on the tarsal conjunctiva.
Vary from simple papillary
hyperplasia to giant papillae. Fig. 2.3A: Papillae—Grade 0
Seen in allergic conjunctivitis,
trachoma and giant papillary
conjunctivitis.
Small papillae along the
medial aspect of upper tarsal
conjunctiva is a normal finding
Grades of papillae:
• Gr 0 = Normal tarsal conjun-
ctiva, no papilla.
Fig. 2.3B: papillae—Grade 1

–23–
 CLINICAL OPHTHALMOLOGY

• Gr 1 = small papillae, smooth

velvety appearance.
• Gr 2 = micropapillae, with a
diameter of 0.3-1 mm.
• Gr 3 = giant papillae, with a
diameter of >1.0 mm.
• Gr 4 = large enormous pro-
truding papillae.

Fig. 2.3C: Papillae—Grade 2

Fig. 2.3D: Papillae—Grade 3

Fig. 2.3E: Papillae—Grade 4

–24–
 DISEASES OF THE CONJUNCTIVA

MEMBRANES
(FIGS 2.4A TO C)
True membranes: Seen in certain
bacterial conjunctivitis, espe-
cially in diphtheria. Removal of
the membrane may cause blee-
ding.
Pseudomembranes: Coagulated
exudates loosely adherent to Fig. 2.4A: Chemosis of
the inflamed conjunctiva. Can conjunctiva
be easily peeled off without
bleeding. Seen in adenoviral
infection, vernal conjunctivitis
and other inflammation.

Fig. 2.4B: True membrane

Fig. 2.4C: Pseudomembrane

–25–
 CLINICAL OPHTHALMOLOGY

ACUTE MUCOPURULENT PURULENT

CONJUNCTIVITIS (FIG. 2.5) CONJUNCTIVITIS (FIG. 2.6)
Marked herperemia, lid edema, Copious purulent discharge, lid
matting of the eyelashes, con- edema, conjunctival chemosis,
junctival chemosis, petechial crusting of eyelashes, mainly
hemorrhage, muco-purulent caused by Gonococcus. Cornea
discharge or flakes of muco- may be involved in severe cases.
pus.
Treatment: Isolation, frequent
Treatment: Frequent eye wash irrigation of eyes with luke-
with lukewarm water, broad- warm saline, penicillin (1:10,000)
spectrum antibiotic eye drops, or ciprofloxacin eye drop
antibiotic ointment at night, pre- hourly, ciprofloxacin eye oint-
vention of spread of the disease. ment at night.

Fig. 2.5: Acute mucopurulent Fig. 2.6: Purulent conjunctivitis

conjunctivitis

–26–
 DISEASES OF THE CONJUNCTIVA

OPHTHALMIA MEMBRANOUS
NEONATORUM (FIG. 2.7) CONJUNCTIVITIS (FIG. 2.8)
In gonococcal infection, hyper- Lid edema, mucopurulent or
acute bilateral purulent con- sanious discharge. Thick gra-
junctivitis within a week in yish-yellow membrane on pal-
neonates. In other cases, it is a pebral conjunctiva. Bleeding is
catarrhal or mucopurulent very common on removal of
conjunctivitis. the membrane

Treatment: Ciprofloxacin eye Treatment: Isolation, crystalline

drop- hourly, ointment at night; penicillin, anti-diphtheric serum,
for Chlamydia, sulphacetamide erythromycin eye ointment.
(10%) eyedrop - 4 times daily; pre-
vention: Proper antenatal care,
asepsis during delivery, antibiotic
eye drop just after birth.

Fig. 2.8: Membranous

conjunctivitis
Fig. 2.7: Ophthalmia neonatorum

–27–
 CLINICAL OPHTHALMOLOGY

ANGULAR CONJUNCTIVITIS
(FIG. 2.9)
Conjunctivitis is limited to inner-
marginal strip at the outer/
inner canthi with excoriation of
surrounding skin. Congestion
of adjacent bulbar conjunctiva.
Treatment: Oxytetracycline eye Fig. 2.9: Angular conjunctivitis
ointment and zinc oxide con-
taining eyedrop.

ADENOVIRAL
CONJUNCTIVITIS
(FIGS 2.10A AND B)
Typical lesion is a kerato-con-
junctivitis with petechial
hemorrhage and follicles. Fig. 2.10A: Adenoviral—acute
Always a tendency of corneal follicular conjunctivitis
involvement (SPKs) and pre-
auricular lymphadenopathy.
Treatment: Astringents and
antibiotics eyedrop; tear sub-
stitutes and weak steroid drops
in corneal involvement.

Fig. 2.10B: Adenoviral conjunc-

tivitis—corneal involvement

–28–
 DISEASES OF THE CONJUNCTIVA

TRACHOMA
(FIGS 2.11A TO E)
Chronic inflammation of the
conjunctiva and the cornea.
Characterized by follicles and
papillary hypertrophy of the
conjunctiva, with pannus forma-
tion over upper part of the
cornea caused by Chlamydia Fig. 2.11A: Trachoma follicles
trachomatis. It is included in
Vision -2020 programme.
Features: Bulbar congestion;
velvety papillary hypertrophy,
follicles—mostly seen in upper
tarsal conjunctiva; pannus—
mainly seen at the upper limbus
and upper part of cornea;
Herbert’s pit at the superior Fig. 2.11B: Trachoma—papillary
limbus—a pathognomonic sign; hypertrophy
scarring of upper tarsal con-
junctiva.
Treatment: Sulphacetmide (20%
or 30%) eyedrop- 4 times daily,
tetracycline eye ointment at
night; Oral tetracycline or azi-
thromycin.

Fig. 2.11C: Trachomatous pannus

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 CLINICAL OPHTHALMOLOGY

Prevention: SAFE strategy (by PHLYCTENULAR

WHO): CONJUNCTIVITIS (FIG. 2.12)
• S = Surgery for trichiasis and Characterised by bleb forma-
entropion tion near or at the limbus in
• A = Antibiotics young children. Pinkish-white
• F = Facial cleanliness or gray in color, with bulbar
• E = Environmental sanitation congestion surrounding the
bleb.
Treatment: Corticosteroid eye
drops, investigation and general
measures.

Fig. 2.11D: Trachoma scar

Fig. 2.11E: Herbert’s pit Fig. 2.12: Limbal phlycten

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 DISEASES OF THE CONJUNCTIVA

VERNAL KERATOCON-
JUNCTIVITIS (VKC)
(FIGS 2.13A TO D)
Bilateral, recurrent, seasonal
(spring) allergic conjunctivitis in
children caused by exogenous
allergens. Presents in one of the
three forms: Palpebral, bulbar
or mixed. Fig. 2.13A: Cobble stone papillae
Palpebral: Cobble-stone like of
papillary hypertrophy of the
palpebral conjunctiva.
Bulbar: Multiple, small, nodule-
like gelatinous thickening
around the limbus, mostly at the
upper.
Discrete superficial spots,
called Horner-Tranta’s dots and Fig. 2.13B: VKC—Cupid’s bow
micropannus around the upper
limbus; epithelial micro-
erosions—leading to corneal
ulceration (Shield ulcer).
Pseudo-gerontoxon—resembles
an arcus senilis with appearance
of ‘cupid’s bow’.

Fig. 2.13C: VKC—Horner Tranta’s

dots

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 CLINICAL OPHTHALMOLOGY

Treatment: Cold compress, GIANT PAPILLARY

topical antihistaminics, soft CONJUNCTIVITIS (GPC)
corticosteroids and mastcell (FIG. 2.14)
stabilizer eyedrops. Foreign body (Soft CL, Artificial
eye & nylon sutures) associated
allergic conjunctivitis with
characteristic giant papillae (>1
mm). Clinical picture is similar
to palpebral vernal conjunc-
tivitis with presence of giant
papillae.
Treatment: As VKC and avoi-
dance of offending agents.
Fig. 2.13D: VKC—shield ulcer

Fig. 2.14: GPC

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 DISEASES OF THE CONJUNCTIVA

PTERYGIUM
(FIGS 2.15A TO D)
Subconjunctival tissue prolifera-
tes as a triangular wing-shaped
tissue-mass to invade the
cornea, involving the Bowman’s
membrane and the superficial
stroma.
Fig. 2.15A: Progressive pterygium
Usually bilateral, may be
asymmetrical, among elderly
individual. Progressive (fleshy)
and stationary (atrophic) types.
Atrophic (stationary): Thin, atte-
nuated with poor vascularity,
no opaque spot (cap) is seen.
Progressive (fleshy): Thick, fleshy
with prominent vascularity,
increasing in size and encroa- Fig. 2.15B: Atrophic pterygium
ching towards the centre of
cornea, opaque infiltrative spot
(cap) with Stocker’s line in front
of the apex.
Recurrent pterygium: With more
scarring and wider.
Malignant pterygium: Recurrent
pterygium with symblepharon Fig. 2.15C: Recurrent pterygium

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 CLINICAL OPHTHALMOLOGY

formation associated with

restriction of ocular movement
on opposite side.
Treatment: Excision of ptery-
gium (subconjunctival dissec-
tion) with conjunctival limbal
autograft (CLAU) is the
treatment of choice. Treatment
of the bare sclera by MMC is Fig. 2.15D: Malignant pterygium
another option.

PSEUDOPTERYGIUM
(FIG. 2.16)
Adhesion of a fold of conjunc-
tiva to the peripheral cornea;
Usually unilateral, stationary,
and at any meridian. A probe
can be passed easily beneath the
neck of the pterygium (Probe
test) Fig. 2.16: Pseudopterygium
Treatment: Simple excision.

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 DISEASES OF THE CONJUNCTIVA

CONJUNCTIVAL CYSTS
(FIGS 2.17A AND B)

Retention cysts: Due to obs-

truction of Krause gland’s duct.
Implantation cysts: Due to the
implantation of conjunctival
epithelium or after an operation
or trauma.
Fig. 2.17A: Retention cyst
Parasitic cysts: As subconjunc-
tival cysticercus.
Treatment: Simple excision in
most cases.

Fig. 2.17B: Implantation cyst

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 CLINICAL OPHTHALMOLOGY

EPIBULBAR LIMBAL
DERMOID (FIGS 2.18A
AND B)
Congenital lesion; solid,
smooth, round white masses
most frequently at the limbus.
Large lesion may also involve
the cornea.
They may be associated
with Goldenhar’s syndrome (pre- Fig. 2.18A: Dermoid—corneal
involvement
auricular skin tags, vertebral
anomalies and hemifacial hypo-
plasia) which may be unilateral
or bilateral. Consists of skin with
sebaceous glands and hair.
Treatment: Excision of the mass
with or without lamellar kerato-
plasty.

Fig. 2.18B: Goldenhar’s

syndrome—unilateral

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 DISEASES OF THE CONJUNCTIVA

DERMOLIPOMA
(LIPODERMOID)
(FIGS 2.19A AND B)
Large, soft, yellowish, movable
subconjunctival masses, located
at the outer canthus or at the
limbus.
Lesions extend beyond
superior fornix and impossible Fig. 2.19A: Dermolipoma
to visualize the posterior limit.
Sometimes, it may be associated
with Goldenhar’s syndrome.
Treatment: Excision of the mass.

CONJUNCTIVAL INTRA-
EPITHELIAL NEOPLASIA
(FIG. 2.20)
Rare unilateral premalignant Fig. 2.19B: Bilateral dermolipoma—
condition, seen in elderly indi- Goldenhar’s syndrome
viduals (previously called
Bowen’s disease). Slightly eleva-
ted, fleshy mass with tuft of
blood vessels at the limbus
which may involve the adjacent
cornea.
Treatment: Excision of the mass
with triple cryo-thawing of the
dissected area. Fig. 2.20: CIN—corneal involement

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 CLINICAL OPHTHALMOLOGY

INVASIVE SQUAMOUS-CELL
CARCINOMA
(FIGS 2.21A AND B)
Slow growing, locally invasive
tumor at limbus arises from
papilloma or carcinoma-in-situ.
Reddish-gray fleshy mass with
broad base, and characterized
Fig. 2.21A: Invasive squamous
by deep invasion into the
cell carcinoma
stroma with fixation to the
underlying structure.
Treatment: Excision of the mass
with triple cryo-thawing of the
dissected area with peropera-
tive MMC.

Fig. 2.21B: Squamous cell

carcinoma—from caruncle
SIMPLE NEVUS (FIG. 2.22)
Single, sharply demarcated, flat
or slightly elevated lesion, has
predilection for the limbus.
Most nevi have a brown color
and 25% are non-pigmented.
Treatment: Excision for cosmetic
reason.
Fig. 2.22: Simple nevus

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 DISEASES OF THE CONJUNCTIVA

PRECANCEROUS MALIGNANT MELANOMA

MELANOSIS (FIG. 2.23) (FIG. 2.24)
Small pigmented tumor which May be pigmented or non-
spread as a diffuse patch of pigmented elevated lesion
pigmented lesion. Mostly occur which affects elderly people.
in elderly patients. In 20% cases,
Has a predilection for limbus.
it proceeds to frank malignancy.
Larger lesion may involve
cornea, adjacent part of eyelid
Treatment: Excision and biopsy
and orbit. Metastasis is
in suspected cases.
common.
Treatment: Excision of the mass
with Cryo and MMC

Fig. 2.23: Precancerous Fig. 2.24: Conjunctival

melanosis melanoma 1

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 CLINICAL OPHTHALMOLOGY

CONJUNCTIVAL XEROSIS BITOT’S SPOT (FIG. 2.26)

(FIG. 2.25) Bilateral lesion in young chil-
Mainly due to vitamin-A defi- dren due to vitamin-A defi-
ciency with associated PEM. ciency. Appears as triangular
Other causes: Burns, pem- patch, with base towards
phigoid, diphtheria, β-blocker limbus and usually on the
or following prolonged expo- temporal side. It may be cheesy
sure, etc. Conjunctiva is pale, or foamy in appearance.
lustureless and with folds and
Treatment: Active prompt
variable pigmentation.
vitamin-A supplementation
Treatment: Active prompt
vitamin-A supplementation
and tear supplementation.

Fig. 2.25: Conjunctival xerosis Fig. 2.26: Bitot’s spot—foamy

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 DISEASES OF THE CONJUNCTIVA

KERATOCONJUNCTIVITIS
SICCA (FIGS 2.27A TO H)
Very common bilateral condi-
tion, leading to dry eye and
ocular surface disorders in
postmenopausal women. Tear
meniscus height is reduced or
absent.
Schirmer’s reading and tear film Fig. 2.27A: KCS—low tear
break-up-time (TBUT) is also meniscus height
reduced.
Presence of corneal filaments
and mucus plaques/debris; A
positive fluorescein, Rose Ben-
gal or Lissamin green staining
of interpalpebral conjunctival
area in a triangular fashion. And
also positive corneal staining.
Corneal staining associated
with other corneal changes, like Fig. 2.27B: Keratoconjunctivitis
sicca—mucous debris
delen, vascularisation, fila-
ments, etc.
Treatment: Tear substitutes,
topical cyclosporine (0.05%) or
‘soft steroids’, punctal occlusion,
etc.

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 CLINICAL OPHTHALMOLOGY

Fig. 2.27C: KCS—rose Bengal Fig. 2.27F: KCS—Lissamine

stain green stain

Fig. 2.27D: KCS—fluorescein stain Fig. 2.27G: KCS—Descemetocele

Fig. 2.27E: KCS—rose Bengal Fig. 2.27H: KCS—

stain vascularization

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 DISEASES OF THE CONJUNCTIVA

OCULAR CICATRICIAL
PEMPHIGOID
(FIGS 2.28A TO C)
Conjunctival inflammation with
fine subepithelial fibrosis and
shrinkage with shortening of
inferior fornix.
Medial symblepharon followed Fig. 2.28A: OCP—Medial
by total symblepharon forma- symblepharon
tion. Keratinization, vasculari-
zation and persistent epithelial
defect of the cornea.
Trichiasis and metaplastic eye-
lashes and total obliteration of
fornices.
Treatment: Tears substitute,
systemic immunosuppressive, Fig. 2.28B: OCP—obliteration of
removal of metaplastic lashes, fornices
etc.

Fig. 2.28C: OCP—keratinization

of ocular surface

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 CLINICAL OPHTHALMOLOGY

STEVENS-JOHNSON’S
SYNDROME
(FIGS 2.29A AND B)
Mucocutaneous vesicullo-
bullous lesions caused by a
hypersensitivity reaction to
certain drugs. Conjunctiva is
involved in 50% of cases. Muco-
purulent conjunctivitis with
Fig. 2.29A: Steven Johnson
membrane or pseudo-memb-
syndrome—skin involvement
rane formation. Oral mucous
membrane lesions.
Secondary scarring of the con-
junctiva and lid margins - with
trichiasis (acquired distichiasis),
symblepharon and obliteration
of the fornices.
Treatment: Tears substitute,
systemic immunosuppressive,
removal of metaplastic lashes,
etc. Fig. 2.29B: SJ syndrome—oral
lesion

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 DISEASES OF THE CONJUNCTIVA

SUPERIOR LIMBIC
KERATOCONJUNCTIVITIS
(FIG. 2.30)
Bilateral keratoconjunctivitis,
sometimes associated with
thyroid dysfunction.
Papillary hypertrophy and
thickening of superior tarsal
conjunctiva. Hyperemia and Fig. 2.30: Superior limbic
thickening of superior bulbar keratoconjunctivitis
conjunctiva.
Positive rose Bengal staining of
upper part. Filaments in
adjacent cornea.
Treatment: Tears substitute,
topical (0.05%) cyclosporine,
excision of upper bulbar
conjunctiva.

CONJUNCTIVOCHALASIS
(FIG. 2.31)
Loose conjunctiva in old age
may appear as conjunctival
folds mainly in the inferior
fornix and overrides onto the
cornea. May be responsible for Fig. 2.31: Conjunctivochalasis

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 CLINICAL OPHTHALMOLOGY

watering and recurrent con-

junctivitis. Fluorescein staining
positive in the lower third of
cornea.
Treatment: Tear substitutes and
conjunctivoplasty.

CONJUNCTIVAL
GRANULOMAS
(FIGS 2.32A AND B)

Pyogenic granuloma: Most

commonly occurs after conjunc-
tival surgery like, pterygium
surgery or symblepharon
operation. Fig. 2.32A: Pyogenic granuloma

Treatment: Excision of the

granuloma.
Rhinosporidiosis: Rare fungal
infection usually after a foreign
body in conjunctiva.

Fig. 2.32B: Granuloma—

rhinosporiodosis

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 CLINICAL OPHTHALMOLOGY

PIGMENT DEPOSITION IN THE CORNEA

(FIGS 3.1A TO D)
Iron
Keratoconus Epithelium
Fleischer’s ring
Old opacity Epithelium
Hudson-Stahli line
Pterygium Epithelium
Stocker’s line
Filtering bleb Epithelium
Ferry’s line
Siderosis Stroma
Blood staining Stroma
Copper
Wilson’s disease Descemet’s membrane
Kayser-Flescher ring
Melanin
Pigment dispersion syndrome Endothelium
Krukenberg’s spindle

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 DISEASES OF THE CORNEA AND SCLERA

Fig. 3.1A: Fleischer’s ring Fig. 3.1C: Stocker’s line

Fig. 3.1B: Hudson Stahli’s line Fig. 3.1D: Kayser Flescher ring

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 CLINICAL OPHTHALMOLOGY

MICROPHTHALMOS
(FIG. 3.2)
Unilateral or bilateral congenital
abnormality in which the axial
length is reduced. Visual acuity
is usually poor and depends
upon the associated anomalies.
Microphthalmos may be with
Fig. 3.2: Microcornea in
or without coloboma.
microphthalmos—right eye

NANOPHTHALMOS
(FIGS 3.3 A AND B)
Uncommon, congenital, bilate-
ral condition, with small globe
in all dimensions (nano means
‘dwarf’). Anatomically the eye
is grossly normal. Very high A
hypermetropia, axial length is
less than 20 mm.
Fundus showed a crowded disk
with vascular tortuosity and
macular hypoplasia

B
Figs 3.3A and B: Nanophthalmos

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 DISEASES OF THE CORNEA AND SCLERA

MEGALOCORNEA (FIG. 3.4)

Rare, congenital, bilateral
condition. Corneal diameter is
more than 13 mm. Very deep
anterior chamber. High myopia
and astigmatism with good
visual acuity. Normal intra-
ocular pressure.
Fig. 3.4: Megalocornea

KERATOGLOBUS (FIG. 3.5)

Congenital bilateral very rare
condition. Mid-peripheral
thinning resulting in protrusion
or bulging of whole cornea, with
an appearance of globular
shape. Very deep anterior
chamber. Acute hydrops in
extreme cases. Fig. 3.5: Keratoglobus

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 CLINICAL OPHTHALMOLOGY

PETER’S ANOMALY
(FIGS 3.6 A AND B)
Central corneal opacity, due to
defect in embryogenesis. In
milder form, it only causes
posterior keratoconus. But in
most cases, it is associated with
anterior polar cataract, iris
adhesion, angle abnormalities,
or secondary glaucoma. Fig. 3.6A: Peter’s anomaly—
posterior keratoconus

Fig. 3.6B: Peter’s anomaly

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 DISEASES OF THE CORNEA AND SCLERA

CORNEAL EDEMA (FIGS

3.7A TO D)
Associated with increased in
corneal thickness due to
accumulation of fluid with
variable degree of loss in
corneal transparency.
Edema may be focal or gene-
ralized; may be with epithelial Fig. 3.7A: Corneal edema with
defect. Descemet’s fold

In long standing cases, the

epithelium tends to be raised
into large vesicles or bullae,
leading to bullous keratopathy.
Important causes: inflammation,
trauma, increased IOP, endo-
thelial dysfunction as in Fuchs’
dystrophy, hypoxia of the
cornea as in contact lens wearer
Fig. 3.7B: Moderate corneal
Treatment: Hypertonic saline edema
drops, thin conjunctival flap,
multiple anterior stromal punc-
ture with BCL, penetrating
keratoplasty (PK) or Descemets’
stripping and endothelial
keratoplasty (DSEK).

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 CLINICAL OPHTHALMOLOGY

Fig. 3.7C: Gross corneal edema Fig. 3.7D: Corneal edema with
bullous keratopathy

BACTERIAL KERATITIS/
ULCER (FIGS 3.8A TO F)
Most frequent causative agents
are Staph. aureus, Pseudomonas
and Strepto. pneumoniae. Signs
vary with the severity and on
causative agents.
Lid edema, marked ciliary
congestion; Epithelial break-
down followed by stromal Fig. 3.8A: Bacterial ulcer
suppuration.
Ulcer usually starts as a grayish-
white circumscribed infiltration;
Edema of the surrounding
tissue; Margins are over

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 DISEASES OF THE CORNEA AND SCLERA

Fig. 3.8B: Bacterial ulcer with Fig. 3.8D: Bacterial corneal ulcer
hypopyon with threatened perforation

Fig. 3.8C: Bacterial ulcer— Fig. 3.8E: Perforated corneal ulcer

Pseudomonas

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 CLINICAL OPHTHALMOLOGY

hanging and the floor is covered

by necrotic material; Overall
look of the ulcer is wet; Hypo-
pyon may be present in variable
amount with flat border.
Corneal abscess: Localized
suppuration in the deeper
stroma under intact corneal
epithelium. Usually associated
with staphylococcal infection. Fig. 3.8F: Corneal abscess

Treatment: Scraping and smear

preparation to identify the
microorganism quickly and
then prompt initiation of
therapy with frequent (hourly)
topical broad-spectrum anti-
biotics. Other therapy includes-
atropine, treat secondary
glaucoma. Therapeutic PK in
extreme cases.

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 DISEASES OF THE CORNEA AND SCLERA

FUNGAL KERATITIS OR
KERATOMYCOSIS
(FIGS 3.9A TO F)
Causative agent may be
Filamentous fungi or Candida.
Typically preceded by ocular
trauma with agricultural and
vegetable matters.
Fig. 3.9A: Fungal keratitis
Relatively painless, dry looking,
elevated yellowish-white lesion
with indistinct margin. Delicate,
feathery, fingerlike projections
into the adjacent stroma.
Massive dense hypopyon which
is immobile with convex upper
border.
Slowly progressive stromal Fig. 3.9B: Fungal keratitis—
destruction may lead to corneal feathery edge
perforation with its sequeale.
Candida keratitis: Gray-white
infiltrate (often as collar-button
abscess) similar to bacterial
ulcer.
Filamentary keratitis: Typical
feathery appearance with fin-
gerlike projection and satellite Fig. 3.9C: Fungal keratitis—
lesion elevated surface

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 CLINICAL OPHTHALMOLOGY

Dematecious fungal keratitis: often

produce pigments on the
surface of the ulcer.
Treatment: Topical antifungal
agents—natamycin (5%),
amphotericin B (0.15%), or
voriconazole – 1-2 hourly. May
require therapeutic PK in severe
cases.
Fig. 3.9E: Fungal ulcer—ring
infiltration

Fig. 3.9D: Fungal ulcer—convex Fig. 3.9F: Fungal keratitis—

hypopyon dematecious fungus

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 DISEASES OF THE CORNEA AND SCLERA

ACANTHAMOEBA
KERATITIS
(FIGS 3.10A AND B)
Very rare unilateral keratitis
that typically affects the soft
contact lens wearer.
Radial keratoneuritis; progres-
sive chronic stromal keratitis
with recurrent breakdown of Fig. 3.10A: Acanthamoeba
corneal epithelium. Paracentral keratitis—ring infiltrates
ring-shaped ulcer or abscess is
the hall mark of advanced
infection.
Treatment: PHMB, propamidine
isothionate, neomycin, chloro-
hexidine, etc. Therapeutic PK in
resistance cases.

Fig. 3.10B: Acanthamoeba

keratitis—vascularization

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 CLINICAL OPHTHALMOLOGY

SEQUEL OF CORNEAL
ULCER (FIGS 11A TO G)
Nebula, macula, leucoma,
adherent leucoma, anterior
staphyloma, phthisis bulbi.
Vascularization may occur in
any form of opacity.

Fig. 3.11C: Central leucoma

Fig. 3.11A: Nebular corneal

opacity

Fig. 3.11D: Adherent leucoma

Fig. 3.11B: Macular corneal

opacity

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 DISEASES OF THE CORNEA AND SCLERA

Fig. 3.11E: Leucoma with severe vascularization

Fig. 3.11F: Anterior Fig. 3.11G: Phthisis bulbi

staphyloma—partial

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 CLINICAL OPHTHALMOLOGY

DENDRITIC KERATITIS
(HSV) (FIGS 3.12A AND B)
Initially starts as superficial
punctate erosion which coa-
lesce. They send out lateral
branches with knobbed ends, to
form ‘dendritic’ or ‘tree-like’
figure and this is pathognomonic.
Bed of the ulcer stains with Fig. 3.12A: Dendritic keratitis
fluorescein and the swollen
diseased cells at the margin take
up rose Bengal stain.
Treatment: Debridement,
topical antiviral (acyclovir), mild
cycloplegic, oral acyclovir to
prevent recurrence.

Fig. 3.12B: HSV—dendritic

keratitis—rose Bengal staining

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 DISEASES OF THE CORNEA AND SCLERA

GEOGRAPHICAL KERATITIS
(FIG. 3.13A AND B)
Larger epithelial lesion—
‘geographical’ or ‘ameboid’
configuration. May occur as a
continued enlargement of den-
dritic keratitis. Likely to occur
following inadvertent use of
topical steroids.
Fig. 3.13A: HSV—geographical
Treatment: Similar to dendritic keratitis
keratitis.

Fig. 3.13B: Dendrogeographical

ulcer

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 CLINICAL OPHTHALMOLOGY

STROMAL NECROTIC
KERATITIS (FIG. 3.14)
Cheesy and necrotic appearance
of the stroma. May be asso-
ciated with epithelial break-
down and anterior uveitis.
Vascularization, scarring and
even perforation may occur.
Treatment: Oral acyclovir, Fig. 3.14: HSV—stromal necrotic
topical antiviral, cycloplegic and keratitis
judicious use of topical steroids.

METAHERPETIC
KERATITIS (TROPHIC
ULCER) (FIG. 3.15)
Due to persistent defects in the
basement membrane. Margin is
gray and thickened due to
heaped-up epithelium. Not an
active viral disease.
Fig. 3.15: HSV—metaherpetic
Treatment: Artificial tears and keratitis
bandage contact lens (BCL).

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 DISEASES OF THE CORNEA AND SCLERA

DISCIFORM KERATITIS
(FIGS 3.16A AND B)
Deep keratitis with disklike
edema—immunogenic reaction
to HSV. Focal central stromal
edema with fine KPs.
Presence of Descemet’s folds
and increased central corneal A
thickness in severe cases.
Wessely’s immune ring surroun-
ding the edema in long standing
cases (Fig. 3.16C).
Treatment: Topical steroids (full
strength or diluted) with
acyclovir eye ointment in equal
frequency and cycloplegic. B
Figs 3.16A and B: Disciform
keratitis

Fig. 3.16C: Wessely’s immune ring

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 CLINICAL OPHTHALMOLOGY

HERPES ZOSTER
OPHTHALMICUS
(FIGS 3.17A AND B)
Vesicular eruptions around the
eye, forehead and the scalp.
Hutchinson’s rule: When the tip
of the nose is involved, the eye
will also be involved. Ocular
lesions may be acute, chronic or
recurrent nummular keratitis: Fig. 3.17A: Herpes zoster
multiple granular lesions sur- ophthalmicus
rounded by a halo of stromal
haze.
Treatment: Oral acyclovir (800
mg 5 times daily for 7 days),
topical steroids in keratitis or
iridocyclitis and systemic ste-
roids in neuro-ophthalmolo-
gical problems.

Fig. 3.17B: Nummular keratitis

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 DISEASES OF THE CORNEA AND SCLERA

LAGOPHTHALMIC
(EXPOSURE) KERATITIS
(FIG. 3.18)
Owing to dryness and desicca-
tion, the lower third of epithe-
lium is cast off and the raw area
is invaded by microorganism.
Seen in facial palsy, leprosy,
proptosis thyroid exophthal-
mos, comatose patient, etc. Fig. 3.18: Lagophthalmic keratitis

Treatment: Lid taping, tarsor-

rhaphy, lid-load operation and
treatment of the cause.

NEUROTROPHIC KERATITIS
(NTK) (FIG. 3.19)
Occurs in anesthetic cornea
which alters the metabolism of
the epithelium. Mostly seen in
HSV and HZV keratitis. Punc-
tate epithelial erosion involving
the intrapalprbral area. Edema
and exfoliation followed by
epithelial ulceration. Fig. 3.19: Neurotropic keratitis
Treatment: Ointment and pat-
ching, in severe cases amniotic
membrane transplantation
(AMT) or tarsorrhaphy.

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 CLINICAL OPHTHALMOLOGY

MARGINAL KERATITIS
(CATARRHAL ULCER)
(FIGS 3.20A AND B)
Caused by hypersensitivity
reaction to Staphylococcal exo-
toxin. Subepithelial infiltrates at
the periphery, mostly at 4-8
A
o’clock position, or at 10-12
o’clock position.
Treatment: Topical cortico-
steroids, steroid-antibiotic
ointment and simultaneous
treatment of blepharitis.

B
FASCICULAR ULCER
(FIG. 3.21) Figs 3.20A and B: Meibomitis
with marginal keratitis
Phlyctenular ulcer slowly
migrates towards the centre of
the cornea in a serpiginous way
and carries leash of blood
vessels which lie in a shallow
gutter formed by the ulcer.
Treatment: Topical cortico-
steroids, cycloplegic and topical
antibiotic. Fig. 3.21: Phlyctenular keratitis—
fascicular ulcer

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 DISEASES OF THE CORNEA AND SCLERA

INTERSTITIAL KERATITIS
(IK) (FIGS 3.22A AND B)
Inflammation of the corneal
stroma without primary invol-
vement of epithelium or endo-
thelium. Rare bilateral codition,
seen in syphilis, tuberculosis or
Cogan’s syndrome.
Vascularized, midstromal, non- Fig. 3.22A: Interstitial keratitis
suppurative inflammation,
giving a ground glass appea-
rance. In inactive stage, there is
variable stromal scarring with
ghost vessels.
Hutchinson’s triad: IK, deafness
and Hutcinson’s teeth – a part of
congenital syphilis.
Treatment: Systemic penicillin,
topical steroids, cyloplegic and Fig. 3.22B: Interstitial keratitis—
AT drugs in selective cases. ghost vessels

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 CLINICAL OPHTHALMOLOGY

PUNCTATE EPITHELIAL
KERATITIS (PEK)
(FIGS 3.23A AND B)
Punctate epithelial lesions scattered
all over the cornea, usually seen
after acute viral conjunctivitis.
Sometimes, they extend into the
Bowman’s membrane and super- Fig. 3.23A: Punctate
ficial stroma. epithelial keratitis
Treatment: Tear substitutes and
dilute topical steroids.

Fig. 3.23B: Superficial

SCLEROSING KERATITIS punctate keratitis
(FIG. 3.24)
Rare condition may occur in isolation
or with scleritis. Gradual peripheral
stromal thickening and opacifica-
tion. Vascularization and lipid
deposition may also occur.
Treatment: Systemic/topical steroids
and investigations. Fig. 3.24: Acute sclerosing
keratitis

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 DISEASES OF THE CORNEA AND SCLERA

TERRIEN’S MARGINAL
DEGENERATION
(FIGS 3.25A AND B)
Lesion starts as fine yellow-
white punctate stromal opaci-
ties at the upper part of the
cornea. Sharp edge towards the
centre becomes demarcated by A
yellow-white lipid deposits.
Eventually, thinning to form a
peripheral gutter. Overlying
epithelium is intact and
vascularization is prominent.
Treatment: RGP contact lens,
deep lamellar sectorial kerato-
plasty in severe cases or
peripheral PK in perforation.
B
Figs 3.25A and B: Terrien’s
degeneration—marginal gutter
(A) Upper cornea
(B) Lower cornes

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 CLINICAL OPHTHALMOLOGY

PELLUCID MARGINAL as in Terrien’s. Hydrops may

DEGENERATION occur as keratoconus.
(FIGS 3.26A AND B)
Treatment: Correction of
Thinning involves only the astigmatism by RGP contact
inferior cornea with ectasia just lens, tectonic patch graft.
above the area of thinning,
giving rise the appearance of MOOREN’S ULCER
keratoconus. No vasculari- (FIGS 3.27A AND B)
zation (as in Mooren’s or
Terriens), or no lipid deposition Chronic peripheral ulcer of
unknown etiology due to ische-
mic necrosis from vasculitis of
perilimbal vessels.

Fig. 3.26A: Pellucid marginal

A
degeneration

B
Fig. 3.26B: PMD—acute hydrops Figs 3.27A and B: Mooren’s ulcer

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 DISEASES OF THE CORNEA AND SCLERA

Peripheral ulcer with over-

hanging edge. Later involves
the entire circumference and
also spread towards the center.
Perforation may occur with
minor trauma.
Treatment: Peritomy, glue with
BCL, systemic immuno-sup-
pressants, lamellar tectonic
graft, etc.

MARGINAL ULCERS WITH

SYSTEMIC COLLAGEN
VASCULAR DISORDERS
(FIG. 3.28)
Seen in rheumatoid arthritis,
polyarteritis nodosa, SLE, or in
Wegener’s granulomtosis.
Ulceration and thinning; peri-
pheral keratolysis, sclerosing Fig. 3.28: Total peripheral kerato-
keratitis, ‘contact lens cornea’, lysis with contact lens cornea
etc.
Treatment: Systemic and topical
steroids, tear substitutes,
immunosuppressive agents (e.g.
oral azothioprim), peritomy or
peripheral keratoplasty.

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 CLINICAL OPHTHALMOLOGY

BAND-SHAPED
KERATOPATHY (BSK)
(FIGS 3.29A AND B)
Calcific horizontal band, largely
at the palpebral fissure, separa-
ted from limbus by a clear zone.
Begins at periphery- 3 and
9 o’clock position, and then
affects the central area.
Treatment: Scraping of the Fig. 3.29A: Band-shaped
epithelium, treatment with di- keratopathy in JRA
sodium EDTA, and lamellar
keratoplasty in severe cases.

Fig. 3.29B: Band-shaped

keratopathy

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 DISEASES OF THE CORNEA AND SCLERA

SALZMANN’S NODULAR
DEGENERATION (FIG. 3.30)
Uncommon, and mostly uni-
lateral. Elevated subepithelial
bluish-gray nodules in a scarred
cornea and surrounded cornea
is clear.
Fig. 3.30: Salzmann nodular
Treatment: Not necessary, degeneration
photorefractive keratoplasty
(PTK) or lamellar keratoplasty
in case of central lesion.

SPHEROIDAL DEGENE-
Fig. 3.31A: Spheroidal
RATION (FIGS 3.31A AND B) degeneration—primary
Rare, bilateral, small amber
colored granules in the super-
ficial stroma and conjunctiva,
mainly in the interpalpebral
area. Lesions then spread cen-
trally and coalesce to become
denser.
Treatment: Lamellar or pene-
Fig. 3.31B: Spheroidal
trating keratoplasty.
degeneration—corneal opacity

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 CLINICAL OPHTHALMOLOGY

REIS-BUCKLER’S
DYSTROPHY
(FIGS 3.32A AND B)
Relatively common, bilateral
condition. Reduced visual acuity
in second or third decade. Ring-
shaped subepithelial opacities
giving ‘honeycomb’ appear-
ance. Entire cornea is affected
Fig. 3.32A: Reis-Buckler
with more involvement of the
dystrophy
central area.
Treatment: Deep anterior
lamellar keratoplasty or PK.

Fig. 3.32B: Reis-Buckler

dystrophy—severe

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 DISEASES OF THE CORNEA AND SCLERA

GRANULAR DYSTROPHY
(FIGS 3.33A TO C)
Autosomal dominant bilateral
disease. Lesions appear as
discrete, crumb-like white
granules within the anterior
stroma of the central cornea.
Stroma in between the opacities A
and the peripheral cornea
remains clear.
Treatment: DALK or PK.

C
Figs 3.33A to C: Granular
dystrophy—more confluent

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 CLINICAL OPHTHALMOLOGY

MACULAR DYSTROPHY
(FIGS 3.34A AND B)
Autosomal recessive, bilateral
with significant impairment of
vision at an early stage. Central,
focal, gray-white poorly defined
opacities in cloudy stroma.
Lesions involve the entire A
thickness of stroma and also
extend upto the limbus.
Treatment: Penetrating kerato-
plasty.

B
Figs 3.34A and B: Macular
dystrophy

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 DISEASES OF THE CORNEA AND SCLERA

LATTICE DYSTROPHY rent levels within the stroma.

(FIGS 3.35A TO D) Recurrent erosions and secon-
Bilateral condition with mixed dary spheroidal degeneration
inheritance. Fine branching are common.
spider-like refractile lines which Treatment: PK; recurrence in the
interlace and overlap at diffe- graft is common.

Fig. 3.35A: Lattice dystrophy— Fig. 3.35C: Lattice dystrophy—

type I type III

Fig. 3.35B: Lattice dystrophy— Fig. 3.35D: Lattice dystrophy—

type II with CDK

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 CLINICAL OPHTHALMOLOGY

CORNEA GUTTATA
(FIGS 3.36A AND B)
A common aging process resul-
ting in focal accumulation of
excrescences on the posterior
surface Descemet’s.
They disrupt the normal endo-
thelial mosaic. With confluent
lesions, appear as dark spots or Fig. 3.36A: Cornea guttata
‘beaten metal’. May be seen in
early stage of Fuchs’ dystrophy.

Fig. 3.36B: Cornea guttata—

beaten metal appearance

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 DISEASES OF THE CORNEA AND SCLERA

FUCHS’ ENDOTHELIAL
DYSTROPHY
(FIGS 3.37A TO D)
Bilateral, autosomal dominant
and more in elderly female.
Central corneal guttata without
any symptom which gradually
spreads towards periphery.
Stroma becomes edematous Fig. 3.37B: Fuchs’ dystrophy-
with endothelial decompen- moderate
sation.

Fig. 3.37A: Fuchs’ dystrophy— Fig. 3.37C: Fuchs’ dystrophy—

Early bullous keratopathy

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 CLINICAL OPHTHALMOLOGY

Epithelial edema with bullous

keratopathy gradually deve-
lops with impairment of vision.
Finally, corneal scarring occurs
with vascularization.
Treatment: Hypertonic saline,
bandage contact lens and ulti-
mately DSEK or PK.
Fig. 3.37D: Fuchs’ dystrophy—
scarring
KERATOCONUS
(FIGS 3.38A TO F)
Bilateral conical protrusion of
the central part of the cornea
with thinning.
Munson’s sign: Bulging of lower
lids in down gaze.
Vogt’s lines (striae): Vertical folds
at the level of deep stroma and
Descemet’s membrane.
Fig. 3.38A: Keratoconus—
Fleischer’s ring: Epithelial iron Munson’s sign
line at the base of the cone.
Rizutti’s sign: Corneal reflection
on the nasal limbus when light
is thrown from the temporal
limbus.

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 DISEASES OF THE CORNEA AND SCLERA

Fig. 3.38B: Keratoconus Fig. 3.38D: Keratoconus—

prominent corneal nerve

Fig. 3.38C: Keratoconus— Fig. 3.38E: Keratoconus—acute

Rizutti’s sign hydrops

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 CLINICAL OPHTHALMOLOGY

Prominent corneal nerves.

Acute hydrops: Sudden corneal
edema due to acute seepage of
aqueous into the corneal stroma
and epithelium resulting from
rupture of Descemet’s mem-
brane.
Variable degree of apical cor-
neal scarring.
Fig. 3.38F: Keratoconus—apical
Treatment: Spectacles, RGP scarring
contact lenses, deep anterior
lamellar keratoplasty (DALK)
or penetrating keratoplasty.

STRIATE KERATOPATHY
(KERATITIS) (FIG. 3.39)
Unilateral corneal edema with
Descemet’s folds; usually after
a cataract surgery. It appears as
delicate gray lines in deeper
cornea. Disappears sponta-
neously. Sometimes, they
persist and end up with corneal Fig. 3.39: Striate keratopathy
decompensation.
Treatment: Like that of corneal
edema.

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 DISEASES OF THE CORNEA AND SCLERA

CORNEAL ABRASION
(FIGS 3.40A AND B)
Common, unilateral condition
usually associated with trauma.
Epithelial defect can be easily
diagnosed by diffuse illumi-
nation and after fluorescein
staining.
Fig. 3.40A: Corneal abrasion
Treatment: Antibiotic ointment
and patching for 24 hours.

FILAMENTARY
Fig. 3.40B: Corneal abrasion—
KERATOPATHY
fluorescein staining
(KERATITIS) (FIG. 3.41)
Formation of epithelial threads
(filaments) on the cornea. which
adhere to the cornea by one
end, while the other moves
freely. Beautifully stained by
fluorescein dye.
Treatment: Removal of fila-
ments by scraping then BCL and Fig. 3.41: Filamentary
frequent artificial tears. keratopathy—fluorescein stain

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 CLINICAL OPHTHALMOLOGY

DESCEMET’S
DETACHMENT
(FIGS 3.42A AND B)
Detachment of Descemet’s
membrane is mainly caused by
surgical trauma. It may be
partial or total and associated
with diffuse or localized corneal
oedema.
Fig. 3.42A: Descemet’s
Treatment: Surgery with detachment—curled
tamponade by air or C3F8 gas to
reattach the membrane.

Fig. 3.42B: Descemet’s

detachment with localized PBK

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 DISEASES OF THE CORNEA AND SCLERA

DESCEMET’S TEAR
(FIGS 3.43A TO E)
Causes: Vertical/oblique tear in
birth trauma; horizontal tear in
congenital glaucoma (Haab’s
striae); elliptical tear in kerato-
C
conus/keratglobus, any direc-
tion in surgical trauma. Figs 3.43B and C: Descemet’s
tear—birth trauma
Treatment: Observation and no
treatment is required.

Fig. 3.43A: Descemet’s tear—

Haab’s striae

E
Figs 3.43D and E: Descemet’s
B tear—keratoconus

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 CLINICAL OPHTHALMOLOGY

CORNEAL DELLEN
(FIGS 3.44A AND B)
May be seen in keratoconjunc-
tivitis sicca (KCS), adjacent to
pterygium or other nodular
limbal lesion. Epithelium is
intact and does not stain with
fluorescein, but pooling may be
present.
Fig. 3.44A: Corneal dellen—KCS
Treatment: Tears substitutes
and treatment of the cause.

Fig. 3.44B: Corneal dellen—KCS

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 DISEASES OF THE CORNEA AND SCLERA

CORNEAL SIGNS IN
AVITAMINOSIS-A
(FIGS 3.45A TO C)
Corneal xerosis (X2):Hazy
lustureless, dry cornea, mainly
in the inferior part.
Keratomalacia (X3A, 3B): Round,
oval, punched out defects,
surrounded by xerotic cornea. Fig. 3.45A: Corneal xerosis—X2
perforation may occur within 24
hours with pseudocornea and
anterior staphyloma formation.
• X3A: when <1/3 cornea is
involved
• X3B: when >1/3 cornea is
involved
Xerophthalmic scar (Xs): Healed Fig. 3.45B: Keratomalacia RE and
sequelae of prior cornea involve- pseudocornea with anterior
ment typically inferior in location. staphyloma LE
It includes nebula, macula,
leucoma, adherent leucoma, etc.
Treatment: A medical emer-
gency; massive dose of vitamin
A; treating malnutrition and
underlying systemic illness;
prophylactic vitamin-A therapy.
Fig. 3.45C: Xerophthalmic scar—
Xs

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 CLINICAL OPHTHALMOLOGY

KERATITIS
MEDICOMENTOSA
(FIGS 3.46A AND B)
Due to preservatives or drug
itself. Initial presentation is
superficial punctate keratitis,
scattered all over the cornea.
Later, patient may present with
dry eye with other signs.
Fig. 3.46A: Keratitis
Treatment: Withdrawal of medicomentosa
specific drug and preservative-
free artificial tears.

Fig. 3.46B: Keratitis

medicomentosa

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 DISEASES OF THE CORNEA AND SCLERA

TUNNEL ABSCESS
(FIGS 3.47A AND B)
Associated with infiltrations
within the tunnel in phako or
SICS. Variable degree of ante-
rior chamber reactions. May
progress into frank endoph-
thalmitis.
Treatment: Exploration and Fig. 3.47A: Tunnel abscess—
scraping the materials for postphakoemulsification
culture and sensitivity, and
tunnel wash with vancomycin
or amphotericin-B. Prognosis is
usually poor.

Fig. 3.47B: Tunnel abscess—

postcataract surgery

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 CLINICAL OPHTHALMOLOGY

CORNEAL TUMORS cinoma of the conjunctiva,

(FIGS 3.48A TO D) pigmented lesions of the
Primary corneal tumors are conjunctiva, etc.
rare. Mainly they are the exten- Treatment: Excision with
sion of the conjunctival or limbal conjunctival resection with or
tumors – like, limbal dermoids, without lamellar keratoplasty
invasive squamous cell car-

Fig. 3.48A: Central corneal Fig. 3.48C: Extension of conjunc-

dermolipoma tival squamous cell carcinoma

Fig. 3.48B: Limbal dermoid on Fig. 3.48D: Conjunctival

dermolipoma melanoma on cornea

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 DISEASES OF THE CORNEA AND SCLERA

BLUE SCLERA
(FIGS 3.49A TO C)
Sclera appears bluer than white,
mainly due to increased visibi-
lity of the underlying uveal
pigment through thin sclera.
Causes: osteogenesis imper-
fecta; buphthalmos; following
diffuse scleritis oculodermal Fig. 3.49B: Blue sclera—oculo-
melanocytosis, ciliary staphy- dermal melanocytosis
loma, etc.

Fig. 3.49A: Blue sclera— Fig. 3.49C: Blue sclera—diffuse

buphthalmos scleritis

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 CLINICAL OPHTHALMOLOGY

EPISCLERITIS
(FIGS 3.50A AND B)
Benign inflammation of the
episcleral tissue, not so serious.
May be Simple—sectorial red-
ness involving the middle
episcleral vessels; or
Nodular—purple solitary nodule
with surrounding injection Fig. 3.50A: Simple episcleritis
which can be moved over the
sclera.
Treatment: Oral anti-inflam-
matory agents, dilute topical
steroids, or non-steroidal anti-
inflammatory eyedrops.

Fig. 3.50B: Nodular episcleritis

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 DISEASES OF THE CORNEA AND SCLERA

ANTERIOR SCLERITIS Diffuse anterior scleritis:

(FIGS 3.51A TO F) Involves either a segment or the
Inflammation of sclera asso- entire anterior sclera. Diffuse
ciated with collagen disorders redness and distortion of
in 50% of cases. May be diffuse, pattern of deep episcleral
nodular or necrotizing. vascular plexus.

Fig. 3.51A: Diffuse anterior Fig. 3.51C: Nodular scleritis—

scleritis multiple

Fig. 3.51B: Nodular scleritis— Fig. 3.51D: Necrotizing scleritis

solitary with inflammation

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 CLINICAL OPHTHALMOLOGY

Nodular scleritis (non-

necrotizing): Extremely tender,
usually solitary or multiple firm
immobile nodule separated
from the overlying congested
episcleral tissue.
Anterior necrotizing scleritis
with inflammation: Avascular
patches with scleral necrosis and Fig. 3.51E: Necrotizing scleritis—
melting. Marked thinning of the thinning
sclera with increased visibility
of underlying uvea.
Necrotizing scleritis without
inflammation (scleromalacia
perforans): In long standing
rheumatoid arthritis. Painless,
necrotic patch in normal sclera.
Eventually, extreme scleral
thinning with exposure and
bulging of underlying uvea.
Treatment: Systemic and topical Fig. 3.51F: Scleromalacia
corticosteroids, NSAIDs, syste- perforans
mic immunosuppressives in
severe and unresponsive cases,
and investigations for systemic
collagen disorders.

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 DISEASES OF THE CORNEA AND SCLERA

SURGICALLY INDUCED Commonly seen following

NECROSIS OF SCLERA cataract surgery, pterygium
(SINS) (FIGS 3.52A TO D) surgery or glaucoma surgery.
Rare, postoperative immune Treatment: Topical and systemic
mediated necrosis of the sclera. coticosteroids, systemic immu-
May be triggered by excessive nosuppressants, scleral patch
cautery, or use of antimeta- graft in extreme case.
bolites durin surgery.

Fig. 3.52A: Surgically induced Fig. 3.52C: SINS—post-

necrosis of sclera pterygium surgery

Fig. 3.52B: SINS—post- Fig. 3.52D: SINS—post-

pterygium surgery pterygium surgery

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 CLINICAL OPHTHALMOLOGY

SHALLOW ANTERIOR over filtration of filtering bleb;

CHAMBER (FIGS 4.1A TO D) choroidal detachment; wound
Causes: Cornea plana; hyper- leak after intraocular surgery;
metropia; angle closure glau- penetrating injury; malignant
coma; intumescent cataract; glaucoma, etc.

Fig. 4.1A: Normal depth AC Fig. 4.1C: Very shallow AC

Fig. 4.1B: Mild shallow AC Fig. 4.1D: Shallow AC—malignant

glaucoma

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ANTERIOR CHAMBER AND PUPILLARY ABNORMALITIES

DEEP ANTERIOR keratoconus; keratoglobus;

CHAMBER (FIGS 4.2A TO D) buphthalmous; posterior
Causes: Myopia; aphakia/ dislocation of the lens.
pseudophakia; megalocornea;

Fig. 4.2A: Deep AC—myopia Fig. 4.2C: Deep AC—

pseudophakia

Fig. 4.2B: Deep AC— Fig. 4.2D: Deep AC—

megalocornea keratoconus

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 CLINICAL OPHTHALMOLOGY

IRREGULAR ANTERIOR leucoma: iris cyst or tumor;

CHAMBER (FIGS 4.3A TO D) penetrating injury with iris
Causes: Ectopia lentis; iris bombe prolapse; angle recession, etc.
(funnel-shaped); adherent

Fig. 4.3C: Funnel shaped AC—

Fig. 4.3A: Irregular AC—ectopia Iris bombe
lentis

Fig. 4.3B: Irregular AC— Fig. 4.3D: Irregular AC—iris cyst

subluxated lens

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ANTERIOR CHAMBER AND PUPILLARY ABNORMALITIES

ABNORMAL CONTENTS OF
AC (FIGS 4.4A TO J)
Vitreous: Postoperative or after
trauma.
Blood (hyphema): Traumatic or
postoperative.
Pus (hypopyon): Suppurative
corneal ulcer; acute iridocyclitis; Fig. 4.4B: Blood in AC—post-
endophthalmitis. traumatic hyphema

Pseudohypopyon: Liquefied
milky cortex in hypermature
cataract; silicone oil—inverse
hypopyon; malignant cells.
Albuminous and cellular
materials: Fibrinous exudates
or aqueous cells in iritis; dense
exudates in endophthalmitis.
Fig. 4.4A: Vitreous in AC—
aphakia

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 CLINICAL OPHTHALMOLOGY

Fig. 4.4C: Postoperative

hyphema Fig. 4.4E: Hypopyon—
endophthalmitis

Fig. 4.4D: Hypopyon—corneal Fig. 4.4F: Inverse hypopyon—

ulcer emulsified silicone oil

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ANTERIOR CHAMBER AND PUPILLARY ABNORMALITIES

Fig. 4.4G: Pseudohypopyon— Fig. 4.4I: Cells in AC—acute iritis

retinoblastoma

Fig. 4.4H: Pseudohypopyon— Fig. 4.4J: Fibrinous exudate—

liquefied lens cortex iritis

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 CLINICAL OPHTHALMOLOGY

OTHER ABNORMAL air bubble, silicone oil in A/C;

CONTENTS IN A/C (FIGS foreign body in A/C; eyelash
4.5A TO J) in A/C; parasite dead or live;
Crystalline lens, ACIOL, lens cholesterolosis bulbi; caterpillar
fragment after cataract surgery, hair.

Fig. 4.5A: Crystalline lens Fig. 4.5C: Lens fragment worm

Fig. 4.5B: Anterior chamber IOL Fig. 4.5D: Air bubble—

postoperative

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ANTERIOR CHAMBER AND PUPILLARY ABNORMALITIES

Fig. 4.5E: Silicone oil bubble Fig. 4.5H: Fungal granuloma

Fig. 4.5F: Foreign body Fig. 4.5I: Live filarial

Fig. 4.5G: Eyelash Fig. 4.5J: Cholesterolosis bulbi

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 CLINICAL OPHTHALMOLOGY

ABNORMAL PUPIL

CORECTOPIA
(FIGS 4.6A AND B)
Displacement of the pupil from
its normal position, usually
more to the nasal side. May be
associated with ectopia lentis,
irido-corneal endothelial (ICE)
syndrome; after trauma or after Fig. 4.6A: Corectopia—ectopia
cataract surgery. lentis et pupillae

Fig. 4.6B: Corectopia—ICE

syndrome

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ANTERIOR CHAMBER AND PUPILLARY ABNORMALITIES

POLYCORIA
(FIGS 4.7A AND B)
Multiple pupils (True polycoria):
Extremely rare, multiple pupils,
each having a sphincter muscle.
Pseudopolycoria: Not uncom-
mon, found in ICE syndrome;
A
trauma and after surgery.

B
Figs 4.7A and B: Polycoria—ICE
syndrome

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 CLINICAL OPHTHALMOLOGY

PERSISTENT
PUPILLARY MEMBRANE
(FIGS 4.8A AND B)
Continued existence of the part
of anterior vascular sheath of
the lens which normally dis-
appears shortly before birth.
Appears as fine strands of
membrane, running inwards Fig. 4.8A: Persistent pupillary
from the collarette inserting into membrane
the anterior lens capsule.
Usually, it does not interfere
with vision.
Treatment: Rarely, it may block
the pupil, and surgical inter-
vention is then necessary.

Fig. 4.8B: Persistent pupillary

membrane—blocking the pupil

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ANTERIOR CHAMBER AND PUPILLARY ABNORMALITIES

ANISOCORIA Causes: Use of miotic or

(FIGS 4.9A TO C) mydriatic in one eye; Adie’s
Unequal puillary size between pupil; Horner’s syndrome; 3rd
two eyes. Pupil in one eye is nerve palsy; optic atrophy in
normal and the other pupil is one eye; traumatic mydriasis in
miotic or mydriatic. one eye, etc.

A B
Figs 4.9A and B: Anisocoria—post-traumatic

Fig. 4.9C: Anisocoria—third nerve palsy

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 CLINICAL OPHTHALMOLOGY

SMALL (MIOTIC) PUPIL Causes: Extreme of ages; in

(FIGS 4.10A TO D) bright light; opium/morphine
Normally, it varies between 2 addict; pontine haemorrhage;
and 4 mm, but depends on level healed iridocyclitis; use of
of illumination. The miotic pupil miotics (e.g. pilocarpine) and
is less than 2 mm. during sleep.

Fig. 4.10A: Miotic pupil—aging

Fig. 4.10C: Miosis—healed iritis

Fig. 4.10B: Extreme miosis— Fig. 4.10D: Miosis—pilocarpine

opium addict

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ANTERIOR CHAMBER AND PUPILLARY ABNORMALITIES

LARGE (MYDRIATIC) PUPIL

(FIGS 4.11A AND B)
Pupil size is 6 mm or more.
Causes: In dark; 3rd nerve palsy;
optic atrophy; comatose
patient; head injury; absolute
glaucoma; use of mydriatics.

Fig. 4.11A: Mydriasis—optic

atrophy

Fig. 4.11B: Mydriasis—

pharmacological

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 CLINICAL OPHTHALMOLOGY

DIFFERENT PUPILLARY
SHAPE (FIGS 4.12A TO J)
Pupil is irregular and different
in shape.
Causes:
Irregular—in iridocyclitis; after
surgery.
D-shaped—in iridodialysis Fig. 4.12A: Irregular pupil—iritis
Festooned—in healed iridocy-
clitis.
Pear-shaped—in trauma.
Inverted pear-shaped—in
coloboma iris, trauma.
Oval pupil—in acute angle
closure glaucoma.
Updrawn pupil—cataract
surgery with vitreous loss.
Slit-like pupil—in Axenfeld-
Fig. 4.12B: Irregular pupil—
Reiger syndrome.
sphincterotomy

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ANTERIOR CHAMBER AND PUPILLARY ABNORMALITIES

Fig. 4.12C: D-shaped pupil— Fig. 4.12E: Festooned pupil—

iridodialysis iridocyclitis

Fig. 4.12F: Inverted pear

Fig. 4.12D: Pear-shaped pupil—
shaped—incomplete coloboma
iris trauma

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 CLINICAL OPHTHALMOLOGY

Fig. 4.12G: Inverted pear- Fig. 4.12I: Updrawn pupil—

shaped—perforating injury cataract surgery

Fig. 4.12H: Oval pupil—acute Fig. 4.12J: Slit-like pupil—

attack ACG Axenfeld Reiger’s syndrome

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ANTERIOR CHAMBER AND PUPILLARY ABNORMALITIES

LEUKOCORIA
(FIGS 4.13A TO F)
Also known as white pupillary
or Cat’s eye reflex; relatively
common; unilateral or may be
bilateral.

Causes:
Congenital cataract: Unilateral Fig. 4.13A: Leucocoria—conge-
or bilateral; opacity in the lens nital cataract—RE operated
clearly indicates the presence of
cataract.
Retinoblastoma: Average age
18 months; progressive, unila-
teral, malignant condition;
Ophthalmoscopically, a pearly-
white mass with presence of
secondary calcification; trans-
parent lens; intraocular pressure
is high.
Retinopathy of prematurity:
Fig. 4.13B: Leucocoria—
prematurity and low birth
retinoblastoma
weight with history exposure to
oxygen; bilateral in 100% of
cases; first noted in neonatal
period; presence of tractional

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 CLINICAL OPHTHALMOLOGY

retinal detachment; normal

intraocular pressure.
Toxocara endophthalmitis:
Unilateral with h/o contact with
pet cat or dog; 2 to 9 years of
age; anterior segment and
vitreous inflammation; retinal
detachment, low intraocular
Fig. 4.13C: Leucocoria— pressure and eventually, the eye
retinopathy of prematurity may be phthisical.
Persistent hyperplastic pri-
mary vitreous (PHPV): Usually
unilateral and first noted in
neonatal period; associated with
microphthalmos and cataract;
elongated ciliary processes;
intraocular pressure may be
high.
Retinal dysplasia: Unilateral or
bilateral, usually present at
birth; pink or white retrolental
mass; microphthalmic eye with
Fig. 4.13D: Leucocoria—
Toxocara endophthalmitis shallow anterior chamber and
elongated ciliary processes;
associated with severe systemic
abnormalities.

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ANTERIOR CHAMBER AND PUPILLARY ABNORMALITIES

Coat’s disease: Unilateral,

occurs primarily in older boys;
large areas of retinal or sub-
retinal exudates with choles-
terol crystals; dilated and
tortuous central retinal vessels;
eventually, exudative detach-
ment as a retrolental mass.
Choroidal coloboma: Unilateral
Fig. 4.13E: Leucocoria—Coat’s
or bilateral, present at birth;
disease
leuckocoria is only with a large
choroidal coloboma with
microphthalmos; inferonasal in
location as the defect is at the
embryonic fissure, with shiny-
white sclera.

Fig. 4.13F: Leucocoria—PHPV

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 CLINICAL OPHTHALMOLOGY

ANIRIDIA (FIGS 5.1A AND B)

Whole of the iris is appeared to
be missing on external exami-
nation; Ciliary processes and
suspensory ligaments of the
lens are visible; Subluxation of
lens and secondary glaucoma in
25% of the cases. A
Aniridia and Wilms’ tumor are
associated with deletion of the
short arm of chromosome-11
(Miller’s syndrome).

B
Fig. 5.1A and B: Aniridia

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 DISEASES OF THE UVEA

COLOBOMA Coloboma may be typical or

(FIGS 5.2A TO D) atypical; Extends from the pupil
Development imperfect closure to the optic nerve.
of the foetal fissure; Lower nasal May stop short of the optic
sector of the eyeis affected. nerve, iris or else or even parti-
tioned by islands of normal
tissue (bridge coloboma).

Fig. 5.2A: Typical coloboma Fig. 5.2C: Incomplete coloboma

Fig. 5.2B: Choroidal coloboma Fig. 5.2D: Atypical iris

coloboma—congenital

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 CLINICAL OPHTHALMOLOGY

Typical coloboma of the iris: Pear

shaped with broad base to-
wards the pupillary margin; it
may be complete or incomplete.
Atypical coloboma of the iris:
Isolated coloboma with or
without lens coloboma which
occurs at any meridian.
Fig. 5.3A: Oculocutaneous
albinism
ALBINISM (FIGS 5.3A TO C)
Hereditary disorder; absence or
reduction of melanin pigmen-
tation throughout the body.
Two main types: Oculocutaneous
and ocular; iris looks pink and
translucent, owing to lack of
pigment; fundus appears
orange-pink in color; retinal and Fig. 5.3B: Albinism—pink iris
choroidal vessels are difficult to
differentiate.

Fig. 5.3C: Albino fundus—

generalised pallor

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 DISEASES OF THE UVEA

HETEROCHROMIA OF THE
IRIS (FIGS 5.4A TO C)
Two irides show a significant
difference in color; may also
affect a sector, with difference
in color from the remainder.
May be hypochromic (eye with
lighter-colored iris is abnormal)
B
or Hyperchromic (iris on the side
of the disease is darker than its
fellow).

C
Fig. 5.4A: Heterochromia Fig. 5.4B and C: Hypochromic
heterochromia

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 CLINICAL OPHTHALMOLOGY

ANTERIOR UVEITIS Aqueous flare: Proteins leaks

(IRIDOCYCLITIS) through the damaged capillaries,
(Figs 5.5A to O) causing a Tyndall effect and
Acute non-granulomatous, or aqueous cells, may be with
chronic granulomatous type. hypopyon.
Circum-corneal (ciliary) conges- Hyphema in herpetic uveitis; Deep
tion; keratic precipitates (KPs)— and irregular AC: in posterior
which may be small, medium, synechiae; Funnel-shaped AC: in
large, and ‘mutton fat’ types. iris bombe.

Fig. 5.5A: Acute Fig. 5.5C: Medium KPs

nongranulomatous type

Fig. 5.5B: KPs—Arlt’s triangle Fig. 5.5D: Mutton KPs

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 DISEASES OF THE UVEA

Fig. 5.5E: Aqueous flare Fig. 5.5G: Herpetic iridocyclitis—

hyphema

Fig. 5.5F: Aqueous cells Fig. 5.5H: Acute iridocyclitis—iris

bombe

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 CLINICAL OPHTHALMOLOGY

Iris nodules: Koeppe’s nodules: At

the pupillary border and smaller
in size; Busacca’s nodules: on the
surface of the iris, away from
the pupil.
Posterior synechia: Ring (annu-
lar) synechiae; irregular or
‘festooned pupil’; Occlusio
Fig. 5.5I: Koeppe’s nodules pupillae; complicated cataract;
Band-shaped keratopathy (BSK)—
more common in children with
juvenile rheumatoid arthritis
and chronic iridocyclitis.

Fig. 5.5J: Busacca’s nodules

Fig. 5.5K: Ring synechiae—iris
bombe

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 DISEASES OF THE UVEA

Fig. 5.5L: Irregular synechiae—

festooned pupil Fig. 5.5N: Healed iritis—
complicated cataract

Fig. 5.5O: Chronic iridocyclitis

and BSK in JRA
Fig. 5.5M: Occlusio pupillae

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 CLINICAL OPHTHALMOLOGY

CHOROIDITIS white patches of chorio-retinal

(FIGS 5.6A TO D) atrophy with pigmented mar-
Active lesions: Well-defined gins; Perivasculitis: Periphlebitis
yellowish-white patches of is more common—called
chorio-retinal inflammation; ‘candle-wax dripping’, seen in
Inactive lesions: Well-defined sarcoidosis.

Fig. 5.6A: Choroiditis Fig. 5.6C: Choroiditis—juxta

pupillary

Fig. 5.6B: Choroiditis—central Fig. 5.6D: Perivasculitis—candle

wax dripping

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 DISEASES OF THE UVEA

TOXOPLASMOSIS the old scar; In reactivation,

(FIGS 5.7A TO D) white or yellowish white
Bilateral healed chorioretinal lesions with fluffy indistinct
scars; may be unilateral; Focal edges visible at the post-
necrotizing retinitis-is a ‘satellite equatorial fundus – ‘headlight in
lesion’ adjacent to the edge of fog’ appearance.

A
Fig. 5.7C: Toxoplasma scar—
satellite lesion

B
Fig. 5.7A and B: Toxoplasma Fig. 5.7D: Toxoplasma—
choroiditis scar—bilateral reactivation (Cheadlight infog
appearance)

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 CLINICAL OPHTHALMOLOGY

VOGT-KOYANAGI-
HARADA SYNDROME
(FIGS 5.8A TO C)
Rare, idiopathic condition
affects Asians, especially the
Japanese; alopecia, vitiligo and
poliosis; chronic granulomatous
anterior uveitis with multifocal
choroiditis; multiple sensory
retinal detachments may be Fig. 5.8B: VKH syndrome with
with exudation (Harada’s); active uveitis
prognosis is fairly good.

Fig. 5.8A: Vogt-Koyanagi-Harada

syndrome Fig. 5.8C: VKH syndrome—
exudative retinal detachment

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 DISEASES OF THE UVEA

SYMPATHETIC • Following intraocular sur-

OPHTHALMITIS (FIG. 5.9) gery
In the ‘exciting eye’—there is • Following wound leak or
ciliary congestion and evidence blebitis (after glaucoma sur-
of initial insult; in the ‘sympa- gery).
thizing eye’—typical granulo-
matous uveitis with mutton-fat
KPs, iris nodules; Dallen-Fuchs’
nodules scattered throughout
posterior pole.

Fig. 5.10A: Endophthalmitis—

penetrating injury

Fig. 5.9: Sympathetic ophthalmia—

Dallen-Fuchs nodules

ENDOPHTHALMITIS
(FIGS 5.10A TO D)
Exogenous
• Following penetrating in- Fig. 5.10B: Endophthalmitis—
jury. catract surgery

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 CLINICAL OPHTHALMOLOGY

Endogenous: Septic emboli

(metastatic).
Toxic (sterile): Toxic reaction to
the chemicals/drugs used dur-
ing surgery.

Fig. 5.10C: Blebitis—

endophthalmitis

Fig. 5.10D: Metastatic

endopthalmitis

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 DISEASES OF THE UVEA

PANOPHTHALMITIS
(FIGS 5.11A AND B)
Marked lid edema.
Conjunctival chemosis and
congestions.
Anterior chamber is full of pus.
Following corneal ulcer; pene-
Fig. 5.11A: Panophthalmitis—
trating injury or post-surgical.
corneal ulcer

Fig. 5.11B: Panophthalmitis—

post surgical

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 CLINICAL OPHTHALMOLOGY

IRIDOCORNEAL Chandler’s syndrome: Beaten-

ENDOTHELIAL (ICE) silver appearance of corneal
SYNDROME endothelium; with gradual
(FIGS 5.12A TO D) endothelial disturbances and
Rare, unilateral condition typi- corneal edema; iris atrophy is
cally affects women and asso- minimal.
ciated with secondary intrac-
table glaucoma; After meta-
plasia, Descemet’s membrane-
like material covers the anterior
iris surface and angle of the
anterior chamber.
Progressive essential iris
atrophy: Patchy iris atrophy
with partial or complete hole
formation; corectopia; pseudo- Fig. 5.12A: Essential iris atrophy
polycoria, and gradual enlarge-
ment of the iris holes; broad
peripheral anterior synechia.
Iris-nevus syndrome (Cogan-
Reese): Dark-brown nodules on
the iris as small woolen-spherules;
peripheral anterior synechiae and
secondary glaucoma may also
occur; endothelial decompen-
sation appears later.
Fig. 5.12B: Essential iris
atrophy—broad PAS

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 DISEASES OF THE UVEA

IRIDOSCHISIS (FIG. 5.13)

Senile degenerative condition of
the iris; large dehiscences
appear on the anterior meso-
dermal layer of the iris and
strands of tissue may float into
the anterior chamber.

Fig. 5.12C: Cogan Reese

syndrome

Fig. 5.12D: Chandler syndrome Fig. 5.13: Iridoschisis

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 CLINICAL OPHTHALMOLOGY

IRIS ATROPHY
(FIGS 5.14A TO C)
May be diffuse or sectorial;
Diffuse type: occurs in old age,
postcataract or other anterior
segment surgeries; Sectorial type
found in - herpetic iritis; angle
closure glaucoma, after surgery
or trauma. Fig. 5.14B: Iris atrophy—moth-
eaten iris

Fig. 5.14A: Iris atrophy—diffuse Fig. 5.14C: Iris atrophy—

sectorial

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 DISEASES OF THE UVEA

RUBEOSIS IRIDIS
(FIGS 5.15A TO C)
Start as tiny dilated capillaries
at pupillary border; radial iris
neovascularisation with net-
work of new vessels on the iris
surface and the stroma;
New vessels and associated Fig. 5.15A: Rubeosis iridis
fibrous tissue may cover angle
and trabecular meshwork; peri-
pheral anterior synechiae and
intractable neovascular glau-
coma; ectropion uveae is
common in late stage.
Treatment: Panretinal photo-
coagulation; panretinal cryo-
coagulation in presence of Fig. 5.15B: Rubeosis iridis—
opaque media. ectropion uveae

Fig. 5.15C: Rubeosis iridis—new

vessels on lens surface

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 CLINICAL OPHTHALMOLOGY

PRIMARY CHOROIDAL
SCLEROSIS
(FIGS 5.16A AND B)
Diffuse atrophy of the RPE and
choriocapillaries. ‘Tessellated’
appearance of the fundus; occurs
in two forms: diffuse or genera-
lized, and localized sclerosis:
affects the central or circum-
papillary region. Fig. 5.16A: Choroidal sclerosis—
diffuse

Fig. 5.16B: Choroidal sclerosis—

localized

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 DISEASES OF THE UVEA

IRIS CYSTS
(FIGS 5.17A AND B)
May be primary or secondary;
lie on anterior surface of iris,
and grayish-white and filled
with clear fluid.
Primary iris cysts: They are
stromal and occur in young
children. They are filled with Fig. 5.17A: Iris cyst—primary
clear fluid and may often touch
the cornea.
Post-surgical iris cysts: A form
of epithelial downgrowth and
occur following cataract sur-
gery.
Treatment: Surgical excision or
sometimes YAG laser deroo-
fing of the cyst.
Fig. 5.17B: Iris cysts—
post surgical

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 CLINICAL OPHTHALMOLOGY

GYRATE ATROPHY OF THE ANGIOID STREAKS

CHOROID (FIG. 5.18) (FIGS 5.19)
Deficiency of ornithine ketoacid Irregular and jagged network
amino transferase enzyme, resul- of red to brown lines, mainly
ting in hyper-ornithinemia; seen in central fundus; Lesions
scalloped to circular patches of are approximately the width of
chorioretinal atrophy in the far a retinal vessel, which may thus
and midretinal periphery. resemble (‘angioid’); but the
streaks are darker, have an
irregular contour with serrated
edges, and tend to terminate
abruptly.

Fig. 5.18: Gyrate atrophy of Fig. 5.19: Angioid streak

choroid

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 DISEASES OF THE UVEA

CHOROIDAL DETACHMENT
(FIGS 5.20A AND B)
Means separation of the cho-
roids from the sclera; shallow
anterior chamber; shows
smooth, elevated, dark-brown
bullous lesions, which are more
prominent on the temporal and
nasal sides (kissing choroidals).
Fig. 5.20A: Choroidal
Treatment: Systemic steroids, detachment—retinal detachment
and treatment of the cause.

Fig. 5.20B: Choroidal

detachment—kissing choroidals

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 CLINICAL OPHTHALMOLOGY

LISCH NODULES (SPOTS)

(FIGS 5.21A AND B)
Bilateral melanocytic hamar-
tomas found in patients with
neurofibromatosis after pu-
berty. Small brown or yellowish
brown dome-shaped spots or
nodules on the anterior iris
surface.
Fig. 5.21A: Neurofibromatosis

Fig. 5.21B: Lisch nodules

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 DISEASES OF THE UVEA

BRUSHFIELD SPOTS IRIS PEARLS (FIG. 5.23)

(FIG. 5.22)
Bilateral small or large, pearl-
Bilateral, and are usually found like clear nodules on the iris
in Down’s syndrome, may be surface and pupillary margin;
seen in general population; tiny may be seen in lepromatous
yellowish or white spots leprosy; may drop into the AC
arranged in a ring at the junction and eventually disappear.
of middle and outer third of iris
surface.

Fig. 5.23: Iris pearls

Fig. 5.22: Brushfield spot

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 CLINICAL OPHTHALMOLOGY

IRIS NEVUS (FIG. 5.24) BENIGN MELANOCYTOMA

Common, usually unilateral; (NEVUS) (FIG. 5.25)
elevated or flat, localized, dis- Typical benign melanomas of
crete, small pigmented mass; the choroid are flat or slightly
usually does not distort the elevated, oval or circular state-
pupil; may cause heterochromia gray lesions; occurs most fre-
iridis. quently at the posterior half of
the fundus.
Treatment: Not indicated, except
the patient should be followed
up regularly with serial photo-
graphs.

Fig. 5.24: Iris nevus Fig. 5.25: Benign melanocytoma

of choroid

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 DISEASES OF THE UVEA

MALIGNANT MELANOMA
OF IRIS (FIGS 5.26A AND B)
Very rare, slow-growing tumor
with relative low malignant
potential, noticed as a brown or
non-pigmented mass on the iris
surface, usually located in the
inferior half of the iris. A
May start at the angle of A/C.
Pupil is distorted; ectropion
uveae and secondary lens
opacities are seen; May extend
into the anterior chamber angle
giving rise to secondary
glaucoma.

B
Figs 5.26A and B: Malignant
melanoma—iris

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 CLINICAL OPHTHALMOLOGY

CILIARY BODY MELANOMA

(FIG. 5.27)
More common than iris mela-
noma; may present as subluxa-
tion with secondary glaucoma,
as dilated episcleral (sentinel)
blood vessels; as a diffuse mass
around the ciliary body.
Treatment: By enucleation (for Fig. 5.27: Ciliary body melanoma
large tumors) and local resec-
tion (for small tumors).

MALIGNANT MELANOMA
OF CHOROID (FIGS 5.28A
AND B)
Chief symptoms result from the
exudative retinal detachment
with secondary glaucoma; Fig. 5.28A: Choroidal melanoma
typically appears as a pigmen-
ted and elevated oval mass.
Treatment: Small melanoma can
be treated by laser and large
melanoma by enucleation.

Fig. 5.28B: Choroidal

melanoma—FFA

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 DISEASES OF THE UVEA

METASTATIC CARCINOMA
OF UVEA (FIGS 5.29A AND B)
Most frequent primary sites:
Bronchus in males, and breast
in females;
May deposit on iris, ciliary body
or choroid; typically, appear as
solitary or multiple, creamy-
white, placoid or oval lesions Fig. 5.29A: Metastatic carcinoma
which infiltrate laterally. Care- of choroid— from bronchus
ful examination of the other eye
is important.
Treatment: Directed towards
primary disease. Enucleation is
contraindicated unless the eye
is painful and blind.

Fig. 5.29B: Metastatic carcinoma

of iris— from breast

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 CLINICAL OPHTHALMOLOGY

COLOBOMA OF THE LENS

(FIGS 6.1A AND B)
Rare unilateral or bilateral
condition, may occur with
typical coloboma of the uveal
tract; or rarely in isolation.
Notching of the lens at the
inferior equator.
Fig. 6.1A: Coloboma of the lens

Fig. 6.1B: Coloboma of lens—

atypical

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 DISEASES OF THE LENS

ANTERIOR LENTICONUS
(FIG. 6.2)
Rare bilateral condition, often
associated with Alport’s syn-
drome; anterior conical pro-
jection at the center of lens; Oil-
droplet sign and high lenticular
myopia.
Fig. 6.2: Anterior lenticonus

POSTERIOR LENTICONUS
(FIG. 6.3)
Rare bilateral condition, may be
associated with Lowe’s syn-
drome; posterior conical or
globular (lentiglobus) bulge in
the axial zone of the lens.
Fig. 6.3: Posterior lenticonus

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 CLINICAL OPHTHALMOLOGY

SPHEROPHAKIA (MICRO-
SPHEROPHAKIA)
(FIGS 6.4A AND B)
Smaller diameter spherical lens;
may be with subluxation; lenti-
cular myopia; part of Weill-
Marchesani’s syndrome.
Pupillary block glaucoma which A
is aggravated by miotics and
relieved by mydriatics (called
‘inverse glaucoma’).

B
Figs 6.4A and B: Spherophakia

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 DISEASES OF THE LENS

MARFAN’S SYNDROME
(FIGS 6.5A AND B)
Autosomal dominant, multiple
mesodermal dysplasia; lens is
typically subluxated in upward
and inward direction; iris hypo-
plasia causes poor pupillary
dilatation.
Systemic features: Arachno- Fig. 6.5A: Marfan’s syndrome
dactyly (spider fingers), long
extremities, hyper-extensibility
of joints and cardiovascular
anomalies.

Fig. 6.5B: Marfan’s syndrome—

upward subluxation

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 CLINICAL OPHTHALMOLOGY

HOMOCYSTINURIA
(FIGS 6.5C AND D)
Autosomal recessive, an inborn
error to convert methionine to
cystine; lens displacement is
typically downward and out-
ward; Diagnosis is confirmed by
urine test with sodium nitro- C
prusside; Anesthetic hazards
during operation.
Treatment: Spectacles or contact
lenses are used to correct the
optical defects through the
phakic part;
Pars plana lensectomy and
vitrectomy with scleral fixation
IOL. In milder degree of sub-
D
luxation – ECCE with capsular
tension ring (CTR) with PCIOL. Figs 6.5C and D: Ectopia
lentis—homocystinuria

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 DISEASES OF THE LENS

PHACOLYTIC GLAUCOMA PHACOMORPHIC GLAU-

(FIG. 6.6) COMA (FIGS 6.7A AND B)
In some hypermature cataract Rapid swelling of the lens in
the capsule leaks, and large intumescent cataract; anterior
phagocytes filled with lens chamber becomes shallow; causes
material obstruct the trabecular a secondary angle-closure
glaucoma.
meshwork; secondary open-
angle glaucoma. Treatment: Urgent control of
glaucoma and extraction of lens
Treatment: Glaucoma must be with PCIOL.
controlled medically first and
then the lens has to be extracted
with PCIOL.

Fig. 6.6: Phacolytic glaucoma—

deep AC

B
Figs 6.7A and B: Phacomorphic
glaucoma

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 CLINICAL OPHTHALMOLOGY

PHACOTOXIC UVEITIS capsule and anterior cortex;

(FIG. 6.8) may be pyramidal and may
Lens proteins are relatively poor project into the anterior cham-
antigens; sometimes, a granu- ber (pyramidal cataract); may be
lomatous uveitis may develop associated with Peters’ anomaly
and may be with secondary or persistent pupillary mem-
glaucoma. brane.
Treatment: Most of the cases do
Treatment: High dose of syste- not require any treatment.
mic corticosteroids and cyclop-
legic followed by lens extraction.

Fig. 6.9A: Anterior polar cataract

Fig. 6.8: Phacotoxic uveitis

ANTERIOR POLAR
CATARACT
(FIGS 6.9A AND B)
Rare, usually bilateral and
sometimes hereditary; opacity Fig. 6.9B: Anterior polar cataract—
involves the capsule or both persistent pupillary membrane

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 DISEASES OF THE LENS

POSTERIOR POLAR ring appearance; few dense

CATARACT dots are seen within the opacity
(FIGS 6.10A TO D) and at the outer ring; may be
Opacity mostly involves only associated with residue of the
the posterior capsule; some- attachment of hyaloid artery on
times, it forms a plaque on the the posterior lens capsule as
posterior cortex with onion- small dots— Mittendorf’s dots.

A C

B D
Figs 6.10A and B: Posterior Figs 6.10C and D: PPC—onion
polar cataract ring appearance

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 CLINICAL OPHTHALMOLOGY

Treatment: ECCE PCIOL; but

often complicated by posterior
capsular rent and its other
sequale.

ZONULAR (LAMELLAR)
CATARACT
(FIGS 6.11A AND B)
Commonest type of develop- Fig. 6.11A: Zonular cataract
mental cataract presenting with
visual impairment; usually
dominant.
Consists of concentric, sharp
zone (lamellae) of opacity sur-
rounding a clear nuclear core,
and enveloped by the clear
cortex externally. Linear opaci-
ties, like spokes of a wheel
(riders) that extend outwards
are pathognomonic.
Treatment: ECCE PCIOL with Fig. 6.11B: Zonular cataract—
PCCC. riders

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 DISEASES OF THE LENS

BLUE-DOT CATARACT
(FIGS 6.12A AND B)
Bilateral, rather common, and
innocuous; usual detection is
during routine ophthalmo-
logical examination. May co-
exist with other type of conge-
nital cataract.
No treatment is necessary. A

B
Figs 6.12A and B: Blue-dot and
sutural cataract

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 CLINICAL OPHTHALMOLOGY

CORTICAL CATARACT Cupuliform type: Opacity

(FIGS 6.13A TO D) appears in posterior cortex just
Cuneiform type: Starts as wedge- beneath the capsule and
shaped spokes of opacity at the gradually forms a dense
periphery and gradually opacity.
encroaches towards center.

A C

B D
Figs 6.13A to D: Cupiliform cataract

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 DISEASES OF THE LENS

MATURE CATARACT
(FIGS 6.14A AND B)
Lens is white or pearly white in
color; in many developing
countries, patient may present
with bilateral mature cataract.

Fig. 6.14A: Mature cataract

Fig. 6.14B: Bilateral white mature

cataract

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 CLINICAL OPHTHALMOLOGY

HYPERMATURE CATARACT
(FIGS 6.15A AND B)
Morgagnian cataract: Cortex
becomes fluid and the brown
nucleus may sink at the bottom
within the lens capsule; fluid is
milky-white in appearance; a
semicircular line above the
nucleus, which may change its
position. Fig. 6.15A: Hypermature
cataract—morgagnian
Sclerotic cataract: More and more
inspissated, and shrunken in
appearance, due to loss of fluid;
lens is more flat and yellowish-
white in appearance; calcific
deposits in some part of the
capsule.

Fig. 6.15B: Hypermature

cataract—sclerotic

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 DISEASES OF THE LENS

POSTERIOR
SUBCAPSULAR CATARACT
(FIGS 6.16A AND B)
Starts in the posterior axial
region; slowly progresses to
involve entire posterior cortex;
marked diminution of vision, as
it is near the nodal point of the
eye.
Fig. 6.16A: Cupiliform cataract
Opacity is best judged by a slit
lamp with dilated pupil; Appears
as dirty yellowish-white layer
in the posterior cortex; patients
with posterior cortical cataract
always see better in dark (dawn
or dusk).

Fig. 6.16B: Dense cupiliform

cataract

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 CLINICAL OPHTHALMOLOGY

NUCLEAR CATARACT Varies in density and color

(FIGS 6.17A TO D) which gradually spreads
Tends to occur earlier than towards the cortex; with time
cortical variety; more the lens becomes yellow,
commonly seen in myopia, post amber, brown (cataracta
vitrectomy and diabetes. brunescens) or black (cataracta
nigra). Nucleus becomes hard
er with with higher grades.

Fig. 6.17A: Corticonuclear Fig. 6.17C: Brown cataract

cataract

Fig. 6.17B: Nuclear cataract Fig. 6.17D: Black cataract

and PSC

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 DISEASES OF THE LENS

May be associated with cortical

type and called, corticonuclear
cataract. Opacity is better appre-
ciated in dilated pupil.
It usually induces lenticular
myopia and patients may have
better vision in near (second
sight).
Fig. 6.18B: Polychromatic lusture
COMPLICATED CATARACT
(FIGS 6.18A AND B)
Results from disturbances of lens Causes: Chronic iridocyclitis,
metabolism as in inflammatory degenerative myopia, retinal
or degenerative diseases. detachment, retinitis pigmen-
tosa, etc.
Opacity usually commences in
the axial region of posterior
cortex; appears as grayish-
white opacity with irregular
border and it gives bread-
crumbs appearance.
Shows a characteristic rainbow
display of colors, the polychro-
matic lusture.
Fig. 6.18A: Complicated
cataract—posterior cortical

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 CLINICAL OPHTHALMOLOGY

DIABETIC CATARACT
(FIGS 6.19A AND B)
Early onset of nuclear cataract;
posterior and anterior sub-
capsular opacities of varying
degree.
True diabetic cataract: More
common in juvenile diabetics.
Bilateral cortical cataract, con- Fig. 6.19A: Diabetic cataract—
sists of minute white dots of snow flakes
varying size like ‘snowflakes’
(snow-storm cataract).
Treatment: As in adult cataract,
but associated retinopathy
often reduces the visual out-
come.

Fig. 6.19B: Diabetic cataract—

snow flakes

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 DISEASES OF THE LENS

ANTERIOR CAPSULAR
OPACIFICATION
(FIGS 6.20A AND B)
Usually appears within 3 to 6
months after the surgery; Fib-
rosis may be associated with or
without capsular phimosis.
Treatment: In extreme cases
radial YAG laser anterior cap- Fig. 6.20A: Anterior capsular
sulotomy. opacification

Fig. 6.20B: ACO with phimosis

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 CLINICAL OPHTHALMOLOGY

POSTERIOR CAPSULAR without Elschnig’s pearl; sig-

OPACIFICATION (PCO) OR nificantly reduces the vision.
‘AFTER CATARACT’ Posterior capsular fibrosis: Mem-
(FIGS 6.21A TO D) branous, white capsular fibrosis
In adults between 1 to 35% cases formed by the remnants of
after surgery; in infant may be anterior and posterior capsules
upto 100% cases. Membranous of the lens, causes less dis-
white irregular opacity with or turbances in vision.

Fig. 6.21C: PCO—Elschnig’s

Fig. 6.21A: Early fibrous PCO pearl

Fig. 6.21B: PCO—Elschnig’s Fig. 6.21D: YAG capsulotomy

pearl in PCO

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 DISEASES OF THE LENS

Elschnig’s pearls: Subcapsular

cubical cells proliferate and
develop into large balloon-like
cells called Elschnig’s pearl;
causes more disturbances in
vision.
Treatment: YAG-laser capsu-
lotomy.
Fig. 6.22B: Subluxation—vitreous
SUBLUXATION OF LENS in AC
(FIGS 6.22A AND B)
A portion of the supporting Edge of the lens is visible as a
zonules is absent, and the lens golden cresentic line in oblique
lacks support in that quadrant; illumination. May be associated
diagnosis should be confirmed with vitreous prolapse in the
after full dilatation of the pupil. anterior chamber.
Treatment: ECCE with PCIOL
with CTR if the subluxation is
less than 180 degree. In extreme
cases, ICCE with vitrectomy
with scleral fixation lens.

Fig. 6.22A: Subluxation of lens

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 CLINICAL OPHTHALMOLOGY

DISLOCATION OF LENS
(FIGS 6.23A TO C)
Crystalline lens is completely
unsupported by the zonular
fibres; displaced from the pupil-
lary area; presence of signs of
aphakia. Lens dislocation may
be anterior, posterior.
Fig. 6.23A: Anterior dislocation
Anterior dislocation: Lens is of lens
dislocated into the bottom of the
anterior chamber; appears as an
‘oil-globule’ due to total internal
reflection.
Posterior dislocation: Lens can be
seen as translucent or opaque
mass in the vitreous cavity.
Treatment: ICCE (or lensec- Fig. 6.23B: Dislocation of lens in
tomy) with vitrectomy with vitreous
scleral fixation lens.

Fig. 6.23C: Subconjunctival dislo-

cation of lens after trauma

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 DISEASES OF THE LENS

DISPLACEMENT OF THE IOL

(FIGS 6.24A TO F)
Ideally, it should be well cen-
tered and preferable in-the-bag.
Displacement usually associated
with posterior capsular rent of
variable degree.
May be displaced downwards
(sunset sign), upwards or side-
ways. Fig. 6.24A: Foldable IOL in-the-
bag
Diagnosis is usually obvious
after full dilatation of the pupil.
Sometimes only the haptic is
visible in the pupillary area.
An IOL may be dislocated in the
vitreous and the pupillary
aperture remains clear. A
decentration may occur without
a PC rent.
Rarely may dislocate in the
subconjunctival space after a Fig. 6.24B: IOL—downward
trauma, called pseudo-phacocele. displacement—sunset sign

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 CLINICAL OPHTHALMOLOGY

Fig. 6.24C: IOL—sideway Fig. 6.24E: Subconjunctival dis-

displacement location of IOL—pseudophacocele

Fig. 6.24D: Decentration of IOL Fig. 6.24F: IOL dislocation—

haptic visible

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 DISEASES OF THE LENS

APHAKIA
(FIGS 6.25A AND B)
Commonest cause: Surgical; and
may be traumatic.
Deep anterior chamber; jet black
pupil; tremulousness of the iris;
associated peripheral iridec-
tomy.
Fig. 6.25A: Good surgical
Treatment: Aphakic glasses, aphakia
contact lens or secondary ante-
rior chamber or scleral fixation
IOL.

Fig. 6.25B: Traumatic aphakia

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 CLINICAL OPHTHALMOLOGY

CONGENITAL GLAUCOMA
(BUPHTHALMOS)

Primary (Figs 7.1A to C)

Congenital or infantile glau-
coma is due to simple outflow
obstruction; rare, unilateral or
bilateral condition. Autosomal
recessive; boys are more affec-
ted than girls. Fig. 7.1A: Primary congenital
glaucoma
Eyeball becomes enlarged, if the
IOP becomes elevated prior to
age of three years; cornea is
enlarged, globular and steamy;
horizontal curvilinear lines are
seen on the back of the cornea,
known as Haab’s striae; blue
discolouration of sclera; deep
anterior chamber; cupping of
the disc
Treatment: Examination under
anesthesia; goniotomy, trabe-
culotomy or trabeculectomy Fig. 7.1B: Primary infantile
and trabeculotomy, and visual glaucoma
rehabilitation.

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 GLAUCOMA

Fig. 7.1C: Congenital glaucoma—Haab’s striae

Secondary (Fig. 7.1D)

Associated with other systemic
diseases, like - aniridia, rubella
syndrome, neurofibromatosis,
Sturge Weber syndrome, meso-
dermal dysgenesis (Axenfeld-
Rieger’s anomaly, Peter’s
anomaly, etc.
Treatment: Same as primary Fig. 7.1D: Axenfeld-Reiger’s
type. anomaly

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 CLINICAL OPHTHALMOLOGY

PRIMARY ANGLE-CLOSURE
GLAUCOMA (PACG)
Acute Attack (Figs 7.2A to D)
Circumcorneal ciliary conges-
tion; cornea steamy and insen-
sitive; shallow anterior cham-
ber; pupil is mid-dilated and
oval; iris shows atrophic chan-
Fig. 7.2B: PACG—acute attack—
ges adjacent to the sphincter oval pupil
muscle; glaucom-fleckens are
small grayish-white anterior
subcapsular opacities occur in
the pupillary zone - diagnostic
of previous attack of angle-
closure glaucoma.

Fig. 7.2C: PACG—PAS formation

Fig. 7.2A: PACG—acute attack—

ciliary congestion Fig. 7.2D: Glaucomfleckens in
Acute ACG

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 GLAUCOMA

Peripheral anterior synechiae

develop, mostly in the upper
part of the angle, but gradually
spread around the whole cir-
cumference.
Treatment: ACG is always
surgical. Oral acetazolamide,
I/V mannitol, then pilocarpine
(2-4%) eyedrops initially, follo- Fig. 7.2E: YAG laser
wed by YAG laser or surgical PI
in initial stage. If the PAS is more
– trabeculectomy is the treat-
ment of choice.
Treatment of the fellow eye by
YAG laser PI (Fig. 7.2E).

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 CLINICAL OPHTHALMOLOGY

CHRONIC PACG (FIG. 7.3) ABSOLUTE GLAUCOMA

Angle becomes slowly and (FIG. 7.4)
progressively closed; creeping Reddish-blue zone surrounding
angle closure; variable degree the limbus; cloudy cornea, may
of cupping of the disk. be bullous changes; shallow
anterior chamber; iris atrophy
Treatment: Trabeculectomy.
with ectropion uveae; dilated
and grayish pupil.
Treatment: Cyclocryopexy.

Fig. 7.3: PACG—chronic angle- Fig. 7.4: Absolute glaucoma

closure

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 GLAUCOMA

SLIT LAMP GRADING OF ‘corneal thickness’ (CT) 1 mm

THE ANGLE (VAN HERICK) inside the limbus.
(FIGS 7.5A TO D)
Four grades:
Used with a fair accuracy; useful • Grade 4: PAC = 1CT = wide
when a gonioscopy is difficult open-angle
to perform or gonioscope is not • Grade 3: PAC = 1/4th to ½
available. CT = open-angle
Angle is judged by estimating • Grade 2: PAC = 1/4th CT =
the depth of the ‘peripheral moderately narrow
anterior chamber’ (PAC) and • Grade 1: PAC < 1/4th CT =
then comparing it to the adjacent extremely narrow

Fig. 7.5A: van Herick grading— Fig. 7.5B: van Herick grading—
Grade 4 Grade 3

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 CLINICAL OPHTHALMOLOGY

CUPPING OF THE OPTIC

DISK (FIGS 7.6A TO L)
Asymmetry of the cupping (C : D
ratio difference more than 0.2);
cupping starts as focal
enlargement (notching) at the
infero-temporal quadrant. It
may be superior or both.

Fig. 7.5C: van Herick grading—

Grade 2

Fig. 7.5D: van Herick grading— Fig. 7.6A and B: Glaucoma

Grade 1 cupping—asymmetry

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 GLAUCOMA

Fig. 7.6C: Glaucoma cupping— Fig. 7.6E: Glaucoma cupping—

inferior notching neuroretinal rim thinning

Fig. 7.6D: Glaucoma cupping - Fig. 7.6F: Glaucoma cupping—

bayonetting sign nasal shifting of blood vessels

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 CLINICAL OPHTHALMOLOGY

Fig. 7.6G: Glaucoma cupping— Fig. 7.6I: Glaucoma cupping—

overpassing phenomena near total

Fig. 7.6H: Glaucoma cupping— Fig. 7.6J: Glaucoma total

baring of blood vessels cupping—bean pot cupping

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 GLAUCOMA

Bayonetting sign—double angu-

lations of blood vessels, pass
sharply backwards and then
turn along the steep wall of the
excavation before angling again
onto the floor of the cup.
Thinning of the neural rim; Nasal
shifting of retinal blood vessels;
Over passing of blood vessels. Fig. 7.6K: Glaucoma cupping—
total pallor
Splinter hemorrhages at the disk
margin; Baring of circumlinear
blood vessels may be seen at the
disc margin; Near total cupping.
Total cupping: Appears as a white
disk with loss of all neural rim,
and bending of all retinal vessels
at the margin of the disk - called
bean-pot cupping.
Total pallor of the disc, as there is
glaucomatous optic atrophy;
visible upto the margin of disk Fig. 7.6L: Glaucoma cupping—
laminar dot sign. laminar dot sign

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 CLINICAL OPHTHALMOLOGY

GLAUCOMA CAPSULAR
(FIGS 7.7A AND B)
Secondary glaucoma with pseu-
doexfoliation syndrome; depo-
sition of fibrillar basement
membrane-like material block-
ing the trabecular meshwork.
White exfoliative materials on
the anterior lens capsule, pupil- Fig. 7.7A: Pseudoexfoliation of
lens capsule
lary margin and angle of the
anterior chamber.
Treatment: Same as PAOG.

Fig. 7.7B: Pseudoexfoliative

glaucoma

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 GLAUCOMA

PIGMENTARY GLAUCOMA
(FIGS 7.8A AND B)
Pigment dispersion occurs
throughout the anterior seg-
ment; loss of pigments from the
iris – transillumination positive.
Deposition of pigment on the
corneal endothelium in a ver-
tical line called Krunkenberg’s Fig. 7.8A: Pigmentary glaucoma
spindle; accumulation of pig-
ment along the Schwalbe’s line,
especially inferiorly, as a dark
line - Sampaolesi’s line.
Treatment: Same as POAG.

Fig. 7.8B: Pigmentary

glaucoma—Sampaolesi’s line

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 CLINICAL OPHTHALMOLOGY

INFLAMMATORY
SECONDARY GLAUCOMA
(FIGS 7.9A AND B)
Associated with inflammation of
other ocular structures.
Causes: Glaucomato-cyclitic
crisis (Posner-Schlossmann
syndrome); hypopyon corneal
ulcer; adherent leucoma, etc.
A
Treatment: Medical and if
necessary surgical.

B
Figs 7.9A and B: Glaucoma with
iridocyclitis—iris bombe

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 GLAUCOMA

GLAUCOMA ASSOCIATED dislocation of lens; angle

WITH TRAUMA recession; Penetrating injury.
(FIGS 7.10A TO D) Chemical injury: Both by acid or
Blunt injury: More than one alkali burn.
mechanism are involved: Treatment: Antiglaucoma
hyphema; subluxation or medication, but no miotics.

Fig. 7.10A: Traumatic hyphema— Fig. 7.10C: Glaucoma with

glaucoma subluxation—pupillary block

Fig. 7.10B: Angle recession Fig. 7.10D: Lens matter

glaucoma glaucoma

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 CLINICAL OPHTHALMOLOGY

MALIGNANT (CILIARY
BLOCK) GLAUCOMA
(FIG. 7.11)
Total shallowing (both central
and peripheral) of the anterior
chamber; poor response to
conventional antiglaucoma
medication.
Two types: cilio-lenticular block:
After trabeculectomy and cilio-
vitreal block: after cataract
operation (mainly ICCE).
Treatment: USG-localization of
aqueous pocket in vitreous;
lens extraction in phakic cases;
YAG laser hyaloidotomy in Fig. 7.11: Malignant glaucoma—
pseudophakic cases; vitrec- ciliovitreal block
tomy in aphakic cases.

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 GLAUCOMA

NEOVASCULAR
GLAUCOMA
(FIGS 7.12A AND B)
Secondary glaucoma due to
neovascularization of the angle
in rubeosis iridis.
Three stages—preglaucoma-
tous stage: rubeosis iridis; open
angle glaucoma stage: due to Fig. 7.12A: Glaucoma—rubeosis
intense neovascularisaton at the iridis
angle; angle closure glaucoma
stage: due to gonio-synechia and
PAS formation.
Treatment: Prophylactic pan-
retinal photocoagulation, ante-
rior retinal cryopexy and cyclo-
photocoagulation.

Fig. 7.12B: Neovascular

glaucoma—total PAS

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 CLINICAL OPHTHALMOLOGY

FILTERING BLEB
ABNORMALITIES
(FIGS 7.13A TO F)
• Normal/good functioning
filtering bleb
• Failed filtering bleb
• Cystic filtering bleb
• Multilocular filtering bleb
• Overhanging filtering bleb Fig. 7.13A: Good filtering bleb

Fig. 7.13B: Normal functioning

bleb

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 GLAUCOMA

Fig. 7.13C: Failed filtering bleb Fig. 7.13E: Multilocular filtering

bleb

Fig. 7.13D: Cystic filtering bleb Fig. 7.13F: Over hanging bleb

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 CLINICAL OPHTHALMOLOGY

OVERFILTERING BLEB choroidal folds and hypotonic

(FIGS 7.14A TO D) maculopathy.
Shallow anterior chamber; cor- Treatment: Repair of the bleb
neal folds due to hypotony; to reduce overfiltration.

Fig. 7.14A: Over filtering bleb Fig. 7.14C: Over filtering bleb—
hypotony— corneal folds

Fig. 7.14B: Over filtering bleb— Fig. 7.14D: Over filtering bleb—
shallow AC hypotony—choroidal folds

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 GLAUCOMA

LEAKING FILTERING BLEB

(FIGS 7.15A AND B)
Shallow anterior chamber;
corneal and fundal changes
may be present; positive
Seidel’s test.
Treatment: Repair of the
filtering bleb.
Fig. 7.15A: Leaking bleb

Fig. 7.15B: Leaking bleb—

positive Seidel’s test

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 CLINICAL OPHTHALMOLOGY

BLEBITIS (BLEB
INFECTION)
(FIGS 7.16A AND B)
Suppurative infection of the bleb
mainly by bacteria. The bleb
appears yellowish white in
colour with surrounding con-
gestion; anterior chamber reac-
tion and hypopyon. Eventually
Fig. 7.16A: Bleb infection—
it progresses to endophthal- blebitis
mitis.
Treatment: Systemic and topical
broad-spectrum antibiotics with
surgical revision of the bleb.

Fig. 7.16B: Bleb infection—

blebitis

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 GLAUCOMA

WIND-SHIELD WIPER
SYNDROME (FIG. 7.17)
Seen after trabeculectomy
surgery with releasable suture.
The loose end of suture moves
like a wiper of windshield.
Careful double passing of the
suture and flush trimming are
important to avoid this pro- Fig. 7.17: Wind-shield wiper
blem. syndrome

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 CLINICAL OPHTHALMOLOGY

ASTEROID HYALOSIS
(BENSON’S DISEASE)
(FIG. 8.1)
Usually bilateral, that affects
aged patients; appear as nume-
rous, white, round or discoid
bodies suspended throughout,
or in a portion of the solid
vitreous; represents calcium
soap crystals from degeneration Fig. 8.1: Asteroid hyalosis
of vitreous fibrils.
Asymptomatic and do not
require treatment.

SYNCHISIS SCINTILLANS
(FIG. 8.2)
Unilateral, with previous h/o
vitreous hemorrhage or inflam-
mation; crystals appear as gol-
den glittering particles which
settle at the bottom of vitreous
cavity; can be thrown upwards Fig. 8.2: Synchisis scintillans—
by ocular movements, to form posterior vitreous
a ‘golden shower’.
No effective treatment.

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 DISEASES OF THE VITREOUS AND RETINA

VITREOUS CELLS (FIG. 8.3)

Seen in Iridocyclitis (when cyclitis
is predominant);
Intermediate uveitis: as inferior
peripheral vitreous snow-ban-
king; infective endophthalmitis:
cells or frank exudates in the
vitreous and posterior uveitis: Fig. 8.3: Vitreous cells in
panuveitis
cells are most dense adjacent to
the lesions.

VITREOUS HEMORRHAGE
(FIGS 8.4A TO D)
May occur as a preretinal or an
intravitreal phenomenon.
• retinal break - traumatic or by
vitreous traction; Fig. 8.4A: Vitreous hemorrhage
• Proliferative retinopathies:
rupture of new vessels;
• Acute posterior vitreous
detachment (PVD);
• Bleeding disorders; peri-
phlebitis or Eales’ disease
May be seen as minute red or
dark spots, as red mass, or with
no fundal view. Organized
Fig. 8.4B: Vitreous
vitreous hemorrhage may hemorrhage—PDR

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 CLINICAL OPHTHALMOLOGY

appear clotted with membrane

formation.
Treatment: Investigation,
medical, pars plana vitrectomy
with endo-laser photocoagu-
lation.

Fig. 8.4C: Organized vitreous

hemorrhage

Fig. 8.4D: Vitreous hemorrhage—

membrane formation

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 DISEASES OF THE VITREOUS AND RETINA

MISCELLANEOUS
VITREOUS OPACITIES
(FIGS 8.5A TO F)
Pigment cells (‘tobacco dust’):
consist of macrophages contai-
ning retinal pigment epithelial
cells; mainly visible in the
anterior vitreous- in retinal
tears with PVD, or RRD
Fig. 8.5A: Vitreous membrane
Cotton ball exudates: as in sarcoi- with tobacco dust
dosis or candidiasis.
Parasite: May be live or dead
parasite—cysticercosis, gnatho-
stomiasis.
Foreign bodies: metallic, silicone
oil, air bubble and other gasses,
and intravitreal triamcinolone
injection.

Fig. 8.5B: Fungal exudates in

Candida endophthalmitis

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 CLINICAL OPHTHALMOLOGY

Fig. 8.5C: Cysticercus in vitreous Fig. 8.5E: Metallic foreign body in

vitreous

Fig. 8.5D: Gnathostoma in Fig. 8.5F: Intravitreal

vitreous triamcinolone

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 DISEASES OF THE VITREOUS AND RETINA

VITREOUS PROLAPSE IN
AC (FIGS 8.6A AND B)
In Aphakia, it may herniate into
the AC. In ECCE in case of PC
rent; in subluxation or dislo-
cation of IOL.
There may be touch with
cornea or with the wound
Treatment: Careful vitrectomy Fig. 8.6A: Vitreous knuckle in AC
with other procedures. in aphakia

Fig. 8.6B: Vitreous prolapse in

AC—subluxated lens

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 CLINICAL OPHTHALMOLOGY

PHAKOMATOSIS
(FIGS 8.7A TO D)
A group of conditions (hamar-
tomas) in which there are con-
genital, disseminated, usually
benign tumors of the blood
vessels or neural tissues. Often
ocular, cutaneous, and intra-
cranial in location. Fig. 8.7A: Tuberous sclerosis—
Neuro-fibromatosis (von adenoma sebaceum
Reclinghausen): most common
type, with typical subcutaneous
nodules and café-au-lait spots,
iris nodule- Leish’s nodule,
plexiform tumors of lids with
ptosis thickened corneal nerves.
Tuberous sclerosis (Bourne-
ville): diagnostic triad are
epilepsy, mental retardation
and adenoma sebaceum; called Fig. 8.7B: Retinal astrocytoma
‘epiloia’: eip (epilepsy), loi (low
IQ), a (adenoma sebaceum);
ocular lesion: astrocytoma optic
disc.

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 DISEASES OF THE VITREOUS AND RETINA

Angiomatosis retinae (von

Hipple-Lindau): a reddish,
slightly elevated tumour is seen
in the retina which is nourished
by dilated large retinal artery
and vein.
Encephalo-trigeminal angio-
matosis (Sturge-Weber): port- C
wine stain along the distribution
of trigeminal nerve; choroidal
hemangioma with congenital
glaucoma.

D
Figs 8.7C and D: Angiomatosis
retinae

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 CLINICAL OPHTHALMOLOGY

RETINOCHOROIDAL
COLOBOMA (FIGS 8.8A TO C)
Large oval, or semicircular
sharp white area inferior to the
optic disk; sometimes, it may
include the disk.
May appear as an isolated
coloboma or with a bridge of
normal retinochoroidal tissue in Fig. 8.8B: Retinochoroidal isolated
between, giving rise to ‘double coloboma—double disk appea-
disc’ or ‘triple disk’ appearance. rance

Fig. 8.8A: Retinochoroidal Fig. 8.8C: Retinochoroidal isolated

coloboma colobomas—triple disk appea-
rance

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 DISEASES OF THE VITREOUS AND RETINA

CENTRAL RETINAL
ARTERY OCCLUSION
(FIGS 8.9A TO F)
Painless, sudden loss of vision;
occlusion may affect the central
retinal artery (CRAO) or a
peripheral branch.
Retina loses its transparency,
and becoming opaque and Fig. 8.9B: Cherry red spot
milky-white, especially around
the posterior pole; a cherry-red
spot appears at the fovea. In
presence cilioretinal artery (25%
cases), macula may often
spared.

Fig. 8.9A: CRAO—cherry red Fig. 8.9C: Branch retinal artery

spot occlusion

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 CLINICAL OPHTHALMOLOGY

Branch occlusion occurs at a

bifurcation and usually by an
embolus; an atheromatous
embolus may be visible as a
refractile body (Hollenhorst
plaque) within the artery.
After a week or so, retina
appears normal with optic
atrophy with pale disc. Fig. 8.9E: Hollenhorst plaque

Treatment: Emergency digital

massage, paracentesis, I/V
acetazolamide, CO2 inhalation,
etc. Prognosis is invariable poor,
if the obstruction is more than 6
hours.

Fig. 8.9D: CRAO—patent Fig. 8.9F: CRAO—optic atrophy

cilioretinal

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 DISEASES OF THE VITREOUS AND RETINA

CENTRAL RETINAL
VENOUS OCCLUSION
(FIGS 8.10A TO D)
Non-ischemic CRVO
Mild tortuosity and dilatation of
all branches of the central retinal
vein; ‘dot’ and ‘blot’; and ‘flame’
shaped hemorrhages are seen A
throughout the retina; Sclerosed
veins may be seen in old CRVO.
Treatment: Treatment of predis-
posing factors.

B
Figs 8.10A and B:
Non-ischemic CRVO

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 CLINICAL OPHTHALMOLOGY

Ischemic CRVO
Marked tortuosity and engor-
gement of the retinal veins;
massive superficial flame-sha-
ped and deep hemorrhages
throughout the fundus.
Cotton-wool exudates are com-
mon; optic disc is swollen and C
hyperemic; macular edema and
hemorrhages; sometimes,
called ‘Blood and Thunder’ fun-
dus.
Treatment: Patient should be
followed up closely to prevent
rubeosis iridis and neovascular
glaucoma.

D
Figs 8.10C and D: Ischemic
CRVO

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 DISEASES OF THE VITREOUS AND RETINA

BRANCH RETINAL VENOUS

OCCLUSION (FIGS 8.11A TO F)
BRVO may occur near the optic
disc and involves a major qua-
drant, at a peripheral crossing
with an artery. Blockage of the
superior temporal vein fre-
quently involves the macula.
Fundus shows: dilated and Fig. 8.11A: BRVO—at the disk
tortuous veins; flame-shaped, margin
and ‘dot’ and ‘blot’ hemorr-
hage in the affected quadrant;
edema and cotton-wool spots
Sometimes there is hemiretinal
venous occlusion, involving the
upper half or lower half of retina.
There may be tributary venous
occlusion.
Treatment: Fundus fluorescein
angiography (FFA) to know the
macular perfusion status and
later macular grid photocoagu-
lation or to treat neovascula- Fig. 8.11B: BRVO—at the AV
rization. crossing

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 CLINICAL OPHTHALMOLOGY

C E

D F
Figs 8.11C and D: Hemiretinal Fig. 8.11F: ST BRVO—
venous occlusion tributary—macular involvement

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 DISEASES OF THE VITREOUS AND RETINA

PRERETINAL
HEMORRHAGE
(FIGS 8.12A TO F)
Usually solitary and located at
the posterior pole obscuring the
visualization of underlying
retinal vessels.
Initially round, but later turn A
into boat-shaped hemorrhage due
to settling by gravity. Absorp-
tion occurs from the top with
yellow-white discoloration.
Causes: trauma, Valsalva retino-
pathy, proliferative retino-
pathies, Terson’s syndrome
(with subarachnoid hemor-
rhage)
Treatment: Laser hyaloidotomy B
to drain the blood into the Figs 8.12A and B: Preretinal
vitreous cavity. hemorrhage

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 CLINICAL OPHTHALMOLOGY

C
Fig. 8.12E: Preretinal
hemorrhage—absorbed

D
Figs 8.12C and D: Preretinal Fig. 8.12F: Preretinal
hemorrhage hemorrhage—YAG hyaliodotomy

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 DISEASES OF THE VITREOUS AND RETINA

SUBRETINAL
HEMORRHAGE
(FIGS 8.13A AND B)
Blood is between the photo-
receptors and RPE layer. Large
bright red area with indistinct
outline. Overlying retina is
slightly elevated with visible
A
retinal blood vessels. May be
associated with sub-RPE
hemorrhage in some cases.
Cause: Blunt trauma, choroidal
neovascularization, etc.

B
Figs 8.13A and B: Subretinal
hemorrhage—FFA

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 CLINICAL OPHTHALMOLOGY

SUB-RPE HEMORRHAGE
(FIGS 8.14A AND B)
Blood from choroids seeps into
the space between Bruch’s
membrane and RPE. Solitary or
multiple dark-red area with
distinct outline. FFA shows
blocked background choroidal
A
fluorescence.
Cause: Subretinal choroidal
neovascular membranes.

B
Figs 8.14A and B: Sub-RPE
hemorrhage—FFA

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 DISEASES OF THE VITREOUS AND RETINA

CHOROIDAL HEMORRHAGE
(FIGS 8.15A AND B)
Solitary very dark-red area with
well defined outline.
Cause: Blunt trauma, often
associated with choroidal tear
and in severe cases with sub-
RPE hemorrhage.
Figs 8.15A: Choroidal
hemorrhage

Fig. 8.15B: Choroidal

hemorrhage—with RD

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 CLINICAL OPHTHALMOLOGY

ROTH SPOT
(FIGS 8.16A AND B)
Retinal hemorrhage with white
centre.
Causes: Leukaemia, severe
anaemia, dysproteinaemias,
subacute bacterial endocarditis,
HIV retinopathy.
Fig. 8.16A: Roth spot—leukemia

Fig. 8.16B: Roth spot—severe

anemia

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 DISEASES OF THE VITREOUS AND RETINA

NEOVASCULARIZATION neovascularization elsewhere

(NVE).
(FIGS 8.17A TO H)
May involve peripheral retina
May involve the optic nerve and takes the configuration of
head, called neovascularisation ‘sea fan’. New vessels often
of the disc (NVD) and when it bleed, resulting retinal or vitre-
involves central retina, called ous hemorrhage.

A
Fig. 8.17C: Extensive NVE (FFA)

B
Figs 8.17A and B: NVD— Fig. 8.17D: NVD and NVE—PDR
preretinal hamorrhage (FFA) (FFA)

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 CLINICAL OPHTHALMOLOGY

E G

F H
Figs 8.17E and F: NVE—sea fan Figs 8.17G and H: Neovas-
neovascularization (FFA) cularization—tractional RD (FFA)

New vessels may be flat, ele- Causes: PDR, old CRVO or

vated or mixed and associated BRVO, retinal vasculitis, Eales’
with variable degree of fibrosis. disease, ROP, Sickle cell retino-
When fibrous tissue contracts, pathy, etc.
it may result in tractional retinal
detachment.

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 DISEASES OF THE VITREOUS AND RETINA

RETINAL COLLATERALS
(FIGS 8.18A AND B)
These shunts are acquired
communication between artery
and vein; artery and artery; and
vein and vein which occur in
response to vascular insult. It is
in larger caliber than that of
A
NVs. Collaterals should not be
lasered as they are physiolo-
gical.

B
Figs 8.18A and B: Collaterals—
BRVO (FFA)

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 CLINICAL OPHTHALMOLOGY

RETINAL VASCULITIS Active vasculitis appears as fluffy

(FIGS 8.19A TO G ) white perivascular cuffing better
More commonly involves retinal visible on FFA.
vein (periphlebitis), rarely the Periphlebitis in sarcoidosis may
arterioles (periarteritis). Severe appear as ‘candle wax dripping’
periphlebitis may give rise to around the veins. Periarteritis
CRVO or BRVO like pictures. may block a branch arteriole

A B
Figs 8.19A and B: Vasculitis

Fig. 8.19C: Vasculitis—candle-wax dripping

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 DISEASES OF THE VITREOUS AND RETINA

D F

E G
Figs 8.19D and E: Frosted Figs 8.19F and G: Vasculitis—
branch angitis—FFA CRVO (FFA)

Causes: periphlebitis: sarcoi- frosted branch angitis, etc. peri-

dosis, Eales’ disease, inter- arteritis: collagen disorders like,
mediate uveitis, CMV retinitis, SLE, polyarteritis nodosa, etc.

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 CLINICAL OPHTHALMOLOGY

RETINAL HARD EXUDATES

(FIGS 8.20A TO F)
Yellow-waxy deposits or
plaques with fairly distinct
margins; Most frequently seen
in the posterior pole; may vary
in size and configuration,
isolated, ring-shaped, etc.
Causes: Diabetic retinopathy, Fig. 8.20A: Hard exudates—
retinal macroaneurysm or isolated clumps
hemangiomas.

Fig. 8.20B: Hard exudates—ring

shaped

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 DISEASES OF THE VITREOUS AND RETINA

Fig. 8.20C: Hard exudate— Fig. 8.20E: Macular star—

circinate pattern incomplete

Fig. 8.20D: Hard exudates with Fig. 8.20F Macular star—

subretinal exudates Complete BRVO

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 CLINICAL OPHTHALMOLOGY

SOFT EXUDATES OR plasmic debris in the nerve fiber

COTTON WOOL SPOTS layer as a result of ischemia.
(FIGS 8.21A TO D)
Causes: CRVO or BRVO, hyper-
White, cotton-wool like spots tensive retinopathy, HIV micro-
with indistinct margins; the angiopathy, severe anemia, etc.
localised accumulation of axo-

A C

B D
Figs 8.21A to D: Soft and hard exudates

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 DISEASES OF THE VITREOUS AND RETINA

SUBRETINAL EXUDATES frequently associated with

(FIGS 8.22A TO D) elevation of overlying retina.
Yellowish-white, exudative Causes: Chronic leakage from
lesions with indistinct margin in SRNVMs, Coat’s diseases, toxo-
the central or peripheral retina; cariasis.

A C

B D
Figs 8.22A to D: Subretinal exudates in Coats’ disease

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 CLINICAL OPHTHALMOLOGY

MULTIPLE EVANESCENT
WHITE DOT SYNDROME
(MEWDS) (FIGS 8.23A AND B)
Rare, unilateral condition in
young women. Multiple white
dots like lesions at the posterior
pole and mid periphery. They
are at the RPE level and clearly
visible on FFA.
Fig. 8.23A: Multiple evanescent
Prognosis is always good. white dot syndromes

Fig. 8.23B: MEWDS—FFA

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 DISEASES OF THE VITREOUS AND RETINA

APMPEE (FIGS 8.24A AND B)

Typical deep cream-colored
placoid lesions at the posterior
pole within the equatorial lre-
gion. Located at the level of
RPE, appreciated by FFA.
Prognosis is good.

Fig. 8.24A: APMPEE

Fig. 8.24B: APMPEE on FFA

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 CLINICAL OPHTHALMOLOGY

MULTIFOCAL CHOROIDITIS areas chorio-retinal atrophy.

(FIGS 8.25A TO D) Associated with anterior uveitis.
Unilateral or bilateral recurrent
condition affects middle-aged Treatment: Topical/systemic
women. Small discrete fresh and corticosteroids, systemic immu-
old lesions at the mid-periphery nosuppressants, etc.
and posterior pole with variable

A C

B D
Figs 8.25A to D: Active multifocal choroiditis—bilateral (FFA)

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 DISEASES OF THE VITREOUS AND RETINA

FOCAL TOXOPLASMOSIS may be with CME. Extensive

(FIGS 8.26A TO D) leakage of FFA.
Unilateral or bilateral protozoan Treatment: Pyrimethamine with
infection of young adults (bet- folinic acid (or alternately clin-
ween 15-30 years), caused by damycin), sulphadiazine/trime-
Toxoplasma gondii. Focal retinitis thoprim, etc. Steroids if macula
adjacent to the edge of old is involved.
lesion, associated vitritis, and

A C

B D
Figs 8.26A and B: Figs 8.26C and D: Toxo-
Toxoplasmosis—old scar (FFA) plasmosis—reactivation (FFA)

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 CLINICAL OPHTHALMOLOGY

CANDIDA RETINITIS
(FIGS 8.27A AND B)
Rare unilateral or bilateral
fungal infection typically affects
drug-addicts or immunocom-
promised individuals. Solitary
or multiple deep retinal infil-
trates with cotton ball opacities
in the vitreous with vitritis.
Fig. 8.27A: Candidiasis—retinal
Prognosis is poor. lesion

Fig. 8.27B: Candidiasis—cotton

ball opacity in vitreous

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 DISEASES OF THE VITREOUS AND RETINA

CYTOMEGALOVIRUS (CMV)
RETINITIS (FIGS 8.28A TO D)
25% of patients of AIDS suffer
from CMV retinitis and bilate-
rality in 50% cases. Yellowish-
white areas of retinal infiltration
with advancing brush-like
border.
A
Slowly progressive and typi-
cally start at the posterior pole
and spread along the vascular
arcades; hemorrhages in the
midst of retinitis.
Other fundal changes in AIDS
patients: Retinal microvasculo-
pathy as evident by cotton wool
spots, superficial and deep
hemorrhage; immuno complex
deposits in the precapillary B
arterioles; CRVO; immune- Figs 8.28A and B: CMV
recovery uveitis retinitis—CRVO

Other causes of CMV retinitis:

Patient on cytotoxic chemo-
therapy or renal transplant
patient.
Treatment: I/V injection of
gancyclovir or foscarnet.

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 CLINICAL OPHTHALMOLOGY

Fig. 8.28C: Retinal Fig. 8.29A: Acute retinal

microvasculopathy—HIV necrosis—CMV retinitis

Fig. 8.28D: Immuno-recovery Fig. 8.29B: Progressive outer

uveitis retinal necrosis

ACUTE RETINAL NECROSIS

confluent yellowish-white
(FIGS 8.29A AND B)
patches with sheathing and
Extremely rare, devastating occlusion of blood vessels. Most
necrotizing retinitis affects eyes develop multiple retinal
otherwise healthy subjects; holes with RRD.

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 DISEASES OF THE VITREOUS AND RETINA

TUBERCULAR
GRANULOMA
(FIGS 8.30A AND B)
Rare, but not so uncommon in
developing countries. Solitary
choroidal granuloma at the
posterior pole. Often associated
with granulomatous anterior
uveitis. A

Treatment: Full antitubercular

regimens. Good prognosis.

B
Figs 8.30A and B: Tubercular
granuloma—FFA

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 CLINICAL OPHTHALMOLOGY

STARGARDT’S MACULAR
DYSTROPHY
(FIGS 8.31A TO F)
Rare, bilateral, recessive condi-
tion starts around 14 to 16 years;
May results severe visual loss
within five years.
Macula may appear: As isolated A
atrophic maculopathy; atrophic
maculopathy with fish tail-
shaped flecks; or with diffuse
flecks around the posterior pole.
Prognosis is always poor

B
Fig. 8.31A and B: Stargardt atrophic
maculopathy with fish tail-shaped
flecks

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 DISEASES OF THE VITREOUS AND RETINA

D F
Figs 8.31C and D: FFA appearance Figs 8.31E and F: Stargardt—
of same patient (Figs 8.31A and B) maculopathy with flecks

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 CLINICAL OPHTHALMOLOGY

BEST’S VITELLIFORM
MACULAR DYSTROPHY
(FIGS 8.32A AND B)
Very rare, dominant hereditary
condition starts in childhood;
usually bilateral, but often
asymmetrical.
Clinically, it has the following
stages: vitelliform stage: egg yolk- Fig. 8.32A: Vitelliform dystrophy—
like macular lesion. pseudohypo- egg yolk lesion
pyon stage: with partial absorp-
tion; vitelliruptive stage: scram-
bled egg macular lesion; end
stage: with atrophic maculo-
pathy and disciform scarring
Prognosis is always poor.

Fig. 8.32B: Vitelliform dystrophy—

scrambled egg appearance

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 DISEASES OF THE VITREOUS AND RETINA

BULL’S EYE MACULOPATHY nant or X-linked recessive. Bull’s

(FIGS 8.33A TO H) eye macular lesions, with golden
Very rare bilateral macular reflex; vascular attenuation and
dystrophy; autosomal domi- temporal pallor may be present

A C

B D
Figs 8.33A to D: Bull’s eye maculopathy—cone dystrophy (FFA)

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 CLINICAL OPHTHALMOLOGY

E G

F H
Figs 8.33E to H: Bull’s eye maculo-
pathy— chloroquine toxicity (FFA)

Other causes: chloroquine toxicity: associated retinal vascular

Dose-dependent and occurs attenuation and may not be
after prolonged use, especially reversible. Also in late stage of
when for rheumatoid arthritis; Stargardt’s disease.

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 DISEASES OF THE VITREOUS AND RETINA

MYOPIC MACULOPATHIES
(FIGS 8.34A TO F)
Common, bilateral, often asym-
metrical macular lesions in
pathological myopia; lesions are
usually progressive
Changes are: Lacquer cracks at
the posterior pole; atrophic
maculopathy; macular haemor-
Fig. 8.34A: Myopic
rhage with choroidal neovascu- maculopathy—lacquer cracks
larisation; Fuchs’ pigmented
spot at fovea; macular hole with
or without retinal detachment;
posterior staphyloma.

Fig. 8.34B: Myopic atrophic

maculopathy

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 CLINICAL OPHTHALMOLOGY

Fig. 8.34C: Myopic fundus— Fig. 8.34E: Myopic maculopathy—

Fuchs’s pot posterior staphyloma

Fig. 8.34D: Myopic maculopathy— Fig. 8.34F: Myopic maculopathy

hemorrhage from CNV (FFA) -tesselated fundus

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 DISEASES OF THE VITREOUS AND RETINA

DRY AGE-RELATED Associated with soft drusen;

MACULAR DEGENERATION sharply demarcated areas of
(AMD) (FIGS 8.35A TO D) macular hypo- or depigmen-
Dry AMD is common, bilateral tation; visible underlying
condition, often bilateral; most choroidal vessels (geographical
common form of macular atrophy).
degeneration; affecting the FFA shows widespread win-
patient above sixty years of age. dow defect with late staining.

A C

B D
Figs 8.35A to D: Dry AMD—geographical atrophy (FFA)

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 CLINICAL OPHTHALMOLOGY

WET AMD (FIGS 8.36A TO F)

Wet AMD is a common bilateral
disease affecting the elderly
people; characterized by for-
mation or subretinal neovas-
cular membranes (SRNVMs) at
the macula.
SRNVMs consist of prolifera- A
tions of fibrovascular tissue
from the choriocapillaries;
clinically appears as pinkish
yellow slightly elevated sub-
retinal lesion of variable size.
FFA of SRNVMs shows charac-
teristic lacy pattern in early
phase, followed by hyper-
fluorescence and late leakage.
B
Extensive subretinal macular
fibrosis occurs in end stage. Figs 8.36A and B: Wet AMD—
bleeding SRNVMs (FFA)

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 DISEASES OF THE VITREOUS AND RETINA

C E

D F
Figs 8.36C and D: Wet AMD— Figs 8.36E and F: Wet AMD—
classical SRNVMs (FFA) scarring (FFA)

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 CLINICAL OPHTHALMOLOGY

CYSTOID MACULAR
EDEMA (FIGS 8.37A AND B)
An accumulation of fluid in the
outer plexiform (Henle’s) layer
and inner nuclear layer of the
retina, in the macular region;
shows an irregularity and blur-
ring of the foveal reflex. FFA A
shows typical ‘flower-petal’ or
‘spoke’ pattern of leakage at the
fovea during the late phase.
Causes: Cataract surgery, chro-
nic iridocyclitis, pars planitis,
YAG capsulotomy, retinitis
pigmentosa, diabetes, etc.

B
Figs 8.37A and B: Cystoid
Macular edema (FFA)

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 DISEASES OF THE VITREOUS AND RETINA

CENTRAL SEROUS Macula appears as an oval or

RETINOPATHY circular dark swelling, about the
(FIGS 8.38A TO D) size of the optic disk, often with
glistening ring-reflex.
Detachment of the neurosen-
sory retina from the RPE by FFA shows characteristic ‘smoke-
serous fluid; characterized by stack’-pattern or gradual ‘ink-
sudden shallow elevation of the blot’-pattern leak under the
neuroretina in the macular area neuro-retina.
with indistinct margin.

Fig. 8.38A: Central serous Fig. 8.38C: Central serous

retinopathy retinopathy

Fig. 8.38B: CSR—ink-blot Fig. 8.38D: CSR—smoke-stack

pattern on FFA pattern on FFA

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 CLINICAL OPHTHALMOLOGY

RPE DETACHMENT
(FIGS 8.39A AND B)
Separation of RPE from the
Bruch’s membrane. Unilateral
or bilateral sharply demarcated
dome-shaped lesions of varying
size at the post pole.
FFA shows area of hyper-
fluorescence which increases in Fig. 8.39A: RPE detachment—
intensity but not in size in late bilateral
phase.
Prognosis is usually good.

Fig. 8.39B: PED—FFA

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 DISEASES OF THE VITREOUS AND RETINA

MACULAR HOLE Pseudohole: Discontinuity of an

(FIGS 8.40A TO F) epiretinal membrane over the
macula.
May be full thickness or
lamellar; idiopathic; a common
age-related condition with bila-
teral affection in 15% cases.
Stage I: Yellow foveolar spot
with loss of depression.
Stage II: Central foveal defect
with an elevated retinal rim.
Stage III: Central round foveal
defect with a central smaller Fig. 8.40A: Macular hole—
stage II
operculum.
Stage IV: Central round foveal
defect with complete separation
of operculum; multiple yellow
deposits at the level of RPE
within the hole.
FFA shows a corresponding
circular zone of hypofluores-
cence.
Other types: Macular hole in
myopia; traumatic macular hole
lamellar hole after prolonged Fig. 8.40B: Macular hole—
CME. stage III

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 CLINICAL OPHTHALMOLOGY

Fig. 8.40C: Macular hole— Fig. 8.40E: Macular hole

stage IV

Fig. 8.40D: Macular hole— Fig. 8.40F: Macular hole (FFA)

yellow deposits

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 DISEASES OF THE VITREOUS AND RETINA

EPIRETINAL MEMBRANE
(FIGS 8.41A AND B)
Appears as a transparent mem-
brane with fine retinal striation
and cause preretinal macular
fibrosis. Associated vascular
tortuosity is best judged by FFA.
Later it becomes more opaque
A
with more wrinkling.

B
Figs 8.41A and B: Epiretinal
membrane—BRVO on FFA

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 CLINICAL OPHTHALMOLOGY

FUNDUS
FLAVIMACULATUS (FIGS
8.42A AND B)
Rare bilateral condition with
recessive inheritance; Yello-
wish-white fish-tail like flecks at
the posterior pole and mid-
periphral retina; flecks may A
occur in isolation or with macu-
lopathy, as in Stargardt’s
disease.

B
Figs 8.42A and B: Fundus
flavimaculatus

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 DISEASES OF THE VITREOUS AND RETINA

FUNDUS ALBIPUNCTATUS
(FIGS 8.43A AND B)
Rare, bilateral, recessive condi-
tion with congenital stationary
night blindness; multiple tiny
yellowish-white dots from
posterior pole to the periphery;
macula is spared and visual
A
acuity remains normal.

B
Figs 8.43A and B: Fundus
albipunctatus

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 CLINICAL OPHTHALMOLOGY

HARD DRUSENS
(FIGS 8.44A TO F)
Very common age-related con-
dition; usually not associated
with subsequent development
of macular degeneration.
Multiple, bilaterally symmet-
rical, small, discrete, yellow- A
white, slightly elevated lesions
at the both posterior poles.
Calcified drusen: Secondary
calcification in long standing
cases gives them glistening-
white appearance with conspi-
cuous margin.
FFA shows multiple RPE-win-
dow defects with hyperfluo-
rescence spots, and late staining
B
of the drusen.

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 DISEASES OF THE VITREOUS AND RETINA

C E

D F
Figs 8.44A to F: Hard drusen on FFA

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 CLINICAL OPHTHALMOLOGY

SOFT DRUSENS
(FIGS 8.45A AND B)
Age-related lesions associated
with increased risk of AMD;
larger than hard drusen with
indistinct edges.
Confluent with time; lesions are
often asymmetrical with secon-
A
dary RPE changes. FFA shows
hyperfluorescence.

B
Figs 8.45A and B: Soft Drusen

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 DISEASES OF THE VITREOUS AND RETINA

TYPICAL RETINITIS
PIGMENTOSA
(FIGS 8.46A TO D)
Typical RP is a bilateral, sym-
metrical, progressive diffuse
pigmentary retinal dystrophy
which predominantly affects the
rods. Patients usually present in
the second decade of life and A
ultimately have severe visual
loss in later life.
Classical triad of RP: Bony-spicule
pigmentation; arteriolar atte-
nuation and waxy-pallor of the
optic disk.
Pigmentary changes are typi-
cally perivascular, and have a
bone-spicule appearance, which
are observed mostly at the
equatorial region of the retina.
B
In late stages of the disease, the
unmasking of the larger choroi- Figs 8.46A and B: Retinitis
dal vessels gives the fundus a pigmentosa
tessellated appearance

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 CLINICAL OPHTHALMOLOGY

Cystoid macular edema, atrophic

or cellophane maculopathy may be
present upto 70% of the patients.

Fig. 8.46C: Retinitis pigmentosa

Fig. 8.46D: Retinitis

pigmentosa—CME

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 DISEASES OF THE VITREOUS AND RETINA

ATYPICAL RETINITIS
PIGMENTOSA
(FIGS 8.47A TO C)
Retinitis punctata albescens:
Multiple scattered white dots,
mostly between the posterior
pole and the equator.
Retinitis pigmentosa sine pig- Fig. 8.47A: Retinitis punctata
albescens—CME
mento: Arteriolar attenuation
and waxy-pallor of the disc with
subnormal ERG.
Unilateral retinitis pigmentosa.
Sectorial retinitis pigmentosa: One
quadrant or one half (usually
inferior) of the fundus.
Pericentric or central retinitis Fig. 8.47B: Retinitis
pigmentosa—sectorial
pigmentosa: RP, except the chan-
ges are confined to central or
pericentral area.

Fig. 8.47C: Retinitis

pigmentosa—central

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 CLINICAL OPHTHALMOLOGY

RP WITH SYSTEMIC
ASSOCIATION (FIG. 8.48)

Laurence-Moon-Biedl syndrome:
RP, mental retardation, obesity,
polydactyly and hypogona-
dism.
Refsum’s disease: RP, peripheral
neuropathy, deafness, ataxia
and icthyosis.
Bassen-Kornzweig syndrome: RP,
ataxia, acanthocytosis, fat mala-
bsorption.
Usher syndrome: RP and sen-
sory-neural deafness.
Cocayne’s syndrome: RP, dwar- Fig. 8.48: Retinitis pigmentosa—
LMB
fism, bird-like face, ataxia,
mental retardation and prema-
ture aging.
Kearn-Sayre syndrome: RP, chro-
nic progressive external oph-
thalmoplegia (CPEO) and heart
block.

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 DISEASES OF THE VITREOUS AND RETINA

RHEGMATOGENOUS
RETINAL DETACHMENT
(FIGS 8.49A AND B)
Detached retina is slightly
opaque, convex and corrugated
in appearance with loss of
underlying choroidal pattern.
Breaks appear as red areas
(holes or tears) of discontinuity
mainly in the peripheral retina. Fig. 8.49A: Rhegmatogenous
retinal detachment—superior RD—
macula

Fig. 8.49B: Rhegmatogenous

RD—choroidal detachment

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 CLINICAL OPHTHALMOLOGY

TRACTIONAL RETINAL
DETACHMENT
(FIGS 8.50A AND B)
Shallow concave detachment
which seldom extends beyond
equator; highest elevation of
retina occurs at vitreoretinal
traction site; mobility of deta-
ched retina is severely reduced;
retinal breaks are usually Fig. 8.50A: Tractional RD—
absent. traumatic

Fig. 8.50B: Tractional RD—

inflammatory

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 DISEASES OF THE VITREOUS AND RETINA

EXUDATIVE RETINAL
DETACHMENT (FIGS 8.51A
AND B)
RD configuration is very much
convex, smooth, non-corru-
gated and bullous; shifting of
fluid is the hallmark of exuda-
tive detachment due to force of
gravity; retinal breaks are
absent. Obvious ocular patho- Fig. 8.51A: Exudative RD—
logy is frequently evident. bullous detachment

Fig. 8.51B: Exudative RD—

choroidal melanoma

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 CLINICAL OPHTHALMOLOGY

HYPERTENSIVE
RETINOPATHY
(FIGS 8.52A AND B)
Focal retinal edema, retinal
hemorrhage and hard exudates
in chronic hypertension; Hard
exudates often deposit around
the macula as macular star.
Cotton-wool patches in acute or Fig. 8.52A: Hypertensive
severe hypertension; Papill- retinopathy
edema including the neuro-
retinal edema may occur in
malignant hypertension.
Various types of arteriovenous
crossing changes and associated
choroidal vascular changes.

Fig. 8.52B: Malignant

hypertension

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 DISEASES OF THE VITREOUS AND RETINA

DIABETIC RETINOPATHY
Non-proliferative DR
(Figs 8.53A to C)
Microaneurysm, vascular chan-
ges; small ‘dot’ and ‘blot’
hemorrhage; intraretinal micro-
vascular abnormalities (IRMA);
Hard exudates. B
Figs 8.53A and B: NPDR—
looping, dot and blot haemorrhage
(FFA)

Fig. 8.53C: NPDR—hard

exudates

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 CLINICAL OPHTHALMOLOGY

DIABETIC MACULOPATHY 500 μm of the fovea; area of reti-

(FIGS 8.54A TO C) nal thickening of 1 dd size (1500
Clinically significant macular μm) or at least part of which
edema (CSME) is defined as: within 1 dd of the centre of
retinal edema or thickening or fovea.
hard exudates at or within

A B

C
Figs 8.54A to C: PDR—CSME

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 DISEASES OF THE VITREOUS AND RETINA

PROLIFERATIVE DR course of major blood vessels,

(FIGS 8.55A TO D) NVE-‘new vessels elsewhere’.
Neovascularization is the Hemorrhage may occur as
hallmark of PDR; new vessels intraretinal, preretinal and
at the disc (NVD), or along the vitreous hemorrhage.

A C

B D
Figs 8.55A and B: Early PDR Figs 8.55C and D: Late PDR
(FFA) (FFA)

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 CLINICAL OPHTHALMOLOGY

ADVANCED hemorrhage; tractional retinal

PROLIFERATIVE DR detachment; brunt out pro-
(FIGS 8.56A TO D) liferative diabetic retinopathy or
neovascular glaucoma.
Central or branch retinal venous
occlusion; recurrent vitreous

A C

B D
Figs 8.56A and B: Advanced Figs 8.56C and D: Advanced
PDR—CRVO with preretinal PDR—featureless retina (FFA)
hemorrhage

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 DISEASES OF THE VITREOUS AND RETINA

RETINOPATHY OF patches in temporal peripheral

PREMATURITY retina; may result in tractional
(FIGS 8.57A TO D) bands at upper temporal
Occurs in premature infants quadrant producing an ectopic
(<1500 gm wt), with exposure macula or dragged disk.
to high concentration of O 2 In severe cases, fibrovascular
during the first 10 days of life. tissue proliferates to form a
mass behind the lens – causing
Appearance of hazy white pseudoglioma.

A C

B D
Figs 8.57A and B: Retinopathy Figs 8.57C and D: ROP—Sea
of prematurity fan neovascularization (FFA)

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 CLINICAL OPHTHALMOLOGY

RETINOBLASTOMA
(FIGS 8.58A AND B)
Leukocoria or ‘amaurotic cat’s eye
reflex’—the most common
presentation in 60% of cases.
Endophytic type: White or pearly-
pink coloured mass with sharp
margin projects into the vitre- A
ous cavity; presence of calcium
deposits giving an appearance
‘cottage cheese’.
Exophytic type gives rise to
exudative retinal detachment
and the tumor itself is difficult
to visualize.
Treatment: Enucleation, radio-
therapy, chemotherapy, photo- B
coagulation and in extreme Figs 8.58A and B: Large
cases exenteration. endophytic retinoblastoma

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 DISEASES OF THE VITREOUS AND RETINA

SUBRETINAL
CYSTICERCOSIS
(FIGS 8.59A AND B)
Not so uncommon caused by
Cysticercus cellulose. The white
scolex is clearly visible under
bright illumination. May be
associated with retinal detach- A
ment.
Treatment: Surgical removal of
the intact cyst.

B
Figs 8.59A and B: Subretinal
Cysticercosis

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 CLINICAL OPHTHALMOLOGY

MYELINATED NERVE
FIBERS (FIGS 9.1A AND B)
Congenital—1% of normal
population; 20% cases bilateral.
Appears as white patch with
radial feathery striations at its
peripheral edge; Usually peri-
papillary, but sometimes peri-
pheral and isolated; In optic Fig. 9.1A: Myelinated nerve
atrophy, it disappears. fibers—typical

No treatment is required.

Fig. 9.1B: Myelinated nerve

fibers—peripheral

CONGENITAL OPTIC DISK

PIT (FIG. 9.2)
Isolated unilateral condition;
round or oval depression at the
temporal margin. A central pit
is less common.
No treatment is required.
Fig. 9.2: Congenital optic disk pit

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 DISEASES OF THE OPTIC NERVE

COLOBOMA OF THE OPTIC with inferior excavation with

DISK (FIGS 9.3A TO C) glistening appearance of
Rare, usually unilateral, but underlying sclera; may be asso-
bilateral in case of autosomal ciated with typical coloboma of
dominant variety; large disk other parts.

A B
Figs 9.3A and B: Optic disk coloboma

Fig. 9.3C: Double optic disk—coloboma

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 CLINICAL OPHTHALMOLOGY

MORNING GLORY Vessels have an abnormal

SYNDROME (FIG. 9.4) distribution emerging around
Usually unilateral, congenital the edges in spoke- like fashion;
and with poor vision; Disk looks surrounded by annular cho-
large with core of white tissue. roidal ring.

Fig. 9.4: Morning glory syndrome

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 DISEASES OF THE OPTIC NERVE

TILTED DISK
(FIGS 9.5A AND B)
Due to an oblique entrance of
optic nerve into the globe;
congenital and usually bilateral.
Disk is extremely oval or ‘D-
shaped’, with the vertical axis
directed obliquely.
A

B
Figs 9.5A and B: Tilted disk—
situs inversus optica

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 CLINICAL OPHTHALMOLOGY

NEW VESSELS AT
THE DISK (NVD)
(FIGS 9.6A AND B)
Unilateral or bilateral, depen-
ding upon the cause; lace-like
fine vessels, may be flat or
elevated; vessels may extend to
the peripapillary region.
Causes: PDR, CRVO/BRVO,
central retinal vasculitis, retinal Fig. 9.6A: Neovascularization of
ischemia, etc. disk

Fig. 9.6B: Massive neovascu-

larization of disk

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 DISEASES OF THE OPTIC NERVE

DISK HEMORRHAGE
(FIGS 9.7A AND B)
Seen as splinter hemorrhage
over the disk and at disk-retina
junction.
Causes: Papilledema, AION,
optic neuritis, open angle glau-
coma, diabetic papillopathy, A
acute PVD, etc.

B
Figs 9.7A and B: Disk
hemorrhage

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 CLINICAL OPHTHALMOLOGY

OPTIC NEURITIS Treatment: I/V methyl pred-

(FIGS 9.8A AND B) nisolne for 3 days followed by
An inflammatory or demyeli- oral prednisolone and inj. Vit B1,
nating disorder of the optic B6 and B12.
nerve from disk to lateral
geniculate body.
Types: Papillitis (optic neuritis),
retrobulbar neuritis and
neuroretinitis.
Signs of papillitis: Sudden
visual loss and pupillary signs
(RAPD), disk edema with
obliteration of the physiological
cup, hyperemia and blurring of Fig. 9.8A: Optic neuritis
the disk margin, hemorrhages
on the disk, slit-like defect in
nerve fiber layer.
Sign of retrobulbar neuritis:
The site of involvement is
behind the globe; visual loss and
pupillary sign are important, no
fundus findings.
Neuroretinitis: Never asso-
ciated with demyelinating
diseases; signs of optic neuritis,
macular star in addition, juxta- Fig. 9.8B: Neuroretinitis
papillary exudates may be seen.

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 DISEASES OF THE OPTIC NERVE

ANTERIOR ISCHEMIC OPTIC

NEUROPATHY (AION)
(FIGS 9.9A TO D)
Two types: Non arteritic AION
and arteritic AION.
Non-arteritic AION: Is a
segmental infarction of the
anterior part of the optic nerve,
A
caused by the occlusion of short
posterior ciliary arteries.
Usually unilateral, aged patient
between 60 and 65 years; Pale,
sectorial (usually upper part)
disk edema which may be sur-
rounded by splinter hemor-
rhages. Associated with sudden
altitudinal hemianopia (usually
B
lower field).
Figs 9.9A and B: Anterior
ischemic optic neuropathy
(Non-arteritic)

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 CLINICAL OPHTHALMOLOGY

Arteritic AION: Caused by

giant cell arteritis, in more
elderly people; Unilateral severe
loss of vision.
A swollen, usually diffuse white
or pale disk, with splinter
hemorrhages around. With
time, the entire optic disk
becomes pale and fellow eye is C
frequently affected.
Tender nodular temporal arte-
ries and in sever cases there may
be scalp necrosis.

D
Figs 9.9C and D: Anterior
ischemic optic neuropathy
(Arteritic)

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 DISEASES OF THE OPTIC NERVE

PAPILLEDEMA
Bilaterial, non-inflammatory
passive swelling of the optic
disk, produced by raised intra-
cranial tension (ICT).
Unilateral papilledema with
optic atrophy on the other side
suggests a frontal lobe tumor A
or olfactory meningioma of
opposite side - Foster-Kennedy
syndrome (Figs 9.10A and B).
Signs depend on duration and
its severity.
Four stages: Early, established,
chronic and atrophic.

B
Figs 9.10A and B: Foster-
Kennedy syndrome: (A) Papille-
dema (B) Optic atrophy
of other eye

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 CLINICAL OPHTHALMOLOGY

Early Papilledema
(Figs 9.10C and D)
Disk hyperemia; Blurring of the
nasal sector of disk margin first,
then the superior and inferior;
Splinter hemorrhages at the
disk-margin; Absent sponta-
neous venous pulsation (also
absent in 20% of general C
population).

D
Fig. 9.10C and D: Early
papilledema

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 DISEASES OF THE OPTIC NERVE

Established (acute)
Papilledema
(Figs 9.10E and F)
Disk elevation is marked; Entire
disk margins become indistinct
and central cup obliterated;
Venous engorgement, flame-
shaped hemorrhage and peri-
E
papillary edema; Patton’s line-
peripapillary circumferential
retinal folds due to accumulation
of fluid

F
Figs 9.10E and F: Established
papilledema—Patton’s line

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 CLINICAL OPHTHALMOLOGY

Chronic Papilledema
(Figs 9.10G and H)
Hemorrhagic and exudative
components gradually resolve.
Optic disk appears as a ‘cham-
pagne cork’- like elevation;
Optico-ciliary shunt may be G
visible; Macular star may be
present.

H
Figs 9.10G and H: Chronic
papilledema—champagne cork
appearance

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 DISEASES OF THE OPTIC NERVE

Atrophic Papilledema
(Figs 9.10I and J)
Dirty-white appearance of the
optic disk, due to reactive glio-
sis, leading to secondary optic
atrophy; Retinal vessels are
attenuated with perivascular
sheathing; Peripapillary pig-
mentary changes.
I

J
Figs 9.10I and J: Atrophic
papilledema

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 CLINICAL OPHTHALMOLOGY

MALIGNANT OPTIC ATROPHY

HYPERTENSION Degeneration of optic nerve
(FIG. 9.11) fibers with loss of their myelin
Presence of severe rise in blood sheaths, and characterized by
pressure; More in secondary the pallor of the optic disk.
hypertension; Bilateral disk Types: Primary, secondary and
edema, flame-shaped hemor- consecutive.
rhage, soft exudates and a
macular star; Variable amount Primary Optic Atrophy
of hypertensive retinal changes; (Fig. 9.12A)
Peripheral pale areas of Disk pallor, with white or grey
choroidal infarcts. colour, without significant
gliosis; Flat disk, margin is
sharply defined, and peripapil-
lary retina is normal looking;

Fig. 9.11: Malignant hypertension

Fig. 9.12A: Primary optic atrophy

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 DISEASES OF THE OPTIC NERVE

Reduction in number of small

vessels crossing the disk;
Thinning of the nerve fiber layer

Secondary Optic Atrophy

(Figs 9.12B(i) and (ii))
Preceded by edema of the optic
nerve head; Dirty-grey color
with blurred margins; Cup is B(i)
full, and lamina cribrosa is
obscured; Narrowing of the
blood vessels with sheathing;
Seen in papilloedema, optic
neuritis or after AION.

B(ii)
Figs 9.12B(i) and (ii): Secondary
(postneuritic) optic atrophy

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 CLINICAL OPHTHALMOLOGY

Consecutive Optic Atrophy Glaucomatous Optic

(Fig. 9.12C) Atrophy (Fig. 9.12D)
Yellowish-waxy pallor of the Total cupping with complete
disk; Disk margins are less pallor of the optic disk. Visible
sharply defined; Marked nar- upto the margin of the disk—
rowing or even obliteration of ‘laminar dot sign’.
arterioles.

Fig. 9.12C: Consecutive optic

Fig. 9.12D: Glaucomatous optic
atrophy in retinitis pigmentosa
atrophy

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 DISEASES OF THE OPTIC NERVE

TEMPORAL PALLOR
(FIGS 9.13A AND B)
Form of partial optic atrophy,
involve a loss of temporal fibers
including the papillo-macular
bundles results in ‘temporal
pallor’.
Temporal side is normally A
relatively pale, because the
retinal vessels emerge from the
nasal side and the temporal side
is normally less vascular.

B
Fig. 9.13A and B: Temporal
pallor

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 CLINICAL OPHTHALMOLOGY

OPTIC DISK HEMANGIOMA

(FIGS 9.14A AND B)
Rare, unilateral; may alo involve
the retina. 25% patients have
von Hippel-Lindau syndrome.
Orange red lesion of the optic
disk with macular hard
exudates.
A
No treatment is required.

B
Fig. 9.14A and B: Optic disk
hemangioma

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 DISEASES OF THE OPTIC NERVE

OPTIC DISK
MELANOCYTOMA
(FIGS 9.15A AND B)
Rare, unilateral benign tumor
in pigmented race. Pigmented
dark lesion, frequently located
eccentrically. May induce disk
swelling and interfere with A
vision.
Only periodic observation is
required.

B
Figs 9.15A and B: Optic disk
melanocytoma

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 CLINICAL OPHTHALMOLOGY

OPTIC DISK
ASTROCYTOMA
(FIGS 9.16A AND B)
Unilateral giant drusen—a
benign condition; associated
with tuberous sclerosis or epiloia.
Semi-trasparent mulberry like
lesion that displays auto-
fluorescence.
Fig. 9.16A: Tuberous sclerosis
No treatment is required.

Fig. 9.16B: Optic disk

astrocytoma

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 CLINICAL OPHTHALMOLOGY

CRANIOSYNOSTOSIS sutures combined with hypo-

Follows premature closure of plasia of the maxilla; often
one/more cranial sutures. A hereditary in nature.
complete arrest of bony growth
perpendicular to the closed suture.
Compensatory growth of the
cranium in other diameters
which causes the typical shape
of the skull.
Common features:
• Bilateral proptosis due to
shallow orbit
• Esotropia or exotropia
• Chemosis of conjunctiva, A
corneal exposure
• Papilledema due to increased
ICT
• Optic atrophy.
Treatment: by craniotomy or
orbital compression to reduce
CSF pressure and papilledema.

CRANIOFACIAL
DYSOSTOSIS (CROUZON)
(FIGS 10.1A AND B)
B
Brachycephaly: (clover leaf Figs 10.1A and B: Cruzon’s
skull) premature closure of all syndrome

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 DISEASES OF THE ORBIT

Ophthalmic features: MEDIAN FACIAL-CLEFT

• Widely separated eyeballs SYNDROME (FIG. 10.2)
(hypertelorism)
• Hypertelorism with telecan-
• Shallow orbits with prop-
thus
tosis • Divergent squint
• Conjuntival chemosis
• Cleft nose, lip and palate
• Corneal problems due to • V-shaped frontal hair line
exposure
(Widow’s peak).
• Divergent squint
• Optic atrophy.
MANDIBULO-FACIAL
DYSOSTOSIS (TRECHER-
COLIN)
• Hypoplasia of the zygoma
and mandible
• Indistinct inferior orbital
margin
• Coloboma (notching) of the
lower lid
• Anti-mongoloid slanting. Fig. 10.2: Median facial-cleft
syndrome

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 CLINICAL OPHTHALMOLOGY

OXYCEPHALY- • Hypertelorism, shallow

SYNDACTYLE (APERT) orbits and proptosis
• Tower skull with flat occiput • Syndactyle, mental retar-
• Hypertelorism, shallow dation.
orbits and proptosis
• Syndactyle, mental retarda- ORBITAL DYSPLASIA
tion. (FIG. 10.4)
• Asymmetry of orbital mar-
HYPERTELORISM (FIG. 10.3) gins, especially the inferior
• Increased separation of the • May be associated with
eyes hypertelorism, hemifacial
• Separated orbits with broad microsomia, Goldenhar
nasal bridge; divergent syndrome, etc.
squint, telecanthus and anti-
mongoloid slanting

Fig. 10.3: Hypertelorism Fig. 10.4: Orbital dysplasia

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 DISEASES OF THE ORBIT

ANOPHTHALMOS OR • To be differentiated from

EXTREME MICROPH- acquired anophthalmos.
THALMOS
Under development of the bony ORBITO-PALPEBRAL
orbit due to extreme microph- (COLOBOMATOUS) CYST
thalmos or anophthalmos (FIG. 10.6)
(Fig. 10.5): • Associated with microph-
• Facial asymmetry is com- thalmos with coloboma
mon • May be with normal but
• Features of anophthalmic deformed globe
socket • Bluish color with upward
• Oculo-digital sign (a blind displacement of globe
child with eye-poking sign) • Congenital cystic eyeball.

Fig. 10.5: Anophthalmic socket— Fig. 10.6: Orbitopalpebral cyst—

oculodigital sign large

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 CLINICAL OPHTHALMOLOGY

PSEUDOPROPTOSIS • Enophthalmos of the oppo-

(FIGS 10.7A TO C) site eye.
One eye may be larger than the
fellow eye.
Causes
• Unilateral high axial myopia
• Unilateral buphthalmos
• Pseudocornea or anterior
staphyloma
• Retraction of the eyelid of
one eye
Fig. 10.7B: Pseudoproptosis—
buphthalmos LE

Fig. 10.7A: Pseudoproptosis— Fig. 10.7C: Pseudoproptosis—lid

myopia RE retraction LE

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 DISEASES OF THE ORBIT

ENOPHTHALMOS misdiagnosed as having con-

(FIGS 10.8A TO C) tralateral proptosis or ipsilateral
A condition in which eyeball is ptosis.
recessed within the orbit. Causes
About 25% of patients with • Phthisis bulbi, unilateral or
enophthalmos are initially bilateral
• Microphthalmos or anoph-
thalmos
• Surgical anophthalmos
• Blow-out fracture
• Horner’s syndrome.

A
Fig. 10.8A: Bilateral
enophthalmos

B C
Figs 10.8 B: Enophthalmos— Figs 10.8 C: Cosmetic correction
phthisis bulbi with artificial eye

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 CLINICAL OPHTHALMOLOGY

CAPILLARY HEMANGIOMA ORBITAL CELLULITIS

(FIG. 10.9) Usually child or in young adults
• Present at birth or early Ethmoidal sinusitis—is the
infancy commonest cause.
• Slowly growing unilateral
proptosis due to heman- Preseptal Cellulitis
gioma mass in the upper (Fig. 10.10)
anterior orbit • Acute periorbital swelling
• Becomes engorged, may and redness
enlarge when the baby cries • Conjunctival chemosis
• May have similar lesion in • Fluctuating mass signifies
eyelids or elsewhere. abscess formation.
• Treatment: Oral antibiotics,
analgesics, hot compress, and
topical antibiotics; drainage of
abscess if necessary.

Fig. 10.9: Capillary hemangioma Fig. 10.10: Preseptal cellulitis

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 DISEASES OF THE ORBIT

Orbital Cellulitis (Fig. 10.11)

• Very sick child with rise in
temperature
• Sudden onset, rapidly grow-
ing unilateral proptosis with
severe pain and chemosis of
the lids
• Eyeball is displaced laterally
and downwards
• Diplopia due to limitation of Fig. 10.11: Orbital cellulitis
ocular movements
• Chemosis and congestion of
the conjunctiva
• Treatment: I/V antibiotics,
analgesics, hot compress,
topical antibiotics.

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 CLINICAL OPHTHALMOLOGY

Lymphangioma
(Figs 10.12A and B)
Benign tumor between 1 and 15
years; May occur in isolation or
be combined with lid or
conjunctival lesions.
Soft bluish mass mainly in the
superior orbit, which may
remain stationary; May also Fig. 10.12A: Lymphangioma
involve the sinuses or oro-
pharynx.
Periodic sudden enlargement
with upper respiratory tract
infection or with spontaneous
bleeding (chocolate cyst).
Visual and motility disturban-
ces are common.

Fig. 10.12B: Lymphangioma—

oropharynx

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 DISEASES OF THE ORBIT

GLIOMA OF THE OPTIC RHABDOMYOSARCOMA

NERVE (FIG. 10.13) (FIG. 10.14)
Ectodermal tumor of the optic Most common primary malig-
nerve; between 2 and 8 years nant orbital tumor in children;
50% cases associated with neu- more in boys; tumor arises from
rofibromatosis. striated muscles; rapidly grow-
ing proptosis with chemosis of
Presents as unilateral proptosis
conjunctiva and lids.
with visual impairment.
Typically, a mass is palpable in
Slow growing unilateral prop-
supero-nasal quadrant.
tosis which is axial; Marcus
Gunn pupil and optic atrophy. Treatment: Combination of
radio- and chemotherapy; in
Enlargement of optic foramen
unresponsive cases, exentera-
in X-ray in 90% cases.
tion of the orbit.

Fig. 10.13: Optic nerve glioma Fig. 10.14: Rhabdomyosarcoma

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 CLINICAL OPHTHALMOLOGY

ORBITAL EXTENSION OF INFLAMMATORY ORBITAL

RETINOBLASTOMA DISEASES (FIG. 10.16)
(FIG. 10.15) Idiopathic, non-neoplastic, non-
In neglected cases, retino- microbial space-occupying
blastoma may present with periocular lesion, which may
proptosis due to direct orbital simulate an orbital neoplasm
extension. (pseudotumor); typical affects
Exenteration followed by males between 20-50 years.
radiotherapy is then required. Unilateral axial proptosis with
variable chemosis of the lids
Conjunctival chemosis and
congestion; limitation of extra-
ocular movements and diplopia.
D/D from thyroid ophthalmo-
pathy and orbital cellulitis.
Treatment: Observation, syste-
mic corticosteroids, and cyto-
toxic agents in resistance cases.

Fig. 10.15: Orbital extension of

retinoblastoma

Fig. 10.16: Inflammatory orbital

diseases

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 DISEASES OF THE ORBIT

THYROID OPHTHALMO-
PATHY (FIGS 10.17A TO C)
Most common cause of
proptosis in adults; unilateral or
bilateral chronic slow growing
axial proptosis; retraction of the
eyelid and lid lag.
Hyperemia of the conjunctiva
near horizontal rectus muscles; Fig. 10.17A: Thyroid
extraocular muscle involvement exophthalmos—unilateral
(most common—inferior rectus,
then medial rectus, least
common—lateral rectus) with
restriction of movements.
Conjunctival chemosis and
severe congestion in advance
cases; corneal involvement like,
exposure keratopathy or dry
eye in late stage.
Compressive optic neuropathy Fig. 10.17B: Thyroid
and disc edema. exophthalmos—bilateral
Chorioretinal folds in late stage.

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 CLINICAL OPHTHALMOLOGY

CAVERNOUS
HEMANGIOMA (FIG. 10.18)
Most common benign tumour
in adults; between 30 and 50
years. unilateral, slow pro-
gressive axial proptosis; may be
associated with chemosis of
conjunctiva.

Fig. 10.17C: Thyroid exoph- Usually not associated with

thalmos—thyroid swelling optic nerve compression unless
it is at the orbital apex.
Treatment: Antithyroid drugs,
artificial tears, systemic cortico-
steroids or cytotoxic agents,
lateral tarsorrhaphy and orbital
decompression in severe cases.

Fig. 10.18: Cavernous

hemangioma

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 DISEASES OF THE ORBIT

ORBITAL VARIX
(FIGS 10.19A AND B)
Usually unilateral, vascular
malformation, at any age.
Nonpulsatile, intermittent axial
proptosis, not associated with a
bruit; Proptosis may be accen-
tuated or precipitated by depen-
dent head posture or by Val- Fig. 10.19A: Orbital varix
salva maneuver.
Associated vascular lesion of the
eyelids or conjunctiva.

Fig. 10.19B: Proptosis—just after

head down position

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 CLINICAL OPHTHALMOLOGY

MENINGIOMA OF OPTIC Tuberculum sellae meningioma:

NERVE (FIG. 10.20) Compresses the optic chiasma.
Occurs predominantly in Sphenoidal-ridge meningioma:
middle-aged women; Ocular Slowly growing, painless, down
features are related to primary and out proptosis fullness of
tumor involvement site. temporal fossa, visual impair-
ment due to optic nerve
dysfunction.
Optic nerve-sheath menin-
gioma: Slowly-growing unila-
teral axial proptosis - the triad of
long-standing visual impair-
ment, a pale swollen optic disc,
and optico-ciliary shunt vessels
are pathognomonic.

Fig. 10.20: Sphenoidal ridge menin- Treatment: Surgical excision of

gioma—temporal fossa fullness the tumor by orbitotomy.

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 DISEASES OF THE ORBIT

CAROTID-CAVERNOUS
FISTULA (FIGS 10.21A
AND B)
Results from an abnormal
communication between the
cavernous sinus and the
internal carotid artery, giving
the classical picture of a
pulsating exophthalmos; may
Fig. 10.21A: Caroticocavernous
be traumatic or spontaneous. fistula
Marked unilateral, sudden
pulsatile proptosis with redness,
chemosis and dilation of the
episcleral blood vessels (caput
medusae).
Ophthalmoplegia due to
involvement of the 3rd, 4th and
6th nerve; retinal venous
congestion with hemorrhage;
raised IOP, due to elevated
episcleral venous pressure.
Fig. 10.21B: Caput medusae of
Treatment: Intracavernous same patient (Fig. 10.21A)
surgery and balloon catheter
embolization.

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 CLINICAL OPHTHALMOLOGY

ORBITAL FAT PROLAPSE often mistaken as lymphoid

(FIGS 10.22A AND B) hyperplasia. Associated with
Not so uncommon, occurs in defects in orbital septum and
old age; unilateral or bilateral, baggy eyelids.

A B
Figs 10.22A and B: Orbital fat prolapse

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 DISEASES OF THE ORBIT

CONTRACTED SOCKET
(FIGS 10.23A TO D)
Contracted socket occurs due to
chronic inflammation, trauma,
prior surgeries, OCP, resulting
in conjunctival shrinkage,
leading to shallowing of the
fornices and inability to wear the
artificial shell.
Fig. 10.23B: Contracted
socket—grade II

Fig. 10.23A: Contracted Fig. 10.23C: Contracted

socket—grade I socket—grade III

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 CLINICAL OPHTHALMOLOGY

According to severity it may be

of following types:
• Gr I – shallowing of inferior
fornix
• Gr II – shallowing of both
inferior and superior forni-
ces
• Gr III – formation of sym-
blepharon bands
Fig. 10.23D: Contracted • Gr IV – gross contracture of
socket—grade IV the whole socket
• Gr V – wet/discharging
contracted socket.

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 CLINICAL OPHTHALMOLOGY

ACUTE DACRYOADENITIS
(FIG. 11.1)

Associated with systemic

diseases like mumps, influenza
or glandular fevers.
Characterized by acute local
pain, swelling and tenderness. Fig. 11.1: Bilateral acute
dacryoadenitis
Drooping of the outer part of
upper lid with an S-shaped curve.
Treatment: Usually self limiting,
but systemic antibiotics and
local hot compress are required
in some cases.

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 DISEASES OF THE LACRIMAL APPARATUS

CHRONIC CANALICULITIS Sometimes with stone forma-

(FIGS 11.2A AND B) tion, called dacryolith.
Commonly caused by Actino- Treatment: Linear incision to
myces israelii (streptothrix). remove the dacryolith.
Chronic infection causes—
discharge, a pouting punctum DACRYOPS (FIG. 11.3)
and concretions within the Swelling in the upper fornix due
canaliculi. to retention of secretion owing
to blockage of one of the
lacrimal ducts.
Treatment: Opening of the sac
to release the fluid.

Fig. 11.3: Dacryops

B
Figs 11.2A and B: Chronic
canaliculitis

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 CLINICAL OPHTHALMOLOGY

PUNCTAL/CANALICULAR
STENOSIS (FIGS 11.4A TO C)
It causes defective drainage of
tears leading to epiphora.
Causes: Senile, infective, due to
injury or drug induced.
Treatment: Periodic punctal
dilatation, Three-snip procedure.
Fig. 11.4B: Punctal stenosis—
senile

Fig. 11.4A: Scarring of lower Fig. 11.4C: Punctal stenosis—

punctum drug (IDU) toxicity

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 DISEASES OF THE LACRIMAL APPARATUS

ACUTE DACRYOCYSTITIS below palpebral ligament,

(FIGS 11.5A TO D) leading
Suppurative inflammation of Treatment: Hot compress,
the lacrimal sac, with an asso- systemic antibiotics, drainage of
ciated cellulitis of the overlying abscess if necessary, and when
tissues; Lacrimal abscess with scar the acute phase subsides,
formation; May often with dacryocystorhinostomy (DCR)
lacrimal fistula formation just or dacryocystectomy (DCT).

Fig. 11.5A: Acute dacryocystitis Fig. 11.5C: Lacrimal abscess—

scar formation

Fig. 11.5B: Lacrimal abscess Fig. 11.5D: Lacrimal fistula

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 CLINICAL OPHTHALMOLOGY

CHRONIC DACRYOCYSTITIS
(FIGS 11.6A TO D)
Most frequently in newborn
infants and middle-aged
women; Chronic mucopurulent
discharge at inner canthus.
Regurgitation positive;
An extraordinary dilatation and
thinning of the lacrimal sac, Fig. 11.6A: Congenital
dacryocystitis
called mucocele or pyocele of the
lacrimal sac.
Hypopyon corneal ulcer:
mostly due to pneumococci.
Treatment
Congenital cases:
Hydrostatic sac massage and
antibiotic drops; probing and
syringing usually at 10-12
months.
Fig. 11.6B: Chronic dacryocystitis
If fails, DCR operation under in adult
GA.

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 DISEASES OF THE LACRIMAL APPARATUS

Adult cases:
Dacryocystorhinostomy (DCR)
is the choice of operation or
otherwise dacryocystectomy
(DCT).

TUMORS OF THE LACRIMAL

SAC
Tumors of the lacrimal sac are Fig. 11.6C: Bilateral mucocele of
extremely rare and represent a the lacrimal sac
potentially life-threatening
condition.
The triad of malignancy:
• A mass below the medial
palpebral ligament
• A chronic dacryocystitis that
irrigates freely, and
• Regurgitation of bloody
mucopus.
Treatment: DCT followed by Fig. 11.6D: Hypopyon corneal
irradiation. ulcer in dacryocystitis patient

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 CLINICAL OPHTHALMOLOGY

LACRIMAL FISTULA
(FIGS 11.7A AND B)
Rare, unilateral or bilateral
condition; may occur in con-
genital or acquired form.
Causing watering from a
separate opening on the skin
just below the medial canthal
ligament; acquired from had a Fig. 11.7A: Congenital lacrimal
history of acute dacryocystitis. fistula

Treatment
In congenital form: Usually no
treatment is required.
In adult form: Fistulectomy along
with DCR or DCT.

Fig. 11.7B: Acquired lacrimal

fistula

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 CLINICAL OPHTHALMOLOGY

APPARENT SQUINT: • Hypertelorism: May simulate

PSEUDOSTRABISMUS a divergent squint
(FIGS 12.1A AND B) • Hypermetropia: An apparent
Here, the visual axes are in fact divergent squint due to
parallel, but the eyes seem to large angle kappa
have squint. • Myopia: An apparent conver-
gent squint due to smaller or
Causes: even negative angle kappa.
• Prominent epicanthic folds: Squint in these conditions may
May simulate a convergent be easily excluded by checking
squint the relative position of corneal
• Telecanthus: Also simulate a light reflections and also by
convergent squint other means.

Fig. 12.1A: Epicanthus—pseudo-

convergent squint

Fig. 12.1B: Telecanthus—

pseudoconvergent squint

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 MOTILITIY DISTURBANCES AND SQUINT

CONVERGENT
CONCOMITANT SQUINT
(ESOTROPIA)

One eye always deviated

inwards.
Typically develops in early
childhood before the binocular
A
reflexes are firmly established.
Amblyopia is a frequent asso-
ciation.
Types of concomitant esotropia.

Infantile Esotropia
(Figs 12.2A and B)
• Develops before 6 months
with large and stable angle
• May have alternate or cross B
fixation
Figs 12.2A and B: Infantile
• Normal refraction for age esotropia
• Poor potential for binocular
vision
• Inferior oblique overaction
may be present initially or
develop later.

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 CLINICAL OPHTHALMOLOGY

Accommodative Esotropia
(Figs 12.3A and B)
• Fully accommodative: Fully
correct by spectacles
• Partially accommodative:
Partly correct by spectacles
• Onset is between 2 and 3
years, rarely earlier
• Hypermetropia
• Atropine refraction is a must.
Fig. 12.3A: Fully accomodative
convergent squint

Fig. 12.3B: Partially accommo-

dative convergent squint

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 MOTILITIY DISTURBANCES AND SQUINT

Non-accommodative
Esotropia (Fig. 12.4)
• Onset during childhood, but
after 6 months of age
• Insignificant refractive error
• No excess accommodative
element Fig. 12.4: Non-accomodative
• Angle of deviation same for convergent squint
distance and near fixation.

Non-refractive
Accommodative Esotropia
• Onset between 6 months and
3 years
• With high AC/A ratio, with
increased accommodative
convergence
• Normal near point of
accommodation
• No significant refractive
error
• Straight eyes for distance, but
esotropia for near.

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 CLINICAL OPHTHALMOLOGY

Sensory Esotropia Consecutive Esotropia

(Fig. 12.5) (Fig. 12.6)
• Caused by unilateral Occurs alter surgical overcor-
reduction in visual acuity at rection of an exotropia.
an early age which interferes
or abolishes fusion DIVERGENT CONCOMITANT
• Other eye remains normal SQUINT (EXOTROPIA)
• Causes: Congenital cataract,
One eye always deviates out-
corneal opacity , coloboma,
wards.
microphthalmos, etc.
More likely to be latent or inter-
mittent than esotropia.
Constant exotropia is usually
seen in older patients.
Amblyopia is less common.

Fig. 12.5: Sensory esotropia

Fig. 12.6: Consecutive esotropia

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 MOTILITIY DISTURBANCES AND SQUINT

Types:
Congenital exotropia
(Figs 12.7A and B)
• Much less common than
congenital esotropia
• Commonly seen in cranio-
facial anomalies like,
Cruzon’s syndrome, hyper-
telorism. Fig. 12.7A: Cruzon’s syndrome

Fig. 12.7B: Hypertelorism

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 CLINICAL OPHTHALMOLOGY

Basic exotropia
(Figs 12.8A and B)
• Initially intermittent then
becomes constant
• Angle of deviation is more
for distant fixation than near
• Myopia may be a common
association.

Fig. 12.8A: Intermittent exotropia

Fig. 12.8B: Basic exotropia

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 MOTILITIY DISTURBANCES AND SQUINT

Sensory exotropia (Fig. 12.9) Alternating squint may be

• Caused by uniocular convergent or divergent type.
sensory visual deprivation
• Commonly in cataract, optic
atrophy, after injury, etc.
Consecutive exotropia
Following overcorrection of a
convergent squint.

Fig. 12.10A: Alternate esotropia

Fig. 12.9: Sensory exotropia—

aphakia RE
ALTERNATING SQUINT
(FIGS 12.10A AND B)
Alternating squint means when
one eye fixes, the other eye
deviates; Either eye can adopt
fixation alternately and freely.
Visual acuity remains almost
normal in each eye.
Chance of amblyopia is least. Fig. 12.10B: Alternate exotropia

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 CLINICAL OPHTHALMOLOGY

VERTICAL SQUINT
(FIGS 12.11A AND B)
Hypertropia: Hyperdeviation
of non-fixing eye in primary
position.
Hypotropia: Hypodeviation of Fig. 12.11A: Left hypertropia—
non-fixing eye in primary gaze. RE fixing

Fig. 12.11B: Hypotropia—

RE fixing

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 MOTILITIY DISTURBANCES AND SQUINT

INFERIOR OBLIQUE uently bilateral and cause

OVERACTION (FIG. 12.12) upshooting on adduction; may
May be unilateral or bilateral be associated with V-pheno-
Primary overaction is freq- menon in esodeviation.

Fig. 12.12: Bilateral inferior oblique overaction—V-phenomenon

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 CLINICAL OPHTHALMOLOGY

TOTAL OPHTHALMOPLEGIA Clinical signs

(FIG. 12.13) • Ptosis
Means involvement of both • Eyeball is slightly proptosed
extrinsic and intrinsic muscles. and divergent
Lesion is in the cavernous sinus • No movement of the eyeball
or in the superior orbital fissure • Fixed dilated pupil
and in bilateral cases; the lesion • Total loss of accommo-
is wisdespread in the brain-stem dation.
due to vascular or inflam-
matory cause.

Fig. 12.13: Total ophthalmoplegia

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 MOTILITIY DISTURBANCES AND SQUINT

EXTERNAL which supplies the intrinsic

OPHTHALMOPLEGIA muscles.
(FIG. 12.14)
Other causes: Chronic progres-
Extrinsic muscles along with sive external ophthamoplegia
levator palpebrae superioris. (CPEO), myasthenia gravis.
Lesion without affecting the Pupillary reactions and accom-
Edinger-Westphal nucleus modation are normal.

Fig. 12.14: External ophthalmoplegia

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 CLINICAL OPHTHALMOLOGY

THIRD (OCULOMOTOR) Intorsion of the eyeball on

NERVE PALSY (FIG. 12.15) attempted downgaze.
Ptosis Ocular movements are
Eyeball rotates outwards (diver- restricted in all gaze except
gent), slightly downwards. lalerally.
Pupil is dilated and fixed.

Fig. 12.15: Right third nerve palsy

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 MOTILITIY DISTURBANCES AND SQUINT

FOURTH (TROCHLEAR)
NERVE PALSY
(FIGS 12.16A AND B)
Trauma: most common cause of
isolated 4th nerve palsy.
Abnormal head posture; eye-
A
ball deviated upwards and
inwards (ipsilateral htpertropia)
wilt extorsion of eyeball.
Restriction of the movements
on downwards and inwards.
Bielschowsky’s head tilt test is
useful to diagnose this.
B
Figs 12.16A and B: Left superior
oblique palsy—Bielschowsky’s
head tilt test

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 CLINICAL OPHTHALMOLOGY

SIXTH (ABDUCENS) NERVE

PALSY (FIG. 12.17)
Most common type, and
commonly occurs in raised
intracranial tension may present
as a false localizing sign.
The eyeball is rotated inwards
(convergent squint).
Defective abduction of the eye.
Face turns towards the field of
action of paralysed muscle.

Fig. 12.17: Right lateral rectus

palsy

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 MOTILITIY DISTURBANCES AND SQUINT

DUANE’S RETRACTION
SYNDROME (FIG. 12.18)
Non-comitant squint, occurs
because of aberrant innervation
which causes contraction of
lateral rectus muscle instead of
relaxation.
Absence of abduction; slight
restriction of the adduction;
retraction of the globe on
attempted adduction; palpebral
aperture of adduction, and
widening on attempted abduc-
tion; and ‘Up-shoot’ or ‘down-
shoot’ of the eyeball on adduc- Fig. 12.18: Duane’s retraction
tion. syndrome I
This is Type I (most common type)
The other types
Type II: Limitation of abduction
with relatively normal abduc-
tion.
Type III: Limitation of the both
abduction and adduction.

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 CLINICAL OPHTHALMOLOGY

SUPERIOR OBLIQUE Normal elevation on abduction.

TENDON-SHEATH Eyes are straight on primary
SYNDROME (BROWN’S position.
SYNDROME) (FIG. 12.19)
There is no overaction of
Superior oblique tendon- superior oblique muscle.
trochlea apparatus.
Limitation of elevation of the
eye on adduction, simulating
inferior oblique muscle palsy.

Fig. 12.19: Brown’s syndrome

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 MOTILITIY DISTURBANCES AND SQUINT

DOUBLE ELEVATOR PALSY Limitation of elevation in all

(FIG. 12.20) positions of upgaze.
May be congenital or acquired. Normal adduction, abduction
Eyeballs are straight in primary and depression movements.
position; mild ptosis.

Fig. 12.20: Double elevator palsy—congenital

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 CLINICAL OPHTHALMOLOGY

STRABISMUS FIXUS
(FIG. 12.21)
Very rare unilateral or bilateral
squinting condition.
Affected eye is fixed in conver-
gent or divergent position due
to fibrous contracture of medial
or lateral rectus muscle.
Fig. 12.21: Strabismus fixus—RE
Forced duction test (FDT) is
positive.

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 CLINICAL OPHTHALMOLOGY

CONTUSIONS (BLUNT
INJURIES)
Ocular injuries by various blunt
instruments vary in severity
depending upon the nature of
impact.
It may be from simple sub-
conjunctival hemorrhage to Fig. 13.1A: Lid laceration
globe rupture; some effects are
progressive or may be delayed.
So during treatment, a guarded
prognosis should be given to
such injuries.

VARIOUS EFFECTS
RESULTING FROM
CONTUSIONS Fig. 13.1B: Black eye—Panda
bear sign
Eyelids (Figs 13.1A to C)
Lid lacerations; Swelling and
ecchymosis (black eye) of the
lids—‘Panda bear’ sign; emphy-
sema of the eyelids.

Fig. 13.1C: Ecchymosis with

emphysema lid

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 OCULAR INJURIES

Conjunctiva
Conjunctival lacerations and
chemosis (Fig. 13.2A)
Sub-conjunctival hemorrhage
(Fig. 13.2B)

Fig. 13.2A: Conjunctival

laceration

Fig. 13.2B: Subconjunctival

hemorrhage

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 CLINICAL OPHTHALMOLOGY

Cornea Blood staining of the cornea

Simple abrasions (Fig. 13.3A); (Figs 13.3C and D)
Rupture of the Descemet’s • Traumatic hyphema with
membrane with folds and raised IOP
corneal edema (Fig. 13.3B) • Endothelial damage and
subsequently

Fig. 13.3A: Corneal abrasion

Fig. 13.3C: Blood staining of
(Fluorescein staining)
cornea

Fig. 13.3B: Descemet’s folds and Fig. 13.3D: Blood staining of

corneal edema with hyphema cornea—early

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 OCULAR INJURIES

• Whole cornea is reddish-

brown or greenish stained
cornea gradually and slowly
clears from the periphery.
• Urgent paracentesis is
required to prevent it.

Sclera
Scleral rupture (rupture of the
globe) (Figs 13.4A and B) Fig. 13.4A: Scleral rupture—
uveal prolapse
Usually near canal of Schlemm
(weakest point) and runs
concentrically with the limbus
Conjunctiva is often intact;
associated uveal prolapse
Eyeball usually collapses with
total loss of vision
Prognosis is often very poor.

Fig. 13.4B: Scleral rupture with

subconjunctival dislocation of IOL

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 CLINICAL OPHTHALMOLOGY

Anterior Chamber
Hyphema (blood in the anterior
chamber)
Blood usually does not get
clotted (Figs 13.5A and B)
Recurrent and more severe
A
bleeding may occur within 24-
72 hours; associated secondary
glaucoma
When the blood gets clotted, the
hyphema appears as small black
ball, called “8 ball hyphema”
(like No.`8’ ball in billiards game)
(Fig. 13.5C).
B
Treatment: Conservative with
systemic/topical steroids, and Figs 13.5A and B: Traumatic
antiglaucoma medication; may hyphema
be urgent paracentesis.

Fig. 13.5C: Blunt trauma—8-ball

hyphema

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 OCULAR INJURIES

Iris Traumatic iridocyclitis—usually

Iridodialysis: iris is partially torn mild.
away from its ciliary Traumatic mydriasis; post-
attachment; biconvex area is traumatic iris atrophy.
seen at the periphery, causing a
D-shaped pupil (Figs 13.6A and
B); a fundal glow is obtained
through the peripheral gap
Traumatic aniridia: partial or
total (Fig. 13.6C).
Anteflexion and retroflexion of
the iris.

Fig. 13.6B: Iridodialysis

Fig. 13.6A: Iridodialysis with D- Fig. 13.6C: Traumatic aniridia

shaped pupil

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 CLINICAL OPHTHALMOLOGY

Ciliary Body
Angle recession: Longitudinal
tear in ciliary body; splitting of
circular fibers from the
longitudinal fibers (Fig. 13.7)
• Deepening of the anterior
chamber
• Widening of the ciliary band
on gonioscopy.
Fig. 13.8A: Vossius’s ring

Concussion cataract: Imbibitions

of aqueous through the dama-
ged capsule, and partly due to
direct mechanical effect on the
lens fibers.
• Localized cataract often
behind the iris (Fig. 13.8B)
• Total cataract in case of
Fig. 13.7: Angle recession capsular tear (Fig. 13.8C)
Crystalline Lens
Vossius’s ring: A circular pig-
mented imprint of the moised
pupil on the anterior lens
surface (Fig. 13.8A).

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 OCULAR INJURIES

Fig. 13.8D: Early rosette cataract

Fig. 13.8B: Traumatic partial
cataract leaves of the feathery
opacities are formed by the
suture acting as a vein from
which the opacities radiate
(Fig. 13.8D); remains statio-
nary, and sometimes, it
may progress into a total
cataract.
• Late rosette cataract: Usually
develops 1-2 years after a
Fig. 13.8C: Traumatic cataract concussion; smaller and
with extremely shallow AC more compact with short
sutural extension; feathery
• Early rosette cataract: Star- opacities lie in the angle
shaped cataract, usually in between two adjacent
the posterior cortex; the sutures (Fig. 13.8E)

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 CLINICAL OPHTHALMOLOGY

Subluxation of the crystalline Dislocation of the lens: anterior

lens (Fig. 13.8F) chamber (Fig. 13.8G) or in the
vitreous cavity (Fig. 13.8H)

Fig. 13.8E: Late rosette cataract Fig. 13.8G: Dislocation of lens in

AC

Fig. 13.8F: Subluxation of lens Fig. 13.8H: Dislocation of lens—

in vitreous cavity

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 OCULAR INJURIES

Vitreous (See Chapter 8) Retina

• Liquefaction of the vitreous Commotio retinae (Berlin’s
• Posterior vitreous detach- edema): Milky white cloudiness
ment at the macular area due to
• Vitreous hemorrhage with oedema, often with a cherry red
its sequelae. spot (Fig. 13.10A); later there
may be pigmentary deposits at
CHOROID (FIG. 13.9) the macula.
Choroidal rupture: rupture is seen Traumatic macular hemorrhage
as one or two curved lines; (Fig. 13.10B) with the formation
concentric with the disk margin of a macular cyst and then a
and on its temporal side; edges macular hole.
of this line are often pigmented
Retinal or preretinal hemor-
rhage (Fig. 13.10C).
Retinal tears at periphery,
especially in myopic subjects.
Rhegmatogenous retinal
detachment (Fig. 13.10D).
Traumatic proliferative vitreo-
retinopathy usually secondary
to vitreous hemorrhage.
Fig. 13.9: Choroidal rupture

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 CLINICAL OPHTHALMOLOGY

Fig. 13.10A: Barlin’s edema— Fig. 13.10C: Traumatic preretinal

cherry red spot hemorrhage

Fig. 13.10B: Traumatic macular Fig. 13.10D: Traumatic tractional

hemorrhage detachment

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 OCULAR INJURIES

Optic nerve
Optic nerve sheath hemorrhage
(Fig. 13.11A).
Peripapillary hemorrhage.
Avulsion of the optic nerve
leading to optic atrophy, which
may be partial or total (Fig.
13.11B).
Fig. 13.11A: Optic nerve sheath
hemorrhage

Fig. 13.11B: Avulsion of optic

nerve with atrophy

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 CLINICAL OPHTHALMOLOGY

Orbit
Blow-out fracture: is typically
caused by a sudden rise in
intraorbital pressure by a
striking object greater than 5 cm
in diameter, like tennis ball or
blow by a fist (Fig. 13.12).
• Periocular ecchymosis and
edema.
Fig. 13.12: Blow-out fracture
• Enophthalmos with pseudo-
ptosis usually appears after
10-14 days; infraorbital nerve
anesthesia Fractures of the
orbital bones
• Nasal bleeding and sub-
conjunctival hemorrhage
Retrobulbar hemorrhage
Orbital emphysema and proptosis.

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 OCULAR INJURIES

PENETRATING
(PERFORATING) INJURIES
Caused by sharp objects or
projectile foreign bodies; all
perforating injuries are
potentially serious and the
patients should be urgently
admitted and treated promptly.
Seriousness arises from: Fig. 13.13A: Conjunctival
• Immediate effect of trauma laceration
• Introduction of infection
• Chance of sympathetic oph-
thalmia.

Immediate Effect of Trauma

Wounds of the lid and conjunc-
tiva (Fig. 13.13A).
Wounds of the cornea (Figs 13.13
B to D).
• May be linear, curved,
Fig. 13.13B: Corneal rupture with
radiating and lacerated iris prolapse
• May be small, large or cor-
neoscleral or at the limbus
• In small perforation Seidel’s
test is positive
• Associated with iris incar-
ceration or frank iris
prolapse.

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 CLINICAL OPHTHALMOLOGY

• May be lamellar; margins associated with vitreous

soon swell-up after the prolapse.
injury, and become cloudy.
Wounds of the lens and its capsule:
Wounds of the sclera: is reco- • Localized lens opacity
gnized by the uveal prolapse • Total cataract with capsular
(Fig. 13.13E) and may be tear (Fig. 13.13F)

Fig. 13.13C: Corneal perforation Fig. 13.13E: Scleral rupture with

with iris incarceration uveal prolapse

Fig. 13.13D: Limbal rupture with Fig. 13.13F: Total cataract—

iris prolapse capsular tear

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 OCULAR INJURIES

• May be with early rosette • Disorganized eye in extreme

cataract (Fig. 13.13G) globe rupture (Fig. 13.13I).
• In case of large capsular
wound, the flocculent white Iatrogenic globe perforation by
cortical matters protrude needle: May happen during
through the capsular peribulbar or retrobulbar block
opening (Fig. 13.13H) and fill (Fig. 13.13J)
the anterior chamber.

Fig. 13.13G: Early rosette Fig. 13.13I: Extensive ruptured

cataract globe

Fig. 13.13H: Cataract with lens Fig. 13.13J: Globe puncture

matter in the AC (repair done) during peribulbar injection

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 CLINICAL OPHTHALMOLOGY

Signs of Globe Perforation

(Figs 13.14A to C)
• Conjunctival chemosis
Shallow or flat anterior
chamber
• Alteration of papillary size,
shape and location
• Focal iris tear or hole
• Injury tract in the cornea,
Fig. 13.14B: Corneal perforation
sclera, lens or retina
• Wound leak (detected by a
positive Seidel’s test)
• Hypotony (checked digi-
tally).

Fig. 13.14A: Conjuctival Fig. 13.14C: Corneal perforation

chemosis in scleral perforation Seidel’s positive

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 OCULAR INJURIES

INTRODUCTION OF
INFECTION
• Purulent keratitis
• Purulent iridoyclitis with
hypopyon (Fig. 13.15A)
• Endophthalmitis (Fig. 13.15B)
• Panophthalmitis in extreme
situation.
Fig. 13.15B: Perforating injury—
endophthalmitis

SYMPATHETIC
OPHTHALMIA
Most dreadful complication of
a penetrating injury—see
Chapter 5.
Fig. 13.15A: Perforating injury—
purulent iritis with hypopyon

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 CLINICAL OPHTHALMOLOGY

FOREIGN BODIES IN
THE EYE
Extraocular Foreign Bodies
Small foreign bodies – e.g. coal,
dust, sand, iron particles,
eyelash, wood-piece, husks of
seeds, wings of insects, etc. may
pitch upon the conjunctiva, Fig. 13.16A: Foreign body—
cornea or the limbus. supratarsal sulcus

Conjunctival Foreign Body

Commonest site: upper subtarsal
sulcus (Fig. 13.16A).
May be embedded in bulbar
conjunctiva, fornix, or at the
limbus (Figs 13.16B and C).
Lid eversion is a must for all
Fig. 13.16B: Foreign body at fornix
cases if the is corneal abrasion
or scratch marks on cornea
Treatment: easy removal with
a sterile cotton bud

Corneal Foreign Body

Foreign body sensation; mar-
ked photophobia and redness.
Fig. 13.16C: Limbal foreign
body—insect wing

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 OCULAR INJURIES

Ciliary Congestion In old cases of iron foreign

It may be superficial, anterior body, there may be associated
stromal, deep stromal, or partly rust ring (Fig. 13.17D).
in the anterior chamber (Figs May be with surrounding infil-
13.17A to C) tration or frank corneal ulcer.

Fig. 13.17A: Foreign body Fig. 13.17C: Foreign body partly

cornea in AC

Fig. 13.17B: Foreign body Fig. 13.17D: Foreign body

cornea—deep cornea—rust ring

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 CLINICAL OPHTHALMOLOGY

Check for tarsal conjunctiva

and chronic dacryocystitis in all
cases of corneal foreign bodies.
Treatment: Removal of foreign
body by a disposable needle
under strict aseptic condition
and broad spectrum antibiotic
drops and ointment for few
days.
Fig. 13.18A: Retained IOFB—
wound of entry—lid
Intraocular Foreign Body
(IOFB)
While chipping the stone, with
an iron-chisel and a hammer, it
is a chip of the chisel (from
cutting edge, or from its
mushroomed head) which
enters the eyes, but not the chip
of the stone.
May pass directly through the
conjunctiva, cornea or sclera, or
sometimes through the lid (Figs Fig. 13.18B: Retained IOFB—
13.18A and B). wound of entry—sclera

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 OCULAR INJURIES

IOFB may retain in anterior Pass through the lens, either by

chamber, on the iris or anterior way of the iris (or pupil, and
chamber angle (Fig. 13.18C to E) causing a traumatic cataract
(Fig. 13.18G).
May lodge in the crystalline
lens, causing cataract or May be in the vitreous or may
siderotic cataract (Fig. 13.18F). rest on retina (Fig. 13.18H).

Fig. 13.18C: IOFB on iris surface Fig. 13.18E: Penetrating injury—

retained FB

Fig. 13.18D: Retained IOFB— Fig. 13.18F: Retained

angle of AC intralenticular iron—siderosis

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 CLINICAL OPHTHALMOLOGY

Rarely pierce the opposite wall

and rest within the orbit (double
perforation); may be associated
with retinal hole, degeneration,
or detachment.

Fig. 13.18G: Retained IOFB—in

the vitreous

Fig. 13.18H: Retained IOFB—iris

hole

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 OCULAR INJURIES

Siderosis Bulbi Retinal pigmentary changes

(Figs 13.19A to C) with attenuated blood vessels.
Chronic irreversible degenera- Prognosis is always poor.
tive changes of the ocular
tissues, caused by retained
intraocular iron foreign body.
Rusty deposition on the
anterior lens surface (earliest
sign).
Frank siderotic cataract of
variable degree.
Iris heterochromia and rusty
Fig. 13.19B: Siderosis bulbi—
discolouration of the cornea.
corneal deposits

Fig. 13.19A: Siderosis bulbi—iris Fig. 13.19C: Siderosis bulbi—

discoloration cataract

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 CLINICAL OPHTHALMOLOGY

Chalcosis Bulbi (Fig. 13.20)

Kayser-Fleischer’s (K-F) ring: A
golden-brown ring at the level
of Descemet’s membrane of the
cornea.
Sun-flower cataract: a brilliant
golden-green sheen in the form
of petals of sun-flower.
Fig. 13.20: Chalcosis bulbi—
Associated retinal changes with sunflower cataract
golden plaques.
Prognosis is always good.

MISCELLANEOUS ORGANIC
MATERIALS
Intraocular eyelashes—cause
proliferation of the hair root
epithelium leading intraocular Fig. 13.21A: Penetraring injury
cysts (Fig. 13.21A). with intraocular eyelashes

Caterpillar hairs – excite a severe

iridocyclitis with granulo-
matous nodules - ophthalmia
nodosa (Fig. 13.21B).
Wood, stone or vegetable materials-
produce severe proliferative
granulomatous reactions.
Fig. 13.21B: Caterpillar hair
within iris

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 OCULAR INJURIES

CHEMICAL INJURIES
(BURNS)
Alkali burns are more dange-
rous than acid burns.
Severity depends on type of
chemical, its quantity, pH of the
solution, concentration of
chemical agents, duration of
exposure and the time of Fig. 13.22A: Chemical injury: Acid
presentation (Figs 13.22A burn—acute phase
and B).

Fig. 13.22B: Chemical injury—

alkali burn—acute phase

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 CLINICAL OPHTHALMOLOGY

Acute Phase (up to 1 week)

• Chemosis of conjunctival
and eyelids
• Congestion and discharge
• Perilimbal ischemia of
variable degree
• Corneal epithelial defects
and stromal clouding
• Increased IOP. Fig. 13.22C: Alkali burn—360
degree limbal ischemia
Early Reparative Phase
(1-3 weeks)
(Figs 13.22C and D)
• Cornea and conjunctival
regeneration
• Persistent corneal epithelial
defects
• Corneal opacity of variable
degree
• Iridocyclitis
Fig. 13.22D: Chemical injury—alkali
burn burn in intermediate phase

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 OCULAR INJURIES

Late Reparative Phase

(3 weeks - months)
(Figs 13.22E to G)
• Irregular scarring of the
cornea
• Corneal thinning and
Descemetocele formation
• Dry eye, due to scarring of
the ducts of lacrimal glands
and goblet cells Fig. 13.22F: Chemical burn—late
• Hypotony due to ciliary phase—corneal opacity with limbal
shock stem cell deficiency
• Symblepharon, entropion
and trichiasis formation.

Fig. 13.22E: Chemical injury— Fig. 13.22G: Chemical injury—

acid burn—late phase late phase severe limbal cell
deficiency

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 CLINICAL OPHTHALMOLOGY

Thermal Burns
(Figs 13.23A and B)
Usually do not involve the
eyeball proper; may be due to
direct burn, by boiled cooking
oil or by molten metal.
Thermal burns of the eyelids
require prompt care to prevent
ectropion; early skin grafting Fig. 13.23A: Thermal injury—
may be required. singing of eyelashes

Associated other features may

be due to asphyxia and carbon
monoxide poisoning.

Fig. 13.23B: Thermal burn—

eye lids

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 OCULAR INJURIES

MISCELLANEOUS INJURIES
Blast Injuries
(Figs 13.24A to C)
More common nowadays by
explosives, bombs or fire
crackers; may be accidental, due
to gas cylinder burst, car-tyre A
burst, etc.
Usually associated with facial
burn or injuries.
Multiple sulphur or other
particles are scattered all over
the external ocular surface; and
some may be intracameral.
Treatment: Difficult, initially
B
scraping and BCL, and later a
lamellar keratoplasty may be Fig. 13.24A and B: Bomb injury
helpful in some cases.

Fig. 13.24C: Blast injury—gas

cylinder explosion

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 CLINICAL OPHTHALMOLOGY

RADIATIONAL INJURIES
(FIGS 13.25A TO C)
Ultra-violet (U-V rays): Results
photo-keratitis (Welder’s
keratitis) or snow blindness, or
photophthalmia.
Infra-red rays (above 700 mm):
They are absorbed by the iris,
and the resultant heat is Fig. 13.25A: Radiation
transmitted to the lens, which keratopathy—dry eye
becomes cataractous (glass-
blower’s cataract).
Solar eclipse with the naked eye,
causes solar retinopathy,
causing a focal macular burn
(eclipse burn or blindness).
Electromagnetic energy of
short wave lengths (X rays or
gamma rays): any part of the
eye is affected, e.g. blepharo-
conjunctivitis (Steven Johnson Fig. 13.25B: Solar retinopathy
syndrome-like picture), kera- (eclipse burn)
titis, radiation cataract and
radiation retinopathy.

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 OCULAR INJURIES

Electric injury or injury after

electrocution: may cause elec-
tric cataract in some cases with
anterior capsular fibrosis; other
organ may also be affected;
retinal damage in various extent
may be associated with this
injuries.

Fig. 13.25C: Electric cataract—

severe anterior capsular fibrosis

–379–
 Index

A irregular 102
Abnormal pupil 108 shallow 100
Acanthamoeba keratitis 59 Anterior ischemic optic
neuropathy 285
Acute hydrops 84
arteritic 286
Acute retinal necrosis 238 non-arteritic 285
Albinism 124 Anterior necrotizing scleritis 96
Alternating squint 335 Anterior uveitis 126
AMD Aphakia 175
dry 247 Asteroid hyalosis 202
wet 248 Avitaminosis-A 89
Angioid streaks 142
Angiomatosis retinae 209 B
Angle recession 354 Bacterial keratitis ulcer 54
Aniridia 122 Baggy eyelids 19
Band-shaped keratopathy 74
Anisocoria 111
Basal cell carcinoma 17
Anophthalmos 303, 106 Bassen-Kornzweig syndrome 264
Anterior chamber 100 Bayonetting sign 187
abnormal contents 103, 106 Belbitis (Bleb infection) 198
deep 101 Benign melanocytoma 146
 CLINICAL OPHTHALMOLOGY

Benson’s disease 202 Central retinal artery occlusion 211

Best’s vitelliform macular Central retinal venous occlusion
dystrophy 242 213
Bitot’s spot 40 ischemic 214
Blast injuries 377 non-ischemic 213
Blepharitis 7 Central serous retinopathy 251
Blepharophimosis syndrome 2 Chalazion 10
Blood staining of the cornea 350 Chalcosis bulbi 372
Blow-out fracture 360 Chandler’s syndrome 136
Blue sclera 93 Chemical injuries 373
Blue-dot cataract 161 acute phase 374
Bowen’s disease 37 early reparative phase 374
Branch retinal venous occlusion late reparative phase 375
215 Chemosis 25
Brushfield spots 145 Choroid
Bull’s eye maculopathy 243 coloboma 119
Buphthalmos 178 detachment 143
Busacca’s noudules 128 hemorrhage 221
rupture 357
C Choroiditis 130
Ciliary body melanoma 148
Canaliculitis 321 Ciliary congestion 367
Candida retinitis 236 Coat’s disease 119
Capillary hemangioma 15, 306 Cocayne’s syndrome 264
Capsular opacification Coloboma 123
anterior 169 choroidal 119
posterior 170 eyelid 2
Carotid-cavernous fistula 315 lens 152
Catarrhal ulcer 68 optic disk 279
Cavernous hemangioma 312 retinochoroidal 210
Cellulitis 9 Commotio retinae 354
orbital 306, 307 Complicated cataract 167
preseptal 307 Congenital cataract 117

–382–
 INDEX

Congenital optic disk pit 278 sclera 351

Conjuctiva vitreous 357
cysts 35 Convergent concomitant squint
intraepithelial neoplasia 37 (esotropia) 329
xerosis 40 accommodative 330, 331
Conjunctivitis consecutive 332
acute mucopurulent 26 infantile esotropia 329
adenoviral 28 non-accommodative 331
angular 28 non-refractive 331
gaint papillary 32 sensory 332
membranous 27 Corectopia 108
phlyctenular 30 Cornea 80
purulent 26 abrasion 85
vernal kerato 31 abscess 56
Conjunctivochalasis 45 Dellen 88
Contact dermatitis 6 edema 53
Contagiosum 16 guttata 80
Contracted socket 317 tumors 92
Contusions (Blunt injuries) 348 ulcer 60
xerosis 89
effects resulting from
Cortical cataract 162
contusions
Craniofacial dysostosis 300
anterior chamber 352
Craniosynostosis 300
choroid 357
Cruzon’s syndrome 300
ciliary body 354
Cystoid macular edema 250
conjunctiva 349
Cytomegalovirus retinitis 237
cornea 350
crystalline lens 354
eyelids 348 D
iris 353 Dacryoadenitis 320
optic nerve 359 Dacryocystitis
orbit 360 acute 323
retina 357 chronic 324

–383–
 CLINICAL OPHTHALMOLOGY

Dacryops 321 Episcleritis 94

Dermatochalasis 20 Exotropia 332
Dermolipoma lipodermoid 37 basic 334
Descemet’s detachment 86 congenital 333
Descemet’s tear 87
sensory 335
Diabetic cataract 168
Diabetic maculopathy 270 External angular dermoid 16
Diabetic retinopathy 269 Exudates
advanced proliferative 272 hard 228
non-proliferative 269 soft 230
proliferative 271 subretinal 231
Disk hemorrhage 283
Fascicular ulcer 68
Dislocation of lens 172, 173
Ferry’s line 48
Divergent concomitant squint 332
Double elevator palsy 345 Filamentary keratopathy 85
Drusens Filtering bleb abnormalities 194
hard 258 Fleischer’s ring 48, 49, 82
soft 260 Focal toxoplasmosis 235
Duane’s retraction syndrome 343 Follicles 23
Foreign bodies in the eye
E conjunctival 366
Ectropion 5 corneal 366
Electric injury 379 extraocular 366
Electromagentic energy 378 intraocular 368
Encephalo-trigeminal
Fourth (Trochlear) nerve palsy 341
angiomatosis 209
Endophthalmitis 133 Fuchs’ endothelial dystrophy 81
Enophthalmos 305 Fundus
Entropion 4 albipunctatus 257
Epibulbar limbal dermoid 36 flavimaculatus 256
Epiretinal membrane 255 Fungal keratitis keratomycosis 57

–384–
 INDEX

G Homocystinuria 156
Hordeolum 9, 10
Glaucoma 178
Horner’s syndrome 12
associated with trauma 191
Horner-Tranta’s dots 31
congenital
primary 178 Hudson Stahli’s line 49
secondary 179 Hutchinson’s triad 69
cupping of the optic disk 184 Hypermature cataract 164
glaucoma capsulare 188 Hypertelorism 302
inflammatory secondary 190 Hypertensive retinopathy 268
malignant (ciliary block) 192 Hypertropia 336
neovascular 193 Hyphema 103
pigmentary glaucoma 189 Hypopyon 103
primary angle-closure 180 Hypotropia 336
absolute 182
acute 180
I
chronic 182
slit lamp grading of the angle Inferior oblique overaction 337
183 Inflammatory orbital diseases 310
Glioma of the optic nerve 309 Infrared rays 378
Goldenhar’s syndrome 36, 37 Invasive squamous cell carcinoma
Granular dystrophy 77 38
Gyrate atrophy of the choroid 142 Iridocyclitis 126
Iridoschisis 137
H Iriodocorneal syndrome 136
Haab’s stria 87 Iris
Hemangioma atrophy 138
capillary 15, 306 cysts 141
cavernous 312 nevus 146
optic disk 296 noudules 128
Herpes zoster ophthalmicus 66 pearls 145
Heterochromia of the iris 125 Iris-nevus syndrome 136

–385–
 CLINICAL OPHTHALMOLOGY

K Lenticonus 153
Kayser-Flescher ring 48 Leukocoria 117
Kearn-Sayre syndrome 264 Lisch nodules 144
Keratic horn 20 Lymphangioma 308
Keratitis
dendritic 62 M
disciform 65 Macular dystrophy 78
geographical 63 Macular hole 253
interstitial 69 Malignant forms 292
lagophthalmic exposure 67 hypertension 292
marginal 68 melanoma 39
metaherpetic 64 choroid 148
neurotrophic 67 iris 147
punctate epithelial 70 Mandibulo-facial dysostosis 301
sclerosing 70 Marfan’s syndrome 155
stromal necrotic 64 Marginal ulcers 73
Keratitis medicomentosa 90 Mature cataract 163
Keratoconjunctivitis sicca 41, 88 Median facial-cleft syndrome 301
Keratoconus 82 Megalocornea 51
Keratoglobus 51 Meibomian gland carcinoma 18
Keratomalacia 89 Meibomitis 8
Koeppe’s nodules 128 Meningioma of optic nerve 314
Krukenberg’s spindle 48, 189 Metastatic carcinoma of uvea 149
Microphthalmos 50
L Miotic pupil 112
Lacrimal fistula 326 Molluscum 16
Lacrimal sac tumor 325 Mooren’s ulcer 72
Lagophthalmos 13 Morning glory syndrome 280
Lash in the punctum 3 Multifocal choroditis 234
Lattice dystrophy 79 Multiple evanescent white dot
Laurence Moon-Biedl syndrome syndrome 232
264 Multiple pupils 109
Leaking filtering bleb 197 Munson’s sign 82

–386–
 INDEX

Myasthenia gravis 12 Optic neuritis 284

Mydriatic pupil 113 Orbital dysplasia 302
Myelinated nerve fibers 278 Orbital fat prolapse 316
Myopic maculopathies 245 Orbital varix 313
Orbito-palpebral (colobomatous)
N cyst 303
Nanophthalmos 50 Overfiltering bleb 196
Necrosis of sclera 97 Oxycephaly syndactyle 302
Neovascularization 223
Neuro-fibromatosis 208 P
Neuroretinitis 284 Panophthalmitis 135
Nevus 38
Papillae 23
New vessels at the disk 282
Papilledema 287
Nodular scleritis 96
early 288
Nuclear cataract 166
established acute 289
chronic 290
O atrophic 291
Ocular cicatricial pemphigoid 43 Pellucid marginal degeneration 72
Ophthalmia neonatorum 27 Penetrating injuries 361
Ophthalmoplegia 338 Perforating injury 365
external 339 Persistent hyperplastic primary
total 338 vitreous 118
Optic atrophy 292 Persistent pupillary membrane
consecutive 294 110
glaucomatous 294 Peter’s anomaly 52
primary 292
Phacolytic glaucoma 157
secondary 293
Phacomorphic glaucoma 157
Optic disk
Phacotoxic uveitis 158
astrocytoma 298
Phakomatosis 208
hemangioma 296
melanocytoma 297 Phthiriasis palpebrarum 14
Optic nerve-sheath meningioma Pigment deposition 48
314 Polar cataract

–387–
 CLINICAL OPHTHALMOLOGY

anterior 158 rhegmatogenous 265

posterior 159 tractional 266
Polycoria 109 Retinal dysplasia 118
Port-wine stain 15 Retinal vasculitis 226
Posterior subcapsular cataract Retinitis pimentosa 261
165 atypical 263
Precancerous melanosis 39 typical 261
Preretinal hemorrhage 217 Retinoblastoma 117, 274, 310
Primary choroidal sclerosis 140 Retinopathy of prematurity
Progressive essential iris atrophy 117, 273
136 Rhabdomyosarcoma 309
Pseudo-gerontoxon 31 Rizutti’s sign 82, 83
Pseudohypopyon 103 Rodent ulcer 17
Pseudomembranes 25 Roth spot 222
Pseudopolycoria 109 RPE detachment 252
Pseudo-proptosis 304 Rubeosis iridis 139, 193
Pseudopterygium 34
Pseudostrabismus/squint 328 S
Pterygium 33
Ptosis 11 Salzmann’s nodular degeneration
acquired 12 75
congenital 11 Sampaolesi’s line 189
senile (aponeurotic) 12 Scleromalacia performas 96
Punctal/canalicular stenosis 322 Siderosis bulbi 371
Pupillary shape 114 Sixth (abducens) nerve palsy 342
Sphenoidal-ridge meningioma
314
R Spheroidal degeneration 75
Radiational injuries 378 Spherophakia 154
Refsum’s disease 264 Squamous cell carcinoma 17
Reis-Buckler’s dystrophy 76 Stargardt’s mascular dystrophy
Retinal collaterals 225 240
Retinal detachment 265 Stevens-Johnson’s syndrome 44
exudative 267 Stocker’s line 48, 49

–388–
 INDEX

Strabismus fixus 346 Tuberculum sellae meningioma

Striate keratopathy 84 314
Sturge-Weber syndrome 15 Tuberous sclerosis 208
Subconjunctival hemorrhage 22 Tunnel abscess 91
Subluxation of lens 171
Subretinal cysticercosis 275 U
Subretinal hemorrhage 219
Ultraviolet 378
Sub-RPE hemorrhage 220
Usher syndrome 264
Superior limbic
keratoconjunctivitis 45
Superior oblique tendon-sheath V
syndrome 344 Vertical squint 336
Symblepharon 14 Vitreous
Sympathetic ophthalmia 365 cells 203
Sympathetic ophthalmitis 133 hemorrhage 203
Synchisis scintillans 202 opacities 205
Systemic collagen vascular prolapse 207
disorders 73 Vogt’s lines (striae) 82
Vogt-Koyanagi-Harada syndrome
T 132
Vossius’s ring 354
Temporal pallor 295
Terrien’s marginal degeneration
71 W
Thermal burns 376 Wessely’s immune ring 65
Third (oculomotor) nerve palsy Wind-shield wiper syndrome 199
340
Thyroid ophthalmopathy 311 X
Titled disk 281
Xanthelesma 19
Toxocara endophthalmitis 118
Xerophthalmic scar 89
Toxoplasmosis 131
Trachoma 29
Trichiasis 3 Z
Tubercular granuloma 239 Zonular (lamelallar) cataract 160

–389–