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OPEMNAIVOKOGY
HIGHLIGHTS OF THE BOOK:
Topic-wise Listing of Questions & their Answers
Answered all Questions of SIA, Osmania & Falcon QBs
Suitable to read ONE-MONTH before Final Exams
All Previous years' Questions till 2022 are covered

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 CONTENTS

Anatomy and Physiology of Eye.

SQs. .. 3
VsQs 4

Optics and Refraction..wes

LOS 5

SQs..
..
9

VSQs 14
 Anatomy and Physiology ofEye
sas
1) Visual fields [13, 09]
Ans.
Visual field is a 3-D area of subject's surroundings that can be seen at any one time around an object
of fixation
It is described as 'island of vision surrounded by a sea of
blindness'
The extent of normal visual field with a 5 mm white colour
object is superiorly 50, nasally 60, inferiorly 70° and
temporally 90°.
The visual field can be divided into central & peripheral field:
Central field includes an area from the fixation point to a
10
circle 30 away. The central zone contains physiologic blind
spot on the temporal side.
Peripheral field of vision refers to the rest of the area beyond Extent of normal visual field of right eye
30° to outer extent of the field of vision.
PERIMETRY is used to evaluate both central and peripheral visual fields using targets of various
sizes and colours.
KINETIC PERIMETRY: In this, the stimulus of STATIC PERIMETRY: In this, the stimulus is at
known luminance is moved from a peripheral fixed position with varying luminance in the field
non-seeing point towards the centre till it is of vision.
perceived. Ex: confrontation method, Lister's Ex: Goldmann perimetry, automated perimetry.
perimetry, scotometry & Goldmann's perimetry.
MANUAL PERIMETRY: Confrontation method, Lister's perimetry, scotometry & Goldmanm's perimetry.

AUTOMATED PERIMETRY: Automated perimeters are computer assisted and test visual fields by a

static method. Ex: Humphrey's Field Analyzer

Advantages of automated perimetry over manual perimetry are:

Flexibility & level of precision
software
Data storage capability, ease of operation, well controlled fixation, menu driven
Can compare results statistically with normal individuals of the same age
group and with previous
tests of the same individual.
Examiner bias is eliminated.

Rignl y

of perimetry: Charting of the visual fields is useful in the

Uses
diagnosis of many diseases like -

ee onenaonal represenation of nomel leld

Glaucoma oA Sand or vision in sea of darkness

Retinal diseases e.g., retinitis pigmentosa

Follow up of laser treatment for diabetic retinopathy
Neurological disorders, e.g., brain tumours, head injury, Merdonal two dimensional represerntaion
of vibual feld (Kinetc perimetny)

multiple sclerosis, cerebral thrombosis, aneurysms.

 VSQs
1) Rods and Cones [17]
Ans.
Sensory organs {photoreceptors)
Present in Outer nuclear layer of retina

2) Ciliary ganglion [15]

Ans.
Ciliary ganglion is a peripheral parasympathetic ganglion placed in the course of oculomotor nerve
near the apex of orbit.
Roots of ciliary ganglion:
Sensory root comes from the nasociliary nerve.
Sympatheticroot comes from internal carotid plexus. These fibres do not relay here and pass along
the short ciliary nerves to
Edinger-Westphal
supply the blood vessels of the nucleus
CN3
Nerve to inferior Ciliary
oblique
eyeball. angion Dilacorpupillae

Parasympathetic root arises Constrictor pupillae

from the nerve to inferior

oblique muscle and carries the Short cilary nerve

preganglionic fibres from the Nasocilary nerve

Edinger-Westphal nucleus.
These fibres relay here and LSympathetic plenus around
oternal carotid
postganglionic fibres pass artery

through the short ciliary nerves.

Short ciliary nerves, branches Supenor cervica
sympathetic gangion
of ciliary ganglion, supply the
sphincter pupillae and ciliary
muscle Roots and distribution of the ciliary ganglion.

Importance:The ciliary ganglion is blocked to produce ilatation of pupil before cataract extraction
***********
 Optics and Refraction
LQs
1) Define Emmetropia. Write about Myopia- etiology, clinical features & management [16, 13, 11]
a. Surgical treatment of myopia [07]
Ans.
Emmetropia (optically normal eye) can be defined as a state of refraction, where in the parallel rays of
light coming from infinity are focused at the sensitive layer of retina with the accommodation being at
rest
Myopia or short-sightedness type of refractive error in
is a
which parallel rays of light coming from infinity are focused in front
of the retina when accommodation is at rest.
Etiological classification
1. Axial myopia (MC form) results from in AP length of the Refraction in a myopic eye
eyeball.
2. Curvatural myopia occurs due to curvature of the cornea, lens or both.
3. Positional myopia is produced by anterior placement of crystalline lens in the eye.
4. Index myopia results from t in refractive index of lens associated with nuclear sclerosis.
5. Myopia due to accommodation occurs in patients with spasm of accommodation.
Grading of mvopia: American Optometric Association (AOA) has defined 3 grades of myopia:
* Low myopia, when the error is s-3D.
*Moderate myopia, when the error is berween-3D to -6D.
*High myopia, when the error is 2-6D.
Clinical varieties of myopia
1. Congenital myopia.
2. Simple or developmental myopia--MC variety
3. Pathological or degenerative myopia.
or
4. Acquired secondary myopia-occurs secondary to some other factors such as: post-traumatic,
post-keratitic, drug-induced, pseudomyopia, space myopia, night myopia, and consecutive myopia.
CONGENITAL MYOPIA

Present since birth, is usually diagnosed by the age of 2-3 years.

Most commonly unilateral. Rarely, it may be bilateral.
High degree of error, about 8 to 10D, is usually presernt
Convergent squint may develop in order to preferentially see clear at its far point
Can be a/w other congenital anomalies such as cataract, aniridia, megalocornea, and congenital
separation of retina.
SIMPLEMYOPIA
It isconsidered as a physiological error not associated with any disease of the eye. Since, the sharpest
rise occurs at school going age, i.e. between 8 years to 12 years so, it is also called school myopia.
Etiology: It results from normal biological variation in the development of eye. It can be
Axial type of simple myopia.
Curvatural type of simple myopia.
Myopia is aggravated by close work, watching TV, smart phones, computers, limited outdoor
activity & not using proper glasses.
 Clinical features of Simple Myopia
Symptoms Signs
Short-sightedness Prominent eyeballs: myopic eyes are typically large
Asthenopic symptoms Anterior chamber is deeper than normal.
Half shutting of the eyes may be Pupils are slightly large & react sluggishly to light
complained by parents of the child. Fundus is normal; rarely temporal myopic
A change in psychological outlook of the crescent maybe seen.
children-Due to poor far vision and Magnitude of refractive error: Simple myopia
normal near vision, the children become usually occurs in children and it keeps on
introvert, studious and develop little increasing till about 18-20 years of age at a rate
interest in the outdoor activities. of about 0.5 0.30 every year
Diagnosis: is confirmed by performing clinical refraction.

PATHOLOGICAL MYOPIA
Pathological/ degenerative/ progressive myopia, is a rapidly progressive error which starts in
childhood at 5- 10 years of age and results in high myopia (>6D) during early adult life which is usually
associated with degenerative changes in the eye. It is less common (about 2% of population).
Etiology Genetic factors General growth process
(play major role)
plays minor role)
1. Role of heredity
Familial More growth of retina
Race: More common in certain races like Chinese,
Stretching of sclera
Japanese, Arabs and Jews. Increased axial length
Degeneration of choroid Features of
Sex: Women> men. Degeneration of retina pathological
> Degeneration of vitreous myopia
2. Role of general growth process -factors such as
nutritional deficiency, debilitating diseases & endocrine Etiological hypothesis for pathological myopia
disturbancesalso influence the progress of myopia.
Clinical features of Pathological Myopla
Symptoms Signs
1) Defective vision Same as Simple Myopia- except:
2) Muscae 1) Fundus examination reveals:
volitantes, i. e. a. Optic disc appears large and pale and at its temporal edge a
floating black characteristic myopic crescent is present.
opacities in front b. Degenerative changes in retina and
of the eyes. choroid:
|3) Difficulty in night Foster-Fuchs' spot may be present at Foster-Fuchs' spot
vision may be the macula. Peripapillary and

complained by Snail track lesions macuiar

degenerabion

very high Total retinal atrophy may occur in an

myopes having advanced case.
marked C. Posterior staphyloma Fundus changes in palhological myopia

degenerative d. Degenerative changes vitreous: liquefaction, vitreous opacities, and

in
changes. posterior vitreous detachment (PVD) appearing as Weiss' reflex.
2) ERG may reveal subnormal electroretinogram due to chorioretinal
atrophy.
Complications: Retinal detachment, Complicated cataract, Vitreous haemorrhage & Choroidal
haemorrhage,
Treatment of myopla
1. Optical treatment of myopla -prescribe appropriate concave lenses
Basic rule of correcting myopia is converse of that in
hypermetropia, i.e., the minimum acceptance providing
maximum vision should be prescribed.
Contact lenses are justified in cases of high myopia as they Refraction in a myopic eye
avoid peripheral distortion produced by spectacles. corrected with concave lens.

2. Surgical treatment of myopla:

Cornea based procedures Lensbased procedures
Radial keratotomy (RK) -for low to moderate myopia.
1) Refractive lens
Orthokeratology-can correct upto -5D of myopia
Laser ablation corneal procedures exchange (RLE): Lens
a. Photorefractive keratectomy (PRK)- can correct upto -6D of extraction with IOL
myopia. implantation of
b. Laser in -situ keratomileusis (LASIK) - refractive surgery of choice appropriate power
can be done for
for myopia of up to -8 D. myopia of > 12D.
Advantages of LASIK Disadvantages
a. Minimal post-op pain. 1) LASIK is more expensive. 2) Phakic refractive
b. Early Recovery of vision 2) It requires greater surgical lens (PRL) or
C. No risk of perforation during surgery skill than RK and PHK. implantable contact
d. No residual haze unlike PRK where sub- 3) There is potential risk of flap lens (ICL) is also
epithelial scarring may occur. related complications being done for
4. Refractive Lenticule extraction (ReLEx): aka SMILE (small incision correction of myopia
Lenticule extraction) can correct myopia up to-10 D. of >8D.
5. Interoorneal ring (ICR) implantation

3. Low vision aids (LVA) are indicated in patients with progressive myopia having advanced
degenerative changes, where useful vision cannot be obtained with spectacles and contact lenses.
Preventive measures:
1) General measures:
»Balanced diet rich in vitamins and proteins.
»Early management of associated debilitating disease.
Visual hygiene.
»Avoidance of excessive near work and excessive use of video display units (VDUs)
» Outdoor activity in childhood may prevent progression of myopia.
2) Genetic counselling: the hereditary transfer of disease may be decreased by advising against
marriage between two individuals with progressive myopia. However, if they do marry, they should
not produce children

2) Define ametropia. Discuss Hypermetropia-types, clinical features, complications and

management [14, 13]
Ans.
Ametropia (a condition of refractive error), is defined as a state of
refraction, when the parallel rays of light coming from infinity (with
accommodation at rest), are focused either in front or behind the
sensitive layer of retina, in one or both the meridians.
The ametropia includes: Myopia, Hypermetropia, and Astigmatism. Refraction in a bypermetropic eye.
Hypermetropia (hyperopia) or long-sightedness is the refractive state of the eye wherein parallel rays8 of 14
of light coming from infinity are focused behind the retina with accommodation being at rest
Etiology: Hypermetropia may be Axial, Curvatural, index, Positional or due to absence of crystalline lens.
1) Axial hvpermetropia (MC): axial shortening of eyeball. 1 mm in AP diameter of the eye = 30 of hypermetropia.
2) Curvatural hypermetropia: curvature of cornea, lens or both.
3) Index hvpermetropia occurs due to in the refractive index of the lens in old age
4) Positional hypermetropia results from posteriorly placed crystalline lens.
5) Absence of crystalline lens either congenital or acquired (following surgical removal) leads to
aphakia- a condition of high hypermetropia.
6) Consecutive hypermetropia may result due to:
a. Overcorrected myopia following refractive surgery le,g, LASIK & inmplantable contact lens]
b. Underpowered intraocular lens (10L) implantation during cataract surgery and refractive
lens exchange (RLE).

Clinical types -There are 3 clinical types of hypermetropia:

1) Simple or Developmental or Physiological hypermetropia (Mc form): It can be axial or curvatural
2) Non-physiological hypermetropia
G Congenital causes Microphthalmos, Microcornea Congenital posterior subluxation of lens etc.
-

Acquired causes - Aphakia, Posterior subluxation of lens, Senile hypermetropia, Consecutive

hypermetropia due to surgically overcorrected myopia etc.
3) Functional hypermetropia: Occurs due to paralysis of accommodation-3 nerve paralysis and
internal ophthalmoplegia
Clinical features
Symptoms Signs
1) Asymptomatic-in young patients Small Size of eyeball.
corrected by mild accommodative effort 2. Cornea may be slighthly smaller than the normal.
2) Asthenopic symptoms develop due to sustained 3. Anterior chamber is comparatively shallow.
accommodative effortstiredness of eyes, 4. Retinoscopy and autorefractometry reveals
frontal or frontotemporal headache, hypermetropic refractive error.
watering and mild photophobia. 5. Fundus examination reveals a small optic disc.
3) Defective vision + asthenopic symptoms. The retina as a whole may shine due to greater
brilliance of light reflections (shot silk
4) Defective vision only if
amountof
appearance).
hypermetropia is very high, the patients
usually do not accommodate (especially 6. A-scan ultrasonography (biometry) reveal short
adults) EE AP length of the eyeball in axial hypermetropia
Complications
1) Repeated rubbing of the eyes (to get relief from fatigue and tiredness)> Recurrent styes,
blepharitis or chalazia.
2) Accommodative convergent squint may develop in children due to excess use of accommodation.
3) Amblyopia may develop.
4) Predisposition to develop primary narrow angle glaucoma.
Treatment
Optical treatment - prescribe convex (plus) lenses (either
Spectacles or Contact lenses)

Relraction in a hypermetropic eye corrected

witn convex lens
 Types of Hypermetropia

Total hypermetropla

Latent hypermetropia Manifest hypermetropia

Camount of hypermetropia usually corrected by the inherent
tone of ciliary muscle- high in children)

Facultative hypermetropia Absolute hypermetropis

(amount of hypermetropia corrected by accomodative effort of patient) Cuncorrected hypermetropia

Surgical treatment of Hypermetropia

Cornea based procedures Lens based procedures
1) Thermal laser keratoplasty (TLK) used for low a) Phakic refractive lens (PRL) or implantable
degree of hyperopia. contact lens (ICL) is being considereda
2) Conductive keratoplasty (CK) can correct surgical option for hyperopia of >+ 4D.
hyperopia of up to 3D. b) Refractive lens exchange (RLE) is a good
3) Hyperopic PRK using excimer laser option for high hyperopia especially in
4) Hyperopic LASIK can correct hypermetropia presbyopic age
up to +4D

sQs
1) Astigmatism [16, 14, 12]
Ans.
Astigmatism is a type of refractive error wherein the refraction varies in different meridians of the eye
due to which light rays fail to converge to a point focus
Broadly, there are 2 types of astigmatism: regular and irregular.
Types of regular astigmatism
Simple Myopic Compound
One meridian focused on Hypermetropic
retina Both meridians are
Other focused in front of focused behind the retina
retina (myopic) (Hypermetropic) but at
Based on different points
Simple Hypermetroplc
Position of the One meridian focused Mixed
two focal lines on retina other
focused behind retina
One meridian focused in
front of retina (myopic
in relation to hypermetropic)
Other focused behind
YpermetroPC
retina Compound Myople
Both meridians are focused Least visually troublesome
in front of retina (Myopic)
but at different points
Most common types

Regular astigmatism
Two principal meridlans are present
and are perpendicular to cach other
Based on the
axis and the With the rule Against the rule Oblique
Vertical meridian Horízontal meridian Two principal meridian are
angle between is more curved is more curved not horizontal and vertical
the two Cornea Cornea

principal
meridians
Wth the rue "Against the rule"
usugmausn asugmaUsm
 REGULAR ASTIGMATISM IRREGULARASTIGMATISM
The astigmatism regular when the
is It ischaracterized by an irregular change
refractive power changes uniformly from of refractive power in different
one meridian to another (i.e., there are 2 meridians
principal meridians).
Corneal astigmatism- occur due to 2 Types
abnormal curvature of cornea (MCC). 1) Curvatural irregular astigmatism
2. Lenticular astigmatism- occur due to seen in corneal scars or keratoconus.
Etiology
abnormalities of the lens 2) Index irregular astigmatism-occur
3. Retinal astigmatism occurs due to due to variable refractive index in
oblique placement of macula different parts of the lens (cataract)
1) Asthenopia (tiredness of eyes
relieved by closing the eyes) Defective vision,
2) Blurring of vision - on reading, letters Distortion of objects, and
Symptoms
are seen to be "running together Polyopia (seeing multiple images).
3) Elongation of objects may be noticed
in
high astigmatism.
»Retinoscopy reveals irregular
1. Half closure of the lid (Like myopes) pupillary reflex.
2. Head tilt- to bring their axes nearer
Slit-lamp examination reveal corneal
to the horizontal or vertical
irregularity or Keratoconus.
meridians.
» Placido's disc test reveals distorted
Signs 3. Oval optic disc may be seen on
circles
ophthalmoscopy.
Different power in 2 meridians is »Photokeratoscopy and computerized
revealed on retinoscopy or corneal topography give
autorefractometry. photographic record of irregular
corneal curvature
1) Retinoscopy.
2) Keratometry reveal corneal astigmatism.
Investigations 3) Astigmatic fan test
4) Jackson's cross cylinder test useful in confirming the power & axis of cylindrical
lenses.
1. Withthe rule Astigmatism
Concave Cylinder at 180 ° or Convex
cylinder at Mnemonic
Optical
90 With CV, Against VC

Against the With conCave [-1 conVexI+) Toric Contact lens

treatment Against conVex I+) conCave
rule
Astigmatism
Convex Cylinder at 180 or
Concave cylinder at 90
1) Astigmatickeratotomy
Surgical
2) AstigmaticLASIK
3) Limbal Relaxing Incision
Techniques
4) Ruiz Procedure for post-keratoplasty astigmatism
5) Phototherapeutic keratectomy performed with excimer laser
(PTK)
Optics of regular astigmatism can be understood from the configuration of a Sturm's conoid
2) Presbyopia [15, 11, 04
Ans.
Presbyopia (eye sight of old age) is not an error of refraction but a condition of physiological
insufficiency of accommodation leading to a progressive fall in near vision.
Pathophysiology: After the age of 40 years, near point of accommodation recedes beyond the normal
reading or working range. This condition of failing near vision due to age-related decrease in the
amplitude of accommodation is called presbyopia.
Etiology
1. Hardening of lens with age
2. Weakness of ciliary muscles & suspensory ligaments with age
3. Excessive Close work
Causes of premature presbyopia are:
Uncorrected hypermetropia.
Chronic simple glaucoma.
Symptomss
near vision - ex: reading small prints, in threading a needle, etc.
1) Difficulty in
2) Vision improves if held further away
3) Asthenopic symptoms due to fatigue of the ciliary muscle
4) Intermittent diplopia may be experienced by few patients
Treatment
Optical treatment prescribe appropriate convex glasses for near work.
Rough guide for providing presbyopic glasses in an emmetrope can be made from the age of the patient.
years: +1 to+ 1.25D
45
S0 years: +1.5 to 1. 750
55 years: +2 to+ 2.25D
60 years: +2.5 to +30
Presbyopic spectacles may be unifocal, bifocal or varifocal.
Surgical treatment:
Refractive surgery for presbyopia, still under trial, includes:
Cornea based procedures Lens based procedures Sclera based procedures
1. Monovision conductive
or
Multifocal accommodating8 1) Anterior ciliary
keratoplasty (CK)
IOL implantation after
2. Monovision LASIK. sclerotomy
cataract surgery 2) Scleral ablation with
3. Presbyopic bifocal LASIK
Monovision with intraocular erbium: YAG laser
4. Presbyopic multifocal (PML)
LASIK
lenses.

**********

3) Contact lens [11, 08, 03]

Ans.
Contact lens is an artificial device whose front surface substitutes the anterior surface of the cornea.
Nomenclature for contact lens
1. Diameters of the contact lens:
a. Overall diameter (OD) of the lens is the linear measurement of the greatest distance across the
physical boundaries of the lens.
 b. Optic zone diameter (02) is the central optic zone of lens which is meant to focus rays on the
retina.
2. Curves of the lens are as follows: Optic zone
a) Base curve (BC) is a curve on the back surface of the
Peripheral Curve
lens to fit the front surface of cornea. Lens edge

b) Peripheral curves-These are concentric to base curve

and are meant to serve as reservoir of tears Back Curve
optic radius
c) Front curve (FC) is the curve on the anterior surface
It determines the power of contact lens.
3. Edge of the lens- It is the polished and blended union of
the peripheral posterior and anterior curves of the lens. Optical zone diameter
Thickness of the lens- measured in the centre of the lens
Overall diameter
5. Tint-It is the colour of the lens.

Types of contact lenses

Depending upon the nature of the material used in their manufacturing, the contact lenses canbe
divided into following 3 types:
Rigid gas permeable
Hard lenses lenses Soft lenses
fsemisoft lenses)
Materials which are
permeable to oxygen HEMA
PMMA
Made up of Ex: Silicone acrylate,
(polymethylmethacrylate) (hydroxyethylmethacrylate).
Cellulose acetate
butyrate
Being soft and oxygen
light in weight, nontoxic, permeable, they are most
Advantages Oxygen permeable
durable and cheap comfortable and so well
tolerated
1. PMMA is impermeable
Wettability, getting cracked,
to thus restricting
Oa
these are also hard & limited Life, inferior optical
Disadvantages the tolerance.
hence not popular quality, more chances of
2. Being hard, it can cause
corneal infections
corneal abrasions.
Indications of contact lens use
1. Optical indications -for patients with refractive error like anisometropia, unilateral aphakia, high
myopia, keratoconus and irregular astigmatism.
2. Therapeutic indications:
a) Corneal diseases, e.g, non-healing corneal ulcers, keratitis & recurrent corneal erosions.
b) Diseases of iris - aniridia, coloboma and albinism to avoid glare.
c)In glaucoma as vehicle for drug delivery.
d) In amblyopia, opaque contact lenses are used for occlusion.
3. Preventive indications:
Prevention of symblepharon and restoration of fornices in chemical bums
Exposure keratitis.
Trichiasis.
4. Diagnostic indications: They are used during gonioscopy, electroretinography, Fundus
photography, Goldmann's 3 mirror examination etc.
5. Operative indications: They are used during goniotomy operation for congenital glaucoma;
vitrectomy etc.
6. Cosmetic indications:
Unsightly corneal scars (colour contact lenses);
()
Ptosis (haptic contact lens); and
(i)
(ii) Cosmetic scleral lenses in phthisis bulbi.
7. Occupational indications include use by sportsmen; pilots; and actors.

Contraindications for contact len

Mental incompetence, and poor motivation;
2. Chronic dacryocystitis; Chronic blepharitis; Chronic conjunctivitis
Dry eye syndromes;
Corneal dystrophies and degenerations; and
5. Recurrent diseases like episcleritis, scleritis and iridocyclitis.

4) Advantage of Intraocular lenses in treatment of Aphakia [09]

a. Signs of Aphakia [07]
Ans. APHAKIA
Absence of crystalline lens > Converging power of eye decreases Light rays come to focus behind
the retina> high degree of hypermetropia & Accommodation is lost fully
Causes
1) Congenital absence of lens.
2) Surgical aphakia occur after removal of lens (MC)
-

3) Aphakia due to absorption of lens matter after trauma in children.

4) Traumatic extrusion of lens from the eye.
5) Posterior dislocation of lens in vitreous.
Clinical features

Symptoms Signs of aphakia

OLimbal/ corneal scar may be seen in surgical aphakia.
Anterior chamber is deeper than normal.
Defective vision for both far
Iridodonesis, i.e., tremulousness of iris can be
and near vision. demonstrated.
Erythropsia and cyanopsia, OPupil is jet black in colour.
i.e., seeing red and blue
Purkinje's image test shows only two images
images fdue to excess entry of UV &
Fundus examination shows hypermetropic small disc.
IR rays in absence of crystalline lens
Retinoscopy & autorefractometry reveal high
hypermetropia.
Treatment
1) Spectacles:
* +10D with cylindrical lenses for surgically induced astigmatism are commonly used.
Disadvantages of spectacles
a. Problem of spherical and chromatic aberrations of thick lenses.
b. Field of vision is limited.
 Prismatic effect of thick glasses.
C.
d. Cosmetically, the eyes look enlarged (Frog Eyes) behind the thick spectacles
2) Contact lenses.
Advantages of contact lenses over spectacles include: No aberrations and prismatic effect of
thick glasses, Wider and better field of vision & cosmetically more acceptable:
Disadvantages: expensive, cumbersome to wear & corneal complications may be associated.
3) Intraocular lens implantation is the best available method of correcting aphakia.
4) Refractive corneal surgery: Hyperopic LASIK may be tried in cases where 1OL cannot be implanted
---**-***-***---*----------------~ ---. *********=*****=***

5) Pseudophakia [200o]
Ans. The condition of aphakia when corrected with an referred to as Pseudophakia or artephakia.
1OL is
Refractivestatus of a Pseudophakic eye: depends upon the power of the 1OL implanted
1) Emmetropia If power of the lOL implanted is exact. It is an ideal situatión
-

2) Consecutive myopia -if 1OL implanted overcorrects the refraction of eye.

3) Consecutive hypermetropia - if under power IOL is implanted.
4) Varying degree of surgically induced astigmatism is also present in pseudophakia.
Signs of pseudophakia (with posterior chamber 10L).
Surgical scar may be seen near the limbus.
Anterior chamber is slightly deeper than normal.
Mild iridodonesis (tremulousness) of iris may be demonstrated.
Purkinje image test shows 4 images.
Shimmering light reflex is present.
Presence of 1OL is confirmed on slit-lamp examination after dilating the pupil.
Visual status and refraction will vary depending upon the power of lOL implanted
Management of pseudophakia:
1 Spectacles
for near vision alone (in pseudophakia with emmetropia) or
Bifocal glasses for both distance and nearvision (in pseudophakia with consecutive refractive
error).
2. LASIK or Advanced surface ablation (ASA) may be required in moderate consecutive
refractive
error.
A
3. Intraocular lens (IOL) exchange or pigiback IOL is required in large consecutive refractive error.

VSQs
1) Uses of convex lenses in Ophthalmology [15]
Ans.
(i) for correction of hypermetropia, aphakia and presbyopia;
(i) As a magnifying lens- in oblique illumination
examination, in indirect ophthalmoscopy & in
many other equipments.
 CONTENTS
Diseases of Conjunctiva.
LQs 3

SQs 9

Diseases of Retina. 13
LQS 13

SQs ... 17
 bf23

Diseases of Conjunctiva
LQs
1. Ophthalmia neonatorum aetiology, symptoms, signs& treatment [09, 85]
a. Purulent conjunctivitis (99]
Ans.
Ophthalmia neonatorum, or neonatal conjunctivitis is a bilateral inflammation of the conjunctiva
occurring in a neonate.
Etiology-Infection may occur in 3 ways: before birth, during birth or after birth
1) Before birth >
through infected liquor amnii in mothers with ruptured membranes.
2) During birth: (MC mode) in vaginally delivered infants.
3) After birth > Ex: during 1st bath of newborn
Clinical features
1) Pain & tenderness in the eyeball Infant is iritable
2) Hyperaemia & chemosis in conjunctiva
3) Periocular vesicles & Corneal involvement (superficial punctate keratitis)-occur in HSV infection.
Conjunctival &
Causative agent Incubation period Smear culture
Discharge
Chemical fsilver nitrate| 6 hours Watery Negative Culture
Copious Intracellular Gram-ve
Gonococcal 2-5 days purulent diplococci culture positive on
discharge blood agar
Non-Gonococcal H Gram +ve or Gram -ve
bacteria {Staph, Strep &&
5-8 days Mucopurulent organisms
Haemophilus species I Positive culture
Neonatal inclusion
conjunctivitis (serotypes D 5-14 days Mucopurulent Positive culture
to K of Chlamydia trachomatis)
Multinucleated giant cells,
Herpes simplex 6-15 days Watery cytoplasmic inclusion bodies
and negative culture
Complications:
Corneal ulcer, which may perforate- corneal opacification or staphyloma formation.
Leukoma; Phthisis bulbi
Differential Diagnosiss Congenital dacryocystitis, Congenital glaucoma
Treatment- Culture sensitivity swabs should be taken before starting the treatment.
1) For Chemicals (silver nitrate) > just wash eye; it is self-limiting & doesn't require any treatment.
2) For Gonococcus:
Topical therapy:
Saline lavage hourly till the discharge is eliminated.
Bacitracin eye ointment 4 times/ day.
Systemic therapy: one of the following regimes can be used for 7 days.
-Ceftriaxone 75-100 mg/ kg/ day IV or IM, gid or
Cefotaxime.100-150 mg/ kg/ day IV or IM, 12 hourly or
 Ciprofloxacin 10-20 mg/kg/day or
Norfloxacin 10 mg/ kg/ day
3) For Other Non-gonococcal bacteria- prescribe broad-spectrum Abx eye drops& Neomycin-
bacitracin eye ointments for 2 weeks.
4) For Neonatal inclusion conjunctivitis -prescribe topical tetracycline 1% or erythromycin 0.5% eye
ointment qid for 3 weeks.
o But, systemic erythromycin (125 mg orally, qid for 3 weeks) should also be given since the presence of
chlamydia agents in the conjunctiva implies colonization of upper respiratory tract as well. Both parents
should also be treated with systemic erythromycin
5) For Herpes simplex conjunctivitis-prescribe topical antivirals (ex: acyclovir 3 % ointment)
Prophylaxis-Antenatal, natal and postnatal care.
a. Antenatal care: Prenatal diagnosis and treatment of birth canal infections.
b. Natal Care: Aseptic delivery. Newborn baby's closed lids should be thoroughly cleansed & dried.
Postnatal care: Clean the eyelids with sterile gauze dipped in Povidon-iodine 2.5% solution or 1%
tetracycline ointment or 0.5% erythromycin ointment.
Single injection of ceftriaxone so mg/ke IM or Vshould be given to infants born to mothers with
untreated gonococcal infection.

2. Trachoma clinical features and management [09, 05, 04]

-

a. Pannus [12, 03, 95]

Complications of Trachoma [11]

aka Egvetian ophthalmia) is a chronic keratoconjunctivitis, affecting the superficial epithelium of

dva and cornea simultaneously. (Trachoma' in Greek means 'rough)

Etiopathogenesis:
Causative organism Chlamydia trachomatis biovar TRIC. (TRIC= Trachoma and Inclusion Conjunctivitis)
-

The organism is epitheliotropic & produces HP (Halberstaedter Prowazek) bodies (intracytoplasmic inclusion
bodies).
Ato K Serotypes of C. trachomatis are together called TRIC agents
(aka Serovars)
OPresently, 12 serovars of Chlamydia trachomatis biovar TRIC have been identified out of which
Serovars A, B, B, and Care a/w hyperendemic (blinding) trachoma.

Serovars D to K are a/w oculogenital chlamydial disease.

Predisposing factors: Inclusion bodies
Epithelial cell
Age-nfancy & early childhood.

Sex: femalesmales
Poor Socioeconomic status; unhygienic and crowded surroundings
Environmental factors like dry weather, exposure to dust, smoke, irritants, sunlight, etc.
Source of infection: conjunctival discharge of the affected person.
Modes of infection:
1) Direct spread - by airborne or waterborne modes.
Papilla
2) Vector transmission through flies. Follicle
Congestion
3) Through contaminated fingers of doctors, nurses and
Pannus
contaminated tonometers, common towel, handkerchief, Herbert's
follicle
bedding and surma-rods.
Prevalence: Trachoma is responsible for 15-20% of the world's
blindness, being second only to cataract. Signs of active trachom
Clinical features- described in 2 phases:
Phase of active trachoma Phase of cicatricial trachoma
Childhood due to active chlamydial Middle age due to chronic inflammation
Occurs in infection Type IV HSN reaction to chlamydial antigens)
Incubation period: 7 to 14 days Here, infection is no longer present, i.e., only trachoma
sequelae are present.
Intheabsence of 2"infection: Mild foreign body sensation, lacrimation, stickiness
Symptoms of the lids & Scanty mucoid discharge.
In thepresence of 2"infection: symptoms resemble acute mucopurulent conjunctivitis
Conjunctival signs
Conjunctival signs 1) Conjunctival scarring, which may be
1) Congestion of upper tarsal & irregular, star-shaped or linear. Linear
forniceal conjunctiva. scar present in the sulcus subtarsalis
2) Conjunctival Follicles look like is called Arlt's line
boiled sago-grains. Sometimes, 2) Concretions-whitish deposits
follicles may be seen on the bulbar formed due to
conjunctiva (pathognomonic of
trachoma).
accumulation of
dead epithelial cells O
3) Papillary hyperplasia - Impart red and mucus in the glands of Henle
and velvety appearance to the 3) Others-pseudocyst, xerosis &
Signs tarsal conjunctiva. symblepharon
Corneal signs Lid Signs: trichiasis, entropion, tylosis,
1) Superficial keratitis in the upper ptosis, madarosis etc.
part. Lacrimal Apparatus: chronic
2) Herbert follicles-present in the dacryocystitis & dacryoadenitis
limbal area (similar to conjunctival Corneal signs
follicles). 1) Regressive pannus (pannus siccus)
3) Progressive pannus, i.e., infiltration vessels extend beyond the area of infiltration
ofthe cornea is aheadof 2) Herbert pits are the pitted scars, left
vascularization. after healing of Herbert follicles
4) Corneal ulcer may develop 3) Blinding sequelae: Corneal opacity,
corneal ectasia, corneal xerosis etc.
o Topical therapy:
Tetracycline or erythromycin 1%
eye ointment BD for 6 weeks or
Sulfacetamide (20%) eye drops ti.d + Remove Concretions with a hypodermic
1% tetracycline eye oint at bed time needle
for 6 weeks Artificial tears for Conjunctival xerosis
Systemic antibiotics regimes: Electrolysis, Cryolysis etc. -for Trichiasis
Azithromycin 20 mg/kg body weight up to Surgery to correct Cicatricial entropion
maximum 1g as single oral dose is as effective
Treatment Measures to treat Corneal Opacity:
as 6 weeks of topical therapy and so IS the
13 DOC. It not used in pregnancy and
is
Penetrating keratoplasty (PK)
children < 6 years of age. Keratoprosthesis (KP) - in B/L blind cases
Tetracycline or erythromycin 250 Punctal occlusion & lateral
mg orally, q.i.d. for 3-4 weeks tarsorrhaphy
Doxycycline 100 mg orally BD for 3-4
weeks
Combined topical & systemic
therapy-preferred in severe
infections
 pannus
Grading of trachoma-WHO classification (FISTO): Progressive pannus Regressive

1) TF: Superficial blood vessels

Trachomatous inflammation-follicular.
Zone of infitration
2) TI: Trachomatous inflammation intense
3) TS: Trachomatous scarring in the tarsal conjunctiva.
4) TT: Trachomatous trichiasis - eyelash rubs the eyeball.
5) CO: Corneal opacity
Complications: Corneal ulcer
Diagnosis
*Clinical diagnosis - made from its typical signs. Clinical grading of each case should be done as per
WHO classification into TE, TI, TS, TT or CO.
Laboratory diagnosis:
Conjunctival cytology: Giemsa-stained smears show PMN reaction with presence of plasma cells
and Leber cells.
ELISA for chlamydial antigens
Polymerase chain reaction (PCR) is also useful.
Prophylaxis for Trachoma: The WHO's GET 2020 program (Global Elimination of Trachoma by 2020),
has adopted the SAFE strategy for prophylaxis against trachoma which includes:
S: Surgery (Tertiary prevention),
A: Antibiotic use (Secondary prevention),
F: Facial hygiene (Primary prevention), &
E: Environmental changes (Primordial prevention).

3. Describe the aetiology, symptoms, signs and treatment of allergic conjunctivitis [88]
a. Vernal conjunctivitis /Vernal Catarrh/Spring Catarrh. [13, 11]
b. Phlyctenular conjunctivitis [03, 95, 91]
c. Phlycten [08, 05]
d. Fascicular ulcer [07
Ans.
Allergic conjunctivitis: It is the inflammation of conjunctiva due to allergic reactions which may be
immediate (humoral) or delayed (cellular) The conjunctiva is 10 times more sensitive than the skin to allergens.
Types of Allergic Conjunctivitis:
1) Simple allergic conjunctivitis It can be seasonal or perennial
2) Vernal keratoconjunctivitis (VKC)-it is seasonal
3) Atopic keratoconjunctivitis (AKC)-adult form of VKC
4) Phlyctenular keratoconjunctivitis (PKC)
5) Giant papillary conjunctivitis
6) Contact Dermoconjunctivitis (Drop Conjunctivitis)

VERNAL KERATOCONJUNCTIVITIS OR SPRING CATARRH3 VKC is a bilateral, interstitial, self-limiting.

allergic inflammation of the conjunctiva having a periodic seasonal incidence.

Etiopathogenesis
oPredisposing factors
1) Sex: boys> girls.
2)Season: More common in summer; hence the name spring catarrh.
3) Climate: More prevalent in tropics, less in temperate zones
4) Other atopic manifestations, such as eczema or asthma, are associated in 40- 75% cases.
5) Family history of atopy is found in 40-60% of patients
 o Pathological Changes: Microscopic structure of conjunctiva
1) Hyperplasia of Conjunctival epithelium 0ppoo00Epithelium
downward
projections into the sub-epithelial tissue.
- Adenoid layer
2) Adenoid layer shows infiltration by mast cells, eosinophils,
plasma cells, Iymphocytes & histiocytes
3) Fibrous layer shows proliferation which later on Fibrous layer
undergoes hyaline changes.
4) Conjunctival vessels also show proliferation,
permeability and vasodilation.
o All these pathological changes lead to formation of multiple papillae in the upper tarsal conjunctiva
Clinical features
Symptoms Signs
»Burning and itching 1) Palpebral form: Usually upper tarsal conjunctiva of both eyes is involved.
sensation which is Hard, flat topped, papillae are arranged in a cobble-stone' or
when patient comes in pavement stone fashion along with conjunctival hyperemia.
a warm humid In severe cases, papillae may hypertrophy to produce
atmosphere. Itching is cauliflower-like 'giant papillae'.
more marked with palpebral 2) Bulbar limbal form. It is characterised by:
form of disease. Dusky red triangular congestion of bulbar conjunctiva in
»Otherassociated palpebral area,
Symptoms: mild Limbal papillae occur as gelatinous, thickened confluent
photophobia, accumulation of tissue around limbus
lacrimation, stringy Presence of whitish raised dots along the limbus (Horner
(ropy) discharge & Tranta's spots)
heaviness of lids. 3) Mixed form: It shows combined features of both palpebral & bulbar forms.
Corneal involvement in VKQ includes the following types of lesions: Cobble stone
1. Punctate epithelial keratitis ement
of papiliae
2. Epithelial erosions-occurs due to coalescence of punctate Tranta's nodule
gelainous
epithelial lesions. membrane
Spring catarh
3. Vernal corneal plaques occurs due to coating of bare areas of
epithelial erosions with a layer of altered exudates
4. Ulcerative vernal keratitis (shield ulcers)
5. Subepithelial scarring (ring scar)
6. Pseudogerontoxon can develop in recurrent limbal disease Palpebral form Bulbar form
Spring catarrh
and is characterised by a classical 'cupid's bow' outline.
Differential diagnosis: Palpebral form of VKC needs to be differentiated from trachoma
Treatment of VKC
»Topicalanti-inflammatory therapy with steroids (luorometholone),mast cell stabilizers (sodum
cromogycate (2%) drops), antihistamines (azelastine, ketotifen), and NSAIDs forms the mainstay of
treatment of VKC. Tacrolimus (0.03% ointment) is an immune-modulator, which can be useful in refractory cases.
Topical lubricants & mucolytics
1. Artificial tears, such as carboxymethyl cellulose, provide soothing effect
2. Acetyl cysteine (0.5%) - mucolytic; useful in the treatment of early plaque formation
»Systemic therapy Oral antihistaminics &steroids in severe cases.
-

»Treatment of large papillae: Supratarsal injection of long-acting steroid or Cryo application, or

Surgical excision.
 Supportive.measures:
Dark goggles to prevent photophobia.
Cold compresses and ice packs have soothing effects.
Maintenance of air-conditioned atmosphere.
Change of place from hot to cold area
»Desensitization
»Treatment of vernal keratopathy
Punctate epithelial keratitis requires steroids
A large vernal plaque requires surgical excision by superficial keratectomy.
Surgical treatment for Shield ulcers > debridement, superficial keratectomy, excimer laser
therapeutic keratectomy; amniotic membrane transplantation to 1 re-epithelialization.

PHLYCTENULARKERATocONJUNCTIVITIS aka microbial allergic conjunctivitis@ It is a characteristic nodular

affection (phlycten) occurring as an allergic response of the conjunctival and corneal epithelium to
some endogenous allergens to which they have become sensitized.
Etiology: It is a delayed hypersensitivity (Type V-cell mediated) response to endogenous microbial
proteins
Causative allergens - Tuberculous proteins, Staphylococcus proteins, proteins of Moraxella bacillus
and certain parasites (worm infestation).
Predisposing factors
Sex: Girls> boys.
Malnutrition, Overcrowding, unhygienic practices etc.
Phlyctenular conjunctivitis
Pathology
1) Stage of nodule formation: exudation & infiltration of WBCs into deep layers of conjunctiva> nodule
formation.
2) Stage of ulceration: Later on, necrosis ocCurs at the apex of the nodule and an ulcer is formed.
3) Stage of granulation: Eventually, floor of the ulcer covered by granulation tissue.
4) Stage of healing
Clinical features Disease is usully U/L (in contrast to vernal keratoconjunctivitis which is B/L).
Symptoms: mild discomfort in the eye, irritation and reflex watering. However, usually there is
associated mucopurulent conjunctivitis due to secondary bacterial infection.
Signs: The phlyctenular conjunctivitis can present in 3 forms: simple, necrotizing & miliary.
Corneal involvement in PKG may ocCur secondarily from extension of conjunctival phlycten; or rarely
as a primary disease. 2 forms are seen -

1) Ulcerative phlyctenular keratitis may occur in the following 3 forms:

a. Scrofulous ulcer is a shallow ulcer formed due to breakdown of small limbal phlycten. Such an
ulcer usualy clears up without leaving any opacity.
b. Fascicular ulcer has a prominent parallel leash of blood vessels. This ulcer
remains superficial but leaves behind a band-shaped superficial opacity after
healing.
C. Miliary ulcer: multiple small ulcers are scattered over a portion of or whole of the cornea.

Diffuse infiltrative phlyctenular keratitis- this appears in the form of central infiltration of cornea
with characteristic rich vascularization from the periphery, all around the limbus.
Differential diagnosis: episcleritis, scleritis, and conjunctival foreign body granuloma.
Management
1. Local therapy
Topical steroids (dexamethasone or betamethasone)
Antibiotic drops and ointment should be added to cover secondary infection
Atropine (1%) eye ointment should be applied once daily when cornea is involved.
2. Specific therapy
a. Tuberculous infection should be excluded by X-rays chest, Mantoux test, TLC, DLC and ESR. In
case, a tubercular focus is discovered, antitubereular treatment should be started
b. Septic focus, in the form of tonsillitis, adenoiditis, or caries teeth, when present shouldbe
adequately treated by systemic antibiotics and necessary surgical measures.
C.Parasitic infestation should be ruled out by repeated stool examination and when discovered
should be adequately treated for complete eradication.
3. General measures-provide high protein diet supplemented with vitamins A, Cand D.

4. Describe the aetiology, symptoms, signs and treatment of membranous conjunctivitis [87
Ans. TRUE MEMBRANE PSEUDOMEMBRANE
»Streptococcus 1. Structure Fibrinous exudate is situated Fibrinous exudate is situated
pyogenes over and within the over the surface of conjunctival
(haemolyticus) causes conjunctival epithelium epithelium.

pseudomembranous 2. On peeling It cannot be peeled off easily. It is separated easily.

3. Bleeding Bleeding occurs when the There is no bleeding.
conjunctivitis. membrane is removed.
Corynebacterium
diphtheriae causes acute membranous conjunctivitis.
Such infections are not known nowadays.

SQs
1) Pterygium [14, 04, 99]
Ans. Pterygium is a wing-shaped fold of conjunctiva encroaching upon the cornea from either side
within the interpalpebral fissure.
Etiology: it is a response to prolonged effect of environmental factors like sunlight (UV rays), dry heat,
high wind and dust
Pathology Pterygium is a degenerative and hyperplastic condition of conjunctiva which proliferates as
vascularised granulation tissue under the corneal epithelium & encroaches the cornea by destroying
the corneal epithelium, Bowman's layer & superficial stroma are destroyed.
Clinical features
Symptoms
Age: Usually seen in old age.
Sex: More common in males doing outdoor work than females
Cosmetic intolerance; Foreign body sensation and iritation.
Defective vision occurs when it encroaches the pupillary area
Diplopia may occur due to limitation of ocular movements.
Signs
Triangular fold of conjunctiva encroaching on the cornea in the area of palpebral aperture is
typical presentation of pterygium.
 Stockerline (deposition of iron) may be seen in corneal epithelium anterior to the advancing head
of pterygium. Body Head
Parts of a fully-developed pterygium are as follows:
Head: Apical part present on the cornea,
Neck: Constricted part present in the limbal area Pterygium
encroaching
Body: Scleral part- extend between limbus & canthus. over cornea Stocker's line
Cap: Semilunar whitish infiltrate present just in front of Neck

the head. Pterygium

Types Pterygium Pseudopterygium

1. Etiology Degenerative Inflammatory
1. Type 1 pterygium extends < 2 mm onto the cornea. process process
2. Type 2 pterygium involves upto 4 mm of the cornea. 2.Age Usually occurs in Can occur at any
3. Type 3 pterygium encroaches onto >4 mm of the cornea elder persons age
3. Site Always situated Can occur at any
and involves the visual axis. in the palpebral site
Complications: Cystic degeneration & infection; neoplastic aperture
4. Stages Either progressive, Alwaysstationary
change to epithelioma, fibrosarcoma or malignant regressive or
stationary
melanoma, may occur rarely.
5.Probe Probe cannot be A probe can be
Differential diagnosis test passed underneath passed under the
neck
Pterygium must be differentiated from pseudopterygium.
Pseudopterygium is a fold of bulbar conjunctiva attached to the cornea. It is formed as a response
to an acute inflammatory episode such as chemical burn, marginal corneal ulcer, corneal trauma
and cicatrizing conjunctivitis.
Treatment
Medical treatment of not much use.
Tear substitutes for dry eye symptom.
Topical steroids for associated inflammation.
Sunglasses to protect from UV rays ( the growth stimulus).
Surgical excision is the only satisfactory treatment which may be indicated for: Cosmetic
disfigurement, Visual impairment, Continued progression threatening to encroach onto the
pupillary area & Diplopia.
Recurrence of the pterygium after surgical excision, can be by any of the following measures:
Surgical excision with free conjunctival limbal autograft (CLAU)
Surgical excision with amniotic membrane graft and mitomycin-C
Surgical excision with lamellar keratectomy and lamellar keratoplasty

2) Sub-conjunctival Haemorrhage [14, 06, 04)

Ans.
Ecchymosis or subconjunctival haemorrhage may vary in extent from small petechial haemorhage to
an extensive one spreading under the whole of the bulbar conjunctiva and thus making the white
sclera of the eye invisible.
Etiology:
1. Trauma (MCC) local trauma to the conjunctiva (Ex: due to surgery & subconjunctival inj.) or
retrobulbar haemorrhage (Ex: due to trauma of orbit) which spreads below the bulbar conjunctiva.
2. Inflammations of the coniunctiva: Petechial subconjunctival haemorhages are usually associated
with acute haemorrhagic conjunctivitis caused by picornaviruses, pneumococcus, leptospirosis etc.
 3. Venous congestion of head (Ex: in whooping cough, epileptic fits, strangulation or compression of jugular veins)
sudden rise in pressurerupture of conjunctival capillaries
4. Vascular diseases such as arteriosclerosis, HTN & DM Spontaneous rupture of fragile capillaries
5. Blood dyscrasias like anaemias, leukaemias and dysproteinaemias.
6. Bleeding disorders like purpura, haemophilia and scurvy.
7. Acute febrile systemic infections such as malaria, typhoid, diphtheria, meningococcal septicaemia,
measles and scarlet fever.
8. Vicarious bleeding associated with menstruation is an extremely rare cause of subconjunctival
haemorrhage.
Clinical features.
Symptom: Red eye is the most predominant feature
Sign: Fresh bright red blood is visible under the conjunctiva
Most of the time it is absorbed completely within 7 to 21 days. During
absorption colour changes are noted from bright red to orange and
then yellow. Subconjunctival haemorrhage
In severe cases, some pigmentation may be left behind after
absorption.
There may be symptoms of associated causative disease

Treatment
No needed; resolves spontaneously in 2 weeks
Rx

Treat the cause when discovered.

Placebo therapy with astringent eye drops
Psychotherapy and assurance to the patient
*Cold compresses to check the bleeding in the initial stage and hot compresses may help in
absorption of blood in late stages.

3) Angular Conjunctivitis [05]

Ans.
It is a type of chronic conjunctivitis characterised by mild grade inflammation confined to the
conjunctiva and lid margins near the angles a/w maceration of the surrounding skin.
Etiology
Causative organisms: Moraxella Axenfield (MA, aka diplobacilli) is MCC. Rarely, staphylococci may
also cause angular conjunctivitis.
Source of infection: usually nasal cavity.
Mode of infection: Infection is transmitted from nasal cavity to the eyes by contaminated fingers or
handkerchief,
Predisposing factors are same as for 'simple chronic conjunctivitis'

Pathology: MA bacillus produces a proteolytic enzyme which collects at the angles by the action of
tears and thus macerates the epithelium of the conjunctiva, lid margin and the skin. The maceration is
followed by mild grade chronic inflammation. Skin may show eczematous changes.

Clinical features
 Symptoms Signs
Irritation, burning Hyperaemia of bulbar conjunctiva near
sensation and the canthi.
discomfort in the eyes. Hyperaemia of lid margins near the
H/o dirty-white foamy angles.
discharge at the Excoriation of the skin around the
angles. angles.
Redness in the angles Foamy mucopurulent discharge at the Signs of angulor conjunctvits

of eyes. angles
Complications: blepharitis & shallow marginal catarhal corneal ulceration.
Treatment Conjunctival Excoritation
Prophylaxis - treatment of associated nasal infection & good personal congestion of skin
Angular conjunctivitis
hygiene.
Curative treatment consists of:
1. Oxytetracycline (1 %) eye ointment, 2-3 times a daily for 9-14 days.
2. Zinc lotion instilled in day time and zine oxide ointment at bed time inhibits the proteolytic
ferment and thus helps in reducing the maceration.

4) Follicular Conjunctivitis [13, 03]

Ans.
It is the inflammation of conjunctiva, characterised by formation of follicles, conjunctival hyperaemia
and discharge from the eyes. Follicles are formed due to localised aggregation of lymphocytes in the
adenoid layer of conjunctiva.
Etiology
Exposure to certain chemicals and toxins, e-g, pilocarpine, atropine etc.
Viruses, e.8, herpes and adenovirus Follicular conjunctivitis

Any conjunctivitis of long duration may cause this condition.

Symptoms: Foreign body sensation, slight initation, redness, watering. mild mucoid discharge, mild
photophobia
Signs: Multiple follicles are present in the lower fornix. There is no scarring which differentiates it from trachoma

Types
1) Inclusion conjunctivitis-It is caused by serotypes D to K of Chlamydia trachomatis > produce
inclusion bodies similar to those occurring in trachoma. The primary source of infection is contaminated
water of swimming pools (hence the name swimming pool conjunctivitis).
2) Epidemic keratoconjunctivitis-It is caused by adenovirus. It is treated by adenine arabinoside (Ara-A).
3) Pharyngoconjunctival fever- It is also caused by adenovirus. A/w pharyngitis & feve
4) Acute herpetic conjunctivitis-It is common in young children. A/w Corneal dendritic ulcers
5) New castle conjunctivitis-It is caused by new castle virus from infected owls.
Complicationss Follicles may persist for several years but always resolve without scaring
Treatment
Astringent eyedrops are applied frequently; Choose Antibiotic/Antiviral based on the causative agent
Supportive Treatment: Improve general health and nutrition of the patient.
Treat associated adenoids, tonsils and upper respiratory tract infection promptly and adequately.
 of 23
Diseases of Retina
LQs
1) Diabetic retinopathy classification, ocular fundus signs and treatment [16, 11, 10, 071
a. Dot and blot haemorrhages [13] Vascular and haematological changes seen in
diabetes mellitus
b. Retinal hemorrhages [12]
Ans. Thickening of capillary basement membrane
capillary endothellal cell damage
Diabetic retinopathy (DR) refers to retinal changes seen in patients RBCS: detormation and rouleaux formation
Increased sickiness of platelets
with diabetes mellitus. Increased plasma viscosity
Loss of capillary pericytes
Risk factors
Microvascular occlusion
1. Duration of diabetes after the onset of puberty is the most
important determining factor Retinal ischaemia
2. Sex: Females> males (4:3). Capillary leakage-
3. Poor metabolic control Microaneurysms
Haemorrnage
Retinal oedema
4. Heredity: It is transmitted as autosomal recessive trait. Hard exudates
Arteriovenous shunts
Other risk factors include Pregnancy, HTN, smoking, obesity, (Intraretinal microvascular
abnormalities-IRMA)
anaemia and hyperlipidaemia. Neovascularisation
Flowchart depicting pathogenesis of
diabetic retinopathy
Pathogenesis:
Microangiopathy
Hyperglycemia, in uncontrolled diabetes mellitus, is the
starting point for development of DR. Microvascular Microaneurysm Capilary leakage
Occlusion andhaemorrhage
Retinal ischaemia

Retinal oedema and Arteriovenous shunt Neovascularization

hard exudates formation
Pathogenesis of diabetic retinopathy

Classification of Diabetic
Ophthalmoscopic features
Retinopathy
Microaneurysms in the macular area (the earliest detectable
1. Non-proliferative lesion): These appear as red dots and leak fluid and also fluorescein
Diabetic Retinopathy dye on FFA. They look like cluster of Grapes at end of vascular twigs
(NPDR) Retinal haemorrhages: Both deep (dot & blot haemorrhages in outer -

plexiform layer) and superficial haemorrhages (flame-shaped-in

It can be mild, moderate, nerve fibre layer), occur from rupture of microaneurysms
severe & very severe (ETDRS Retinal oedema
Classification} Hard exudates (lipid deposition) -seen in macular area;
Dot and blot Cotton-wool spots- represent areas of nerve fibre infarcts
Venous abnormalities (beading, looping and dilatation) occur
haemorrhages

Microanwurysms
adjacent to area of capillary non-perfusion.
Hard exudales
Intraretinal microvascular abnormalities (IRMA) seen as fine
irregular red lines connecting arterioles with venules, represent A
V shunts
2. Proliferative diabetic Occurrence of neovascularization over the changes of very severe
retinopathy (PDR) NPDR is the hallmark of PDR. It results in the formation of:
 14 of 23
Fibrovascular epiretinal membrane Neovascularization .
formed due to condensation of Fibrous bands

connective tissue around the new

vessels
= Vitreous detachment and vitreous
Proliferative retinopathy
haemorrhage
1 permeability of the
Diabetic Macular Oedema (DME) occurs due to
retinal capillaries. It can be Clinically significant macular edema (CSME) or clinically
non-significant macular edema (non-CSME)
Clinico-angiographic classification of diabetici aculopathy:
1) Focal exudative maculopathy- FFA reveals focal leakage with
adequate macular perfusion
3. Diabetic maculopathy 2) Diffuse exudative maculopathy-FFA reveals diffuse leakage
(Changes in macular region) 3) Ischaemic maculopathy occurs due to microvascular blockage. FFA
-

shows areas of non-perfusion in the form of foveal avascular zone (FAZ)

4) Mixed maculopathy: In it combined features of ischaemic &&

exudative maculopathy are present

oCT (Optical coherence tomography) classification of DME:
1) Non-tractional DME - Ex: Cystoid macular oedema (CME)
2) Tractional DME-Ex: Vitreo-foveal traction (VFT)
It is the end result of uncontrolled PDR & is marked by complications
4. Advanced diabetic eye
such as: Persistent vitreous haemorrhage, Tractional retinal
disease (ADED)
detachment, and Neovascular glaucoma.
Management of Diabetic Retinopathy:
Screening for diabetic retinopathy-The recommendations for are as follows:
First examination, 5 years after diagnosis of type 1 DM & at the time of diagnosis in type 2 DM.
Every year, till there is no diabetic retinopathy or there is mild NPDR.
Every 6 months, in moderate NPDR.
Every 3 months, in severe NPDR.
Every 2 months, in PDR with no high-risk characteristics.
Investigations in a case of DR include: Urine examination, 24-hour urinary protein, Blood sugar
estimation, Renal function tests, Lipid profile, HbA1C, FFA & Optical coherence tomography (OCT)
Treatment of diabetic retinopathy:
*Metabolic control of diabetes melitus & associated risk factors:
Target blood glucose level: fasting <120 mg%, post-prandial <180 mg%, and HbAc <7%.
Target lipid profile (fasting): Cholesterol <200 mg%, Triglycerides <150 mg%, HDL >50 mg%,
and LDL <150 mg%.
Control of associated anaemia: Target hemoglobin >10 mg%.
Control of associated hypertension: Target blood pressure levels:130/80 mm Hg.
"Life style changes - regular exercises, stop smoking and alcohol consumption etc.
Intravitreal anti-VEGF (vascular endothelial growth factor) drugs: e.g, Bevacizumab (1.25 mg) and
Ranibizumab (0.5 mg).
Effects of the anti-VEGFs last for 4-6 weeks and frequent injections are warranted.
There is risk of endophthalmitis
*Intravitreal steroids-ex: triamcinolone acetonide (IVTA) (20 mg) restores inner retinal barier
-

and has some anti-VEGF effects as well. Used along with anti-VEGFs, in recalcitrant cases
There is risk of glaucoma, steroid induced cataract, endophthalmitis etc.
 Laser therapy:
GETDRS had recommended focal laser for focal DME and grid laser for diffuse DME.
Laser helps by stimulating the RPE pump mechanism and by inhibiting VEGF release.
G Laser therapy is performed using double frequency YAG laser 532 nm or argon green laser or
diode laser.
G Ex: Macular photocoagulation (Focal/ Grid) & Panretinal photocoagulation (PRP)
PRP causes destruction of hypoxic retina which is responsible for the production of vasoformative factors.
G Indications for PRP are:
PDR with HRCs
Neovascularization of iris (NVI)
Severe NPDR associated with: Poor
compliance for follow-up, Before
cataract surgery/YAG capsulotomy,
Renal failure, One eyed patient and
Protocols of laser application in diabetic retinopathy: A, focal treatment
B, grid treatment and; C, panretinal pholocoagulation
Pregnancy.
Surgical treatment (Pars plana vitrectomy (PPV)} is indicated in following cases:
Tractional DME with NPDR: PPV+ removal of posterior hyaloid.
Advanced PDR with dense vitreous haemorrhage: PPV+ removal of opaque vitreous gel&
endophotocoagulation.
Advanced PDR with extensive fibrovascular epiretinal membrane: PPV +removal of
fibrovascular epiretinal membrane & endophotocoagulation.
Advanced PDR with tractional retinal detachment: PPV with endophotocoagulation and
reattachment of detached retina + scleral buckling and internal tamponade using intravitreal
silicone oil or gases like sulphur hexafluoride (SF6)

2) Retinoblastoma aetiology, pathology, C/F & management [09, 05, 90].

-

a. Stages of retinoblastoma [15]

b. Amaurotic cat's eye reflex [96]
c. Discuss the differential diagnosis of 'Cat's eye' in children [90]
Ans.
Retinoblastoma is a common congenital malignant tumour of the retina occurring in early childhood.
Etiopathogenesis
Origin: Retinoblastoma is a tumour derived from neurosensory retina. It occurs due to the
proliferation of neural cells which have failed to evolve normally
of all cases, only 10% are familial (inherited by autosomal dominant mode) and the rest about 90% occur
sporadically.
Retinoblastoma (RB) gene has been identified as 14 band on the long arm of chromosome 13 (13q 14) and is a

'cancer suppressor gene.

Deletion or inactivation of both the normal alleles of RB gene by 2 mutations (Knudson's two hit hypothesis)
leads to formation of retinoblastoma.
Microscopic examination shows 2 types of cellular characteristics:
1) Poorly differentiated cells with large hyperchromatic nuclei and scanty cytoplasm along with
necrosis. They resemble the nuclear layer of the retina.
2) Well-differentiated tumour cells may be arranged in 2 special forms: a. Rosettes b. Fleurettes.
a. Rosettes
Flexner-Wintersteiner rosettes-specific for retinoblastoma.
Homer Wright rosettes- not specific for retinoblastoma (can also be seen in neuroblastoma
& medulloepithelioma).
 Pseudorosettes-tumour cells are clustered around blood vessels in necrotic retinoblastoma.
b. Fleurettes: specific for retinoblastoma-flower bouquet type aggregation of tumour cells.
Clear lumen Central neural fibres Area of necrosis

Flexner-Wintersteiner rosettes Homer Wright rosettes Pseudo-rosettes Fleurettes

Symptoms Signs
1. Leucocoria (MC)-Peculiar yellow or white Multiple polypoid masses are seen in the
pupillary reflex called the "amaurotic cat's eye". It fundus. There may be haemorrhages on the
is due to reflection of light from the yellow-white surface of the tumour.
mass in the retrolental area. The tumour mass may spread into the
Squint usually convergent is the 2nd MC presenting vitreous cavity.
symptom. Pseudohypopyon with esotropia
Nystagmus is seen in bilateral cases. (convergent squint).
4. Severe pain may be present due to intraocular Acute secondary glaucoma may occur if
pressure. tumour cells clog the trabecular
5. Enlargement of the globe with protrusion of the meshwork Large Eyeball
eyeball. (Buphthalmos)
Growth of RB 2 types:
-

1. Glioma exophytum-it grows outwards separating the retina from

the choroid. It resembles detachment of retina.
2. Glioma endophvtum-it grows inwards towards the vitreous.
Stages-4 clinical stages:
1) The quiescent stage-It lasts from six months to one year.
2) The glaucomatous stage-enlargement of the globe, proptosis and Exophytic retinoblastoma

severe pain a/w T IOP

3) The stage of extraocular extension -The tumour bursts through
the limbus followed by rapid growth.
4) The stage of metastasis-the tumour spreads by the:
Direct spread (MC route)-occurs via Optic nerve
Lymphatics-Pre-auricular and cervical lymph nodes.
Bloodstream via choroidal vessels. MC sites are bone & liver. Endophytic retinoblastoma
Differential Diagnosis
1) Pseudoglioma -Various conditions other than retinoblastoma, which present as leukocoria are
collectively called as 'Pseudoglioma'.
a. Congenital cataract
b. Inflammatory deposits in the vitreous following a plastic cyclitis or choroiditis.
C. Tuberculosis of the choroid specially the confluent type.

d. Toxocara infestation.
e. Persistent hyperplastic Primary vitreous.
1. Retrolental fibroplasia-it is common in premature babies due to hyperoxygenation.
2) Other causes Coats disease, Choroidal coloboma & Retinal dysplasia.
Diagnosis of Retinoblastoma
1. Examination under anaesthesia - Fundus examination of both eyes after full mydriasis with
atropine (direct as well as indirect ophthalmoscopy), measurement of lOP 8& corneal diameter.
2. LDH levels are raised in the aqueous humour.
3. Plain X-ray orbit -Calcification occurs in 75% cases of retinoblastomas.
4. Ultrasonography, CT scan and MRI confirm the diagnosis & also demonstrate extension to optic
nerve, orbit and CNS, if any
Treatment
Radiation and chemotherapy-Retinoblastoma highly radiosensitive tumour
is a
Standard doseCVE regimen: consists of 3-weekly, 6 cycles of Carboplatin (a86 mgl on day,
Vincristine (o.05 mg) on day 1 & Etoposide (5 mg) on day 1 and2
2. Cryotherapy-used for small tumours located anterior to equator
3. Photocoagulation by argon laser or diode laser- used for small tumour located posterior to
equator
4. Enucleation (removal of whole eyeball with optic nerve)-treatment of choice if tumour involves
more than half of the retina /Optic nerve is involved/ Glaucoma is present.
5. Exenteration of the orbit--t is done in stage 3. It is a mutilating surgical procedure > not preferred
by many surgeons. Hence only Palliative treatment (cVE regimen, Debulking, External beam radiotherapy) is
given in Stage 3 & 4
Prognosis
1) It is always bad if untreated.
2) It is fair if the eye is removed before the onset of extraocular extension.
3) Prognosis is poor if the optic nerve is involved, tumour cells are undifferentiated and in 3rd and 4th
clinical stages.
4) Spontaneous regression with massive necrosis and calcification may occur occasionally due to the
immunological mechanisms.

sQs
1. Retinal detachment-its classification, predisposing factors and clinical features. [17]
a. Tractional retinal detachment [13]
Ans.
Retinal detachment (RD} is the separation of neurosensory retina proper from the pigment epithelium.
Senile acute Predisposing Aphakia
posterioir reunal (Endodonesis)
Retinal tear vitreous degenerattons
Sensory detachment
retra
(acute PVD)
Serous
Classification Retinal break Trauma
gannnenonnteésas Ploment epithelum
Clinico-etiologically retinal detachment can be
classified into three Iypes: Choroid The degeneraled fluid vitreous seeps through the retinal
Rhegmatogenous or primary retinal detachment. Dreak and collects as subretinal fluid (SRF) between
2 Tractional retinal detachment Secondary the sensory retna and pigmentary epithelium.
Sdlera
retinal
3. Exudative retinal detachment detachment Primary reuinal delachmen Retinal detachment
Flowchart depicting pathogenesis of
rhegmatogenous retinal detachment

Rhegmatogenous RD Tractional RD Exudative (solid) RD

Etiology It occurs due to a break in the occurs due to retina being
It Exudative RD occurs due to
retina in the form of a hole or mechanically pulled away the retina being pushed away
tear. This allows the fluid from from its bed by the by a neoplasm or
 the vitreous to seep through contraction of fibrous tissue accumulation of fluid beneath
and raise the retina from its in the vitreous (vitreoretinal the retina
bed. tractional bands). Causes are:-
Systemic diseases:
Risk Factors are: Risk Factors are: preecclampsia, renal HTN,
Post-traumatic blood dyscrasias &
Age: elderly (40-60 yrs)
G Sex: M>F. retraction of scar tissue polyarteritis nodosa.
Proliferative diabetic Ocular diseases:
GMyopia. retinopathy Congenital:
G Aphakia & pseudophakia. Retinopathy of Nanophthalmos, choroidal
GRetinal degenerations: prematurity coloboma & FEVR;
Ex: Snail track Plastic cyclitis Inflammations:
degeneration, Lattice Sickle cell retinopathy, Harada's disease, posterior
degeneration etc. Vitreomacular traction scleritis, orbital cellulitis
syndrome, etc.
GTrauma.
Incontinentia pigmenti, Vascular diseases: Ex:
Senile posterior Retinal dysplasia, and
Coats disease
vitreous detachment Toxocariasis.
(PVD). Neoplasms, eg,
retinoblastoma (exophytic
type), haemangioma, etc.
Uveal effusion syndrome.
Choroidal neovascularization

Dark spots (floaters) in

front of the eye
Photopsia sensation of
-

flashes of light due to

irritation of retina
Localised relative loss in
Symptoms the field of vision (of Exudative RDcan be
detached retina) differentiated from
Sudden painless loss of Rhegmatogenous RD by:
vision occurs when the Absence of photopsia,
detachment is large GAbsence of holes, tears& folds
andcentral photopsia, floaters & Shifting fluid: changing
retinal tears position of the detached
Plane mirror
Presence of area with gravity is the
examination-no red
vitreoretinal bands hallmark of exudative
glow seen in the area of
with lesions of the retinal detachment
detached retina
Fundus examination causative disease On transillumination
done by direct & indirect GRetinal mobility is test a simple
ophthalmoscope severely reduced and detachment appears
Detached retina looks shifting fluid is absent transparent while solid
greyish-white & raised detachment is opaque
Signs above the surface FFA may show the
b. Detached retina is thrown source of fluid
into multiple folds which
oscillate with the eye
movement
Retinal vessels are dark
with no central light
reflex.
d. In total the retina
RD, is
funnel-shaped being8
 attached to the disc & ora
serrata.
e. A/w retinal degeneration,
plgmentation &
haemorrhage
Visual field charting
Scotomas are present
corresponding to the area
of the detached retina
Electroretinography
(ERG)-it is subnormal or
absent
Ultrasonography
confirms the diagnosis of
retinal detachment in
cases when retina cannot
be visualised, e.g., senile
mature cataract, corneal
opacity, vitreous opacities
Configuration Convex Concave Convex
1) To seal retinal breaks
Photocoagulation or
Cryosurgery or Diathermy Pars plana vitrectomy to
2) To approximate the cut the vitreoretinal
sclera, choroid and Treat the cause
tractional bands &
Treatment detached retina
Ex: Enucleation for
Internal tamponade with
Scleral buckling, intraocular tumourss
either a long-acting gas
Drainage of subretinal or silicon oil
fluid (SRF), Pars plana
vitrectomy etc.
Proliferative vitreoretinopathy (PVR), Complicated (posterior cortical) cataract,
Complications
uveitis and phthisis bulbi
----------
2. Retinitis pigmentosa [(15, 12, 03, 01]
Ans.
slow degenerative, hereditary disease of the retina predominantly affecting the rods more than
It is a
the cones.
Etiopathogenesis:
G Occurs due to consanguinity of the parents
G It appears in the childhood and progresses slowly causing blindness in middle age
GRetinitis pigmentosa is inherited as AD > AR> X-linked recessive disease tin the order of occurrence & Prognasis)
G It is Bilateral - both eyes are equally affected
G Sex: Males > Female
Associations of Retinitis pigmentosa:
Ocular associations: myopia, primary open-angle glaucoma, microphthalmos, conical cornea
(keratoconus) and posterior subcapsular cataract
Systemic associations Ex: Cockayne's syndrome, Refsum's syndrome, Usher's syndrome etc.
-

Symptoms
1) Night blindness is an early complaint (since rods are degenerated early and cones are involved late)
2) Tubular vision - Loss of peripheral vision with preservation of central vision.
3) Central vision is also lost ultimately after many years
Signs
1. Fundus examination
GRetina is studded with jet black spots (pigments) which resemble bone corpuscles with a spidenyoutine.

GRetinal arterioles become extremely attenuated and

thread-like.
Sheathingof
Retinal veins may have a sheath of pigment for part of retinal vein

their course.
Consecutive
Thinning & atrophy of retinal pigment epithelium (RPE) optic atrophy
GOptic disc-It shows features of optic atrophy, i.e, pale, Bone corpuscles
shaped pigment
wax-like, yellowish appearance. Visual retinitis pigmentosa
2. Visual fields

Annular or ring scotoma is present which progress to tubular vision.

There is complete blindness in the later stage.
3. Dark adaptation is increased due to rods dysfunction.
4. The electroretinogram (ERG) and electro-oculogram (EOG) are markedly
subnormal or completely extinguished early in the disease
Some Atypical forms of retinitis pigmentosa
GRetinitis pigmentosa sine pigmento: It is characterised by al the clinical features of typical retinitis
pigmentosa, except that there are no visible pigmentary changes in the fundus.
G Sectorial retinitis pigmentosa: It is characterized by involvement of only one sector of the retina
Differential Diagnosis- Congenital syphilis & Night blindness
Treatment: till date there is no effective treatment for the disease.
1. Measures to stop progression: vasodilators, placental extracts, transplantation of rectus muscles
into suprachoroidal space, acupuncture therapy, ultrasonic therapy etc.
2. Correct any refractive errors-prescribe glasses
3. Low vision aids may be useful. Ex: magnifying glasses' and 'night vision device
4. Systemic acetazolamide (500 mg po) for associated cystoid macular oedema
5. Stem cell therapy is still under trial
6. Rehabilitation of the patient
Prophylaxis: Genetic counselling is advised. There should be no consanguineous marriages
Prognosis: The central vision steadily becomes very poor in advanced life.
-=-=-=-=.

3. Hypertensive Retinopathy [15, 12, 08, 03]]

a. Keith & Wegner grading of hypertensive retinopathy [13]
b. Toxaemia of pregnancy retinopathy [95]
Ans.
Hypertensive retinopathy refers to fundus changes occurring in patients suffering from systemic HTN.
Pathogenesis: factors which play role in the pathogenesis of hypertensive retinopathy are:
3
1) Vasoconstriction of retinal arterioles & choroidal vesselschoroidal & RPE ischaemia >
hypertensive choroidopathy
Vasoconstriction of peripapillary choroid optic nerve head ischaemia hypertensive optic neuropathy
2) Arteriosclerotic changes in the vessels
3) Increased vascular permeability Gunn's sign Salus sig
results from hypoxia & is
responsible for haemorrhages,
Anteriolar Copper Bonne's
exudates, focal retinal oedema, narrowing wire reflex Sign

macular oedema etc. Nomal A-V crossing Stage t and 2 hypertensive retinopathy

Clinical Types Clinical Features

It seen in young patients with elastic retinal arterioles

is
1) Simple hypertension Generalized constriction of the arterioles occur
without sclerosis OSuperficial flame-shaped haemorrhages & cotton wool
exudates may be present.
Seen in elderly (above 50 yrs);
2) Hypertension with Changes at arteriovenous crossings are diagnostic (Gunn's sign,
involutionary (senile) Bonnet sign & Salu's sign)
sclerosis There is deposition of hard exudates
Retinal haemorrhages without any oedema may occur
*It is seen in young patients
a/w chronic glomerulonephritis & the ophthalmic picture is
known as 'albuminuric' or renal retinopathy
3) Chronic hypertension with
*The vessels are narrow and tortuous with nicking at AV
compensatory arteriolar
crossing
sclerosis
*Multiple retinal haemorrhages are seen with oedema, diffuse
cotton wool exudates (early), and hard exudates (later)
*Vision is seriously impaired
»Marked arteriolar narrowing with generalized oedema
exudates papilloedema, Disc pallor macular star along with
superficial flame-shaped haemorrhages & Focal intraretinal
periarteriolar transudates (FIPTs- due to breakdown of blood-
4) Malignant (acute) retinal barrier)
hypertensive retinopathy »Elschnig's spots (focal white spots) & Siegrist streaks (fibrinoid
necrosis) are formed
»Cotton wool spots are also more marked
a/w renal insufficiency
The visual prognosis is grave unless controlled medically
Keith & Wegner grading of hypertensive retinopathy

Grade FundusExamination
Mild arteriolar attenuation, particularly of small branches, with broadening of the
Grade 1
arteriolar light reflex
Marked arteriolar attenuation a/w deflection of veins at arteriovenous crossings
Grade 2
(Salus'sign)
Grade 2+
Copper wiring of arterioles, banking of veins distal to arteriovenous crossings
Grade 3 Bonnet sign), tapering of veins on either side of the crossings (Gunn sign)
Flame-shaped haemorrhages, cotton-wool spots and hard exudates are also
present
Grade 4 Grade 3 + silver-wiring of arterioles and papilloedema
 Management Normal
Mild cases require BP control only.
Silver wiring Arterial
Moderate cases (with retinal haemorrhages, microaneurysms & cotton-wool Grade 4
narrowing
Grade 1

spots): BP control +risk reduction therapy (e.g, cholesterol

lowering agents).
Bonnef's and
Accelerated hypertensive retinopathy (with bilateral disk swelling & gunns signs
lu sign

severe HTN) Patients: stepwise control of BP over a few hours to

Grade 3 Grade 2
avoid a sudden in BP which may perfusion of optic nerve
head and CNS (causing stroke). Hypertensive retinopathy

Retinopathy in Pregnancy-induced Hypertension (aka 'toxaemia of pregnancy'), is a disease of

PIH is characterised by BP, proteinuria and generalised oedema.
In PIH, Retinal changes are marked when BP rises above 200 mm of Hg
130
Narrowing of nasal arterioles Earliest change.
Persistent spasm of vessels causes retinal hypoxia 'cotton wool spots'
- & superficial haemorrhages.
Retinal oedema & exudation is marked & a/w 'macular star or flat macular detachment
Further progression of retinopathy occurs rapidly if pregnancy is allowed to continue.
Prognosis for retinal reattachment is good, as it occurs spontaneously within a few days of termination
of pregnancy.
Management
Changes of retinopathy are reversible and disappear after the delivery

If the patient responds well to conservative Mx, the pregnancy can be continued under dlose observation.
GAdvent of hypoxic retinopathy (cotton wool spots, retinal oedema and haemorrhages), however,
should be considered an indication for termination of pregnancy; otherwise, permanent visual loss or
even loss of life (of both mother and foetus) may occur.

4. Central Retinal Vein Occlusion. [10]

Ans. Retinal vein occlusions are more common than the artery occlusions.
Pressure on the vein by an atherosclerotic retinal artery can cause the occlusion
Predisposing factors: HTN, DM, Hyperviscosity of blood, TIOP, orbital cellulitis, orbital tumors etc.
Site of Oclusion: It is just behind the lamina cribrosa
Symptom: There is Painless sudden onset of impaired vision
Signs:
1) In ischemic CRVO
Retinal veins are dilated, engorged & tortuous. Obstruction to the outflow of blood and stagnation
Retina is covered with multiple haemorrhages (splashed
Rise in intravascular pressure
tomato appearance) & soft exudates.
RAPD Ppresent, Retinal oedema, abnormal leakage and haenmorrhage

Retinal edema
Formation of collaterals and neovasularisation
amplitude of b-wave of electroretinogram (ERG)
In late stages, Neovascularization may be seen at the disc (NVD) or in the periphery (NVE)
2) In non-ischemic CRVO: mild venous congestion, few superficial flame-shaped haemorrhages &
other mild lesions but no RAPD, relatively normal retina
Investigations:
Record Visual acuity, IOP
Gonioscopy to rule out neovascularization of angle (NVA).
Goldmann perimetry & ERG evaluation: to differentiate ischaemic vs non-ischaemic CRVO.
 should be done (to assess state of retinal perfusion) after resolution of retinal haemorrhage
FFA
Routine investigations: to look for predisposing factors
Complications
1. Neovascular glaucoma occurs at a later stage (usually within 3 months - aka 90 days Glaucoma)
due to sclerosis and neovascularisation at the angle of anterior chamber
2. Vitreous haemorrhage and subhyaloid haemorrhage may occur.
3. Complete blindness develops eventually
Differential Diagnosis:
Diabetic retinopathy is generally bilateral and CRVO is usually unilateral.
Ocular ischaemic syndrome (OIS) due to carotid occlusive disease has only dilated ve ins without tortuosity (in CRVo
tortuosity is also seen)
Treatment
1) Observation & monitoring in patients with mild to moderate visual loss (since CRVO resolves with almost
normal vision.)
2) For patientswith.marked visual loss: Intravitreal anti-VEGF drugs: e.g., Bevacizumab & Intravitreal
steroids- ex: triamcinolone acetonide: useful for associated CME & Neovascularisation
3) Treatment of Predisposing factors -Ex: HTN, DM
4) Neovascular glaucoma (NVG) can be prevented by PRP.
5) If NVG develops Pars plana placement of glaucoma drainage device (6DD)

5. Photoretinitis [05
Ans. Photoretinitis aka Solar retinopathy or eclipse retinopathy, refers to retinal injury induced by
direct or indirect sun viewing.
Etiology:
Religious sun gazing, solar eclipse observing, telescopic solar viewing, sun bathing and sun
watching in psychiatric disorders.
Causes other than sun exposure are: Welding arc exposure, Lightening & phototoxicity from
ophthalmic instruments like operating microscope.
Pathogenesis-Solar radiations damage the retina through:
Photochemical effects produced by UV rays& IR rays
Thermal effects may enhance the photochemical effects.
Clinical features
Symptomns Signs
Persistence of negative after-image Shortly after exposure a small yellow spot appear in
of the sun, progressing later into a the foveal region.
+ve scotoma & metamorphopsia. Later, central burnt-out hole in the pigment
Decreased vision which develops epithelium is seen-appears as a bean- or kidney-
within 1 to 4 hours after solar shaped pigmented spot with yellowish white centre
exposure, usually improves within 6 months in the foveal region.
In worst cases,typical macular hole may appear
Treatment:
There is no effective treatment for Photoretinitis, so emphasis should be on prevention.
Eclipse viewing should be discouraged unless there is proper use of protective eye wear filters (to
block UV & IR rays).
Prognosis is guarded, since some scotoma & loss in visual acuity by 1 or 2 lines mostly persists
 CONTENTS

Diseases of Cornea e 000000s0ssssse.

LOS. 3

SQs.. 9
VSQs. 16

www.17
Diseases of Vitreousceeee0eeecee0eeeeeeee0eeece
sQs ... 17
VSQs .. 18
Gmal 12:13 AM wed TT May

X 3 Cornea & Vitreous.pdf

VISeases or uorTea
LQs
1. Discuss symptoms, signs and treatment of herpes simplex keratitis [14]
a. Herpes Zoster Ophthalmicus [17]
b. 4 causes of Superficial Punctate Keratitis [15, 01]
C. Viral keratitis [12, 09]

d. Dendritic corneal ulcer [03, 95]

Ans.
Viral Keratitls
Most of the viruses tend to affect the epithelium of both the conjunctiva and cornea, hence the
typical viral lesions constitute the viral keratoconjunctivitis.
Causative Organisms: Herpes Simplex Virus (most common), herpes zoster & adenovirus keratitis (rare).
Herpes Simplex Keratitis
Etiology: HSV is a DNA virus.
HSV-1 is acquired by kissing or coming in contact with a patient of herpes labialis.
HSV-2 is transmitted to eyes of neonates through infected genitalia of the mother.
Iypes: Primary Herpes (mainly conjunctival lesions seen) & Recurrent Herpes (mainly corneal lesions seen)
Symptoms: Vesicles are seen on lips, nose, cornea (H5v-1 &genitals (Hsv-2
photophobia, visual acuity, ocular discomfort
Signs:
Skin lesions-Vesicles heal without scar formation.
Superficial punctate keratitis
Epithelial lesions occur due to active viral replication
-

1) Superficial punctate keratitis: many in head size plaques of epithelial cels

2) Dendritic ulcer with terminal buds
3) Confluent ulcer-Large geographical pattern type of ulcers
Stromal lesions Contluent
Denditic ulcer

Immune stromal keratitis: occurs due to Type 3 hypersensitivity

Necrotising stromal keratitis
Endothelial lesions -Disciform keratitis: disc shaped areas of deep stroma/endothelial edema -

ocCurs due to type 4 hypersensitivity. Discilom kerabbs

Metaherpetic keratitis -is not an active viral disease, but is a mechanical healing problem due to
persistent defects in the basement membrane of corneal epithelium which occurs at the site of a previous herpetic ulcer
Corneal Anaesthesia-due to 5h cranial nerve palsy
Diagnosis: By immunofluorescence of epithelial scrapings
Complications: Corneal opacity, Iritis and iridocyclitis
Treatment:
Topical Antivirals: Acyclovir-3% eye ointment 5 times daily for 10-14 days.
Topical Steroids can be given (except in epithelial lesions)
Debridement can be done for dendritic ulcers. This protects healthy epithelium from infection
For Metaherpetic keratitis- Promote healing by use of lubricants (artificial tears), bandage soft contact lens
and lid closure (tarsorrhaphy)
Atropine and warm compresses are useful in controlling iritis
Systemic Antivirals Oral acyclovir 40o mg BO 7
-
days. It is the method of choice in recurrent cases
Full thickness keratoplasty is done in cases of permanent corneal opacity. The eye must be quiet for a year at least
 Diseases of Cornea
LaS
1. Discuss symptoms, signs and treatment of herpes simplex keratitis [14]
a. Herpes Zoster Ophthalmicus [17]
b. 4 causes of Superficial Punctate Keratitis [15, 01]
c. Viral keratitis [12, 09]
d. Dendritic corneal ulcer [03, 95]
Ans.
VMiral Keratitls
Most of the viruses tend to affect the epithelium of both the conjunctiva and cornea, hence the
typical viral lesions constitute the viral keratoconjunctivitis.
Causative Organisms: Herpes Simplex Virus (most common), herpes zoster & adenovirus keratitis (rare).
Herpes Simplex Keratitis
Etiolog: HSV is a DNA virus.

HSV-1 is acquired by kissing or coming in contact with a patient of herpes labialís.

G HSV-2 is transmitted to eyes of neonates through infected genitalia of the mother.
Types: Primary Herpes (mainly conjunctival lesions seen) & Recurrent Herpes (mainly corneal lesions seen)
Symptoms: Vesicles are seen on lips, nose, cornea (Hsv-1)& genitals (HSv-2
photophobia, visual acuity, ocular discomfort
Signs:
Skin lesions - Vesicles heal without scar formation.
Superficial punctate keratitis
Epithelial lesions- occur due to active viral replication 7
1) Superficial punctate keratitis: many pin-head size plaques of epithelial cells
2) Dendritic ulcer with terminal. buds
3) Confluent ulcer-Large geographical pattern type of ulcers
Contluent uicer
Stromal lesions Denditic ulcer

Immune stromal keratiti: occurs due to Type 3 hypersensitivity

Necrotising stromal keratitis
Endothelial lesions-Disciform keratitis: disc shaped areas of deep stroma/endothelial edema -

occurs due to type 4 hypersensitivity. Discifom kerabts

Metaherpetic keratitis -
not an active viral disease, but is a mechanical healing problem due to
is

persistent defects in the basement membrane of corneal epithelium which occurs at the site of a previous herpetic ulcer
Corneal Anaesthesia-due to 5 cranial nerve palsy

Diagnosis: immunofluorescence of epithelial scrapings

By
Complications: Corneal opacity, Iritis and iridocyclitis
Treatment:
Topical Antivirals: Acyclovir-3% eye ointment 5 times daily for 10-14 days.
Topical Steroids can be given (except in epithelial lesions)
Debridement- can be done for dendritic ulcers. This protects healthy epithelium from infection
For Metaherpetic keratitis - Promote healing by use of lubricants (artificial tears), bandage soft contact lens
and lid closure (tarsorhaphy)
Atropine and warm compresses are useful in controlling iritis
Systemic Antivirals Oral acyclovir a00 mg BDx7 days. It is the method of choice in recurrent cases
Full thickness keratoplasty is done in cases of permanent corneal opacity. The eye must be quiet for a year at least
 Herpes Zoster Opthalmicus (aka Shingles): It is is an acute infection of Gasserian ganglion of the S 4 of 18
cranial nerve by the varicella-zoster virus (VZV). It is a/w chickenpox infection in childhood.
>Pathogenesis:
often occurs in elderly with cellular immunity, e.g. as in diabetics, alcoholics, cancer
It
patients etc.
It is always unilateral; affecting the gasserian ganglion from where the Unilateral skin
esions on face
virus travels down the ophthalmie (Vi) branch of sth nerve affecting Hutchinson's
the dermatomes supplied by it. UIe

Herpes zoster
Symptoms:
GFever, malaise & Severe neuralgic pain - a/w Acute phase lesions
Rows of vesicular eruption along Vi nerve. Vesicles rupture & cause pitted scar.
GSkin of lid and face becomes red and oedematous Dendritic lesion
apering ends)
Signs
Conjunctivitis
Slit-lamp examination reveals: Superficial punctate keratitis, Nummular keratits

pseudo-dendritic ulcers (no terminal buds), Nummular keratitis & Disciform keratitis
Hutchinson's rule: More chances of HZO if the rash affects the tip of the nose (nasociliary nerve)
Corneal Anaesthesia
Complications: Iridocyclitis, scleritis, Secondary glaucoma, postherpetic neuralgia, cranial nerve
palsies (3rd, 6th, 7th cranial nerves)
Treatment
Topical Antivirals: Acyclovir-3% eye ointment 5 times daily for 10-14 days
Systemic Antivirals-Oral acyclovir 800 mg is given 5 times daily for 14 days
Topical steroids are useful particularly in disciform keratitis, scleritis and iridocyclitis
Systemic steroids are indicated in cranial nerve palsies
Analgesics & anti-inflammatory Drugs - mephenamic acid + PCM or even pethidine (in severe cases)
Antibiotic skin ointment is applied over the skin lesion to prevent secondary infection.
Topical atropine is applied in cases of keratitis, iridocyclitis, and scleritis
Surgical treatment
GLateral tarsorrhaphy
Full thickness keratoplasty is required for visual rehabilitation of patients with dense
scarring. The eye must be quiet for a year at least.

Causes ofSuperficial Punctate Keratitis

1. herpes simplex, herpes zoster, adenovirus, pharyngo-conjunctival fever etc.
Viral infections
2. Chlamydial infections-trachoma and inclusion conjunctivitis.
3. Toxic lesions e.g., due to staphylococcal toxin
4. Trophic lesions e.g., exposure keratitis and neuroparalytic keratitis
5. Allergic lesions e.g, vernal keratoconjunctivitis.
6. Irritative lesions e.g., effect of some drugs such as idoxuridine.
7. Disorders of skin and mucous membrane, such as acne rosacea and pemphigoid.
8. Dry eye syndrome, i.e., keratoconjunctivitis sicca.
9. Specific types of idiopathic SPK e.g., Thygeson's superficial unctate keratitis.
p

10. Photo-ophthalmitis.
 2. Describe aetiology, clinical features, Rx & complications of Bacterial Corneal Ulcer [14, 13, 10]
a. Nebula [14]
Ans.
Etiology: There are 2 factors in the production of purulent corneal ulcer: Damage to corneal
epithelium & Infection of the eroded area.
However, 3 pathogens can ulcerate even the intact corneal epithelium N. gonorrhoeae, N. meningitidis & C. diphtheriae.
Corneal epithelial damage: It may occur in following conditions:
a. Corneal abrasion due to small foreign body, trivial trauma in contact lens wearers.
b. Epithelial drying as in xerosis and exposure keratitis.
c. Necrosis of epithelium as in keratomalacia.
d. Desquamation of epithelial cells as a result of corneal oedema as in bullous keratopathy.
e. Epithelial damage due to trophic changes as in neuroparalytic keratitis.
Sources of infection include:
GExogenous source like conjunctival sac, lacrimal sac (dacryocystitis), infected foreign bodies and
waterborne or airborne infections.
From the ocular tissue Ex: diseases of the conjunctiva readily spread to corneal epithelium,
-

those of sclera to stroma, and of the uveal tract to the

endothelium of cornea.
Causative organisms: Staphylococci, Pseudomonas,
Streptococcus pneumonia, Enterobacteriaceae and Neisseria.
Pathogenesis of corneal ulcer; Pathological changes can be described
under 4 Stages:
1. Stage of progressive infiltration,
B
2. Stage of active ulceration,
3. Stage of regression, and
4. Stage of cicatrization.
Course of corneal ulcer may take 1 of the 3 forms:
a. Ulcer may become localised and heal,
b. Penetrate deep leading to corneal perforation, and
C. Spread fast to involve whole cornea as sloughing corneal ulcer. D

Clinical features: Corneal ulcers may manifest with/without Pathology of cormeal ulcer:A, stage of progressive
infiltration; B, stage of active ulceration; C, stage o
regression,D, stage of cicatrization
hypopyonA
Symptomns Signs
1) Swelling of lids &
Blepharospasm.
1. Pain & foreign body sensation 2 Conjunctiva shows hyperaemia and ciliary congestion.
3) Corneal ulcer
-
ocCur due to mechanical effects of lids
and toxins on the V, nerve endings. Epithelial defect seen in early stage
Watering from the eye occurs GYellowish-white ulcer
due to reflex hyperlacrimation. GCan be oval or irregular in shape
Photophobia -
occurs due to GMargins of the ulcer are swollen and over hanging
stimulation of nerve endings. GFloor is covered by necrotic material
Blurred vision results from GStromal oedema is present surrounding the ulcer area
corneal haze. 4) Anterior chamber may show pus (hypopyon).
5. Redness of eyes -occurs due to 5) Iris may be slightly muddy in colour.
congestion of circumcorneal vessels 6) Pupil may be small due to associated toxin induced iritis.
|7) 1OP may sometimes be raised (inflammatory glaucoma).
Complications of Corneal Ulcer
1) Toxic iridocyclitis - occurs due to absorption of toxins in the anterior chamber.
2) Secondary glaucoma -occurs due to fibrinous exudates blocking the angle of anterior chamber
(inflammatory glaucoma).
3) Descemetocele - develop if ulcer extend up to Descemet's membrane. This is a sign of impending
perforation and is a/w severe pain.
4) Perforation of corneal ulcer: Sudden strain due to cough, sneeze or spasm of orbicularis muscle may convert
impending perforation into actual perforation.
5) Corneal scarring > permanent visual impairment.
Depending upon the clinical course of
ulcer, corneal scar noted may be nebula,
macula, leucoma, ectatic cicatrix or
anterior staphyloma.
When corneal ulcer involves Bowman's
Nebula Macu eucom
membrane and few superficial stromal
lamellae, the resultant scar is called a 'nebula'.
MANAGEMENT OF Herniation
Descemets
omembrane
Protrusionof
CORNEAL ULCER cormea
Normal IODP
Leucoma
Clinical evaluation: 1 1OP

history taking, physical

examination & Ocular Anterior staphyloma Ectatic cicatrix
Descemetocele

examination
LaboratoryInvestigations
1) Routine investigations - CBP, blood sugar,
complete urine and stool examination
2) Microbiological investigations-to identify
optical effects of Leucoma
causative organism and guide the treatment Optical effect of nebula stops al ignt which tails upon t
loss of bnghtness but not definitbon
iTegular astigmatism
Treatment
I. Treatment of Uncomplicated corneal ulcer
Initial therapy should be with any of the following 2 drugs:
a. Fortified Cefazoline 5% & Fortified tobramycin, 1.3%
Topical or
1. Specific antibiotics| b. Fortified vancomycin 5%, and one of Fa (0.3%% ciprofloxacin, or 0.3%
treatment ofloxacin or 0.5% moxifloxacin).
If the response is poor,immediatelychange Abx as per sensitivity report
Systemic a cephalosporin & an aminoglycoside or ciprofloxacin (750 mg BD) may
antibiotics |be given in fulminating cases with perforation
Cycloplegic drugs To reduce pain from ciliary spasm and
2. Non- -1% atropine eye To prevent the formation of synechiae from iridocyclitis.
specific drops Atropine also increases the blood supply to anterior uvea
Supportive Systemic NSAIDs Paracetamol & ibuprofen relieve the pain & oedema
treatment Multi-Vitamins (A, Help in early healing of ulcer
B-complex and C)

3. General Hot fomentation -gives comfort, reduces pain and causes vasodilatation.
measures Dark goEgles may be used to prevent photophobia.
TRest, good diet and fresh air may have a soothing effect
11. Treatment of non-healing cornealulcer:
1) Removal of any known cause of non-healing ulcer
Local causes: 10P, misdirected cilia, impactedforeign body, dacryocystitis etc.
Systemic causes: DM, severe anaemia, malnutrition, patients on systemic steroids etc.
2) Mechanical debridement of ulcer to remove necrosed material may hasten the healing.
3) Cauterisation of the ulcer with pure carbolic acid or 10-20% trichloroacetic acid.
4) Bandage soft contact lens.
5) Peritomy, i.e., severing of perilimbal conjunctival vessels can be performed when excessive corneal
vascularization is hindering healing.

. Treatment of impending perforation:

1. No strain: avoid sneezing, coughing &straining during stool, etc.
2. Pressure bandage should be applied to give some external support
3. IOP by simultaneous use of acetazolamide, IV mannitol, oral glycerol &0.5%timolol eye drops,
4. Tissue adhesive glue such as cyanoacrylate is helpful in preventing perforation.
5. Bandage soft contact lens may also be used.
6. Cover the cornea with Conjunctival flap to give support to the weak tissue.
7. Amniotic membrane transplantation may also be considered as an option.
8. Penetrating therapeutic keratoplasty (tectonic graft) may be undertaken in suitable cases

IV. Treatment of perforated corneal ulcer:

use of tissue adhesive glues, covering with conjunctival flap,
Depending upon the size of perforation, measures lke
bandage soft contact lens or therapeutic keratoplasty should be undertaken.
Best option is an urgent tectonic keratoplasty

3. Describe the aetiology, clinical features, and treatment of interstitial keratitis [15, 02, 96]
a. Causes of Interstitial Keratitis [17]
Ans.
Interstitial keratitis is inflammation of only Corneal Stroma without primary involvement of the
epithelium or endothelium
Causes: Congenital Syphilis, Acquired syphilis, Cogan Syndrome, Trypanosomiasis, Malaria, TB,
Leprosy, sarcoidosis etc.
Syphilitic (Luetic) Interstitial Keratitis.
Pathogenesis; It is a manifestation of local antigen-antibody reaction.
G Treponema pallidum invades the cornea and sensitizes it in the foetal stage.
GLater, fresh invasion by Treponema excites the inflammation in the sensitized cornea.
Clinical features
The disease is generally B/L in inherited syphilis and U/L in acquired syphilis
In Congenital Syphilis-Hutchinson's triad: interstitial keratitis, Hutchinson's teeth & vestibular
deafness.
Clinical features of interstitial keratitis can be divided into 3 stages: initial progressive stage, florid
stage and stage of regression.
1. Initialprogressive stage - pain, lacrimation, photophobia, blepharospasm and circumcorneal injection
followed by a diffuse corneal haze (ground glass appearance). This stage lasts for about 2 weeks.
 2. Florid stage: In this stage, eye remains acutely inflamed. Deep vascularization of cornea develops.
Since,
these vessels are covered by hazy cornea, they look dull reddish pink which is called Salmon patch
appearance Superficial vessels and conjunctiva heap at limbus in
the the form of epulit. This stage lasts
for about 2 months.
3. Stage of regression: The acute inflammation resolves. This stage may last for about 1 to 2 years.
Diagnosis: +ve VDRL or Treponema pallidum immobilization test confirms the diagnosis.
Treatment
Topical treatment for keratitis:
Topical corticosteroid drops e.g., dexamethasone 0.1% drops
Atropine eye ointment
Dark goggles to be used for photophobia.
Keratoplasty done in cases where dense corneal opacities are left.
Systemic treatment: Penicillin & steroids.
Tuberculous Interstitial Keratitis
The features of tubercular interstitial keratitis are similar to syphilitic interstitial keratitis except
that it is more frequently unilateral and sectorial (usually involving a lower sector of cornea).
Treatment consists of systemic antitubercular drugs, topical steroids and cycloplegics.
Cogan's Syndrome
comprises the interstitial keratitis of unknown etiology, acutetinnitus, vertigo, and deafness.
It
It typically occurs in middle-aged adults and is often bilateral.
G Treatment: topical and systemic corticosteroids.

4. Hypopyon Corneal ulcer -

Etiology, signs, symptoms, laboratory findings, Dx & treatment [08, 03]
a. Ulcus serpens [16
Ans.
Etiopathogenesis: Keratic
precprtates
Cormeal ulcer
Causative organisms: Comeai ulca

Hypopyon corneal ulcer' =Ulcus Serpens Hypopyonn

Pneumococcus
Corneal ulcer with hypopyon' caused by
other organisms such as Staphylococci, Streptococci, Gonococci, Moraxella and Pseudomonas.
Factors predisposing to development of hypopyon: chronic dacryocystitis {pneumococcus}, old
people, alcoholics etc.
Mechanism of development of hypopyon: Corneal ulcer is associated with some iritis owing to
diffusion of bacterial toxins. When the iritis is severe the outpouring of leucocytes from the vessels is
so great that these cells gravitate to the bottom of the anterior chamber to form a hypopyon. Once
the ulcerative process is controlled, the hypopyon is absorbed.
Clinical features: same as bacterial corneal ulcer.
During initial stage of ulcus Serpens, there is little pain. As a result, the treatment is often unduly
delayed.
Characteristic features of ulcus Serpens are:
It is a greyish white or yellow disc-shaped ulcer occurring nearthe centre of cornea
Ulcer has a tendency to creep over the cornea in a serpiginous fashion.
Violent iridocyclitis is commonly associated with a definite hypopyon.
Hypopyon increases in size very rapidly and often results in secondary glaucoma.
Ulcer spreads rapidly and has a great tendency for early perforation.
 Management ofhvpopyoncornealulcer: same as for other bacterial corneal ulcer
Special points which need to be considered are:
Secondary glaucoma should be anticipated and treated with Anti-glaucoma drugs
Source of infection, i.e., chronic dacryocystitisif detected, should be treated by dacryocystectomy

sQs
1) Mention various causes of loss of Corneal Transparency. Write a note on Vascularization of Cornea.
(171
a. Adherent leucoma [13, 03]
b. Leucoma grade corneal opacity [06]
C. Corneal opacity [05]

Ans.
The word 'corneal opacification' literally means loss of normal transparency of cornea.
Cornea is an avascular Causes of Corneal Opacity
Tears in the endothellum and Descemet's membrane (STUMPED) Corneal ulcers and inflammation (STUMPED)L
structure. Small loops derived from the Congenltal
anterior ciliary vessels invade its periphery for SSclerocornea
about 1 mm. Actually, these loops are not in T:Tears In Descemet's membrane
the cornea but in the subconjunctival tissue U:Ulcer
which overlaps the cornea. M: Metabolic conditions such as mucolipidosis, mucopolysaccharidosis
P:Posterior corneal defect such as Peters anomaly
E Endothelal dystrophy such as congenital hereditary endothelial dystrophy

Clinical
D: Dermoid.
features: Loss of Acqulred
Post-trauma following chemical injuries, mechanical injuries
vision (when dense opacity Corneal degenerations
Postinfection or inflammation of cornea following infective or non-infective keratitis.
covers the pupillary area) or
blurred vision (due to astigmatic effect)
Tvpes of cornealopacity
1. Nebular corneal opacity: It is a faint opacity-occurs
due to superficial scars
2. Macular corneal opacity: It is a semi-dense opacity
produced when scarring involves about half the A
Diagrammatic depiction of corneal opacity A
corneal stroma. Nebular: B, Macular; C, Leucomatous: D, Acherent ieucoma
3. Leucomatous corneal opacity (leucoma simplex): It is a
dense white opacity which results due to scarring of more than half of the stroma.
4. Adherent leucoma: It results when healing occurs after perforation of
cornea with incarceration of iris
5. Corneal facet: Sometimes, the corneal surface is depressed at the site of
healing (due to less fibrous tissue); such a scar is called facet.
6. Kerectasia: In this condition, corneal curvature is at the site of opacity
(bulge due to weak scar).
7. Anterior staphyloma: {refer 6th sQ}
Secondary changes seeninlong-standingcornealopacity: hyaline
degeneration, calcareous degeneration, pigmentation and atheromatous Anterior staphyloma:

ulceration.
Treatment
1) Optical iridectomy- done in cases with central macular or Leucomatous corneal opacities,
provided vision improves with pupillarydilatation.
2) Phototherapeutic keratectomy (PTK) performed with excimer laser is useful in superficial (nebular)
corneal opacities
3) Keratoplasty can be done in uncomplicated cases where optical iridectomy is not of much use.
4) Cosmetic-coloured contactlens BEST option for an eye with ugly scar having no potential for
vision
5) Tattooing of scar- suitable only for firm scars in a quiet eye without useful vision

2) Corneal edema [16]

Ans. The water content of normal cornea is 78%. It is kept constant by a balance of factors which draw
water in the cornea (e.g., 1OP and swelling pressure of the stromal matrix) and the factors which draw
water out of cornea (viz. the active pumping action of corneal endothelium, and the mechanical
barrier action of epithelium and endothelium).
Disturbance of any of the above factors leads to corneal oedema, wherein its hydration becomes
above 78%, central thickness increases and transparency reduces.
Causes of corneal oedema
1) IOP
2) Endothelial damage
Due to injuries, such as birth trauma (forceps delivery), surgical trauma during intraocular
operation, contusion injuries and penetrating injuries.
Due to corneal dystrophies such as, Fuchs dystrophy, congenital hereditaryendothelial
dystrophy and posterior polymorphous dystrophy.
GSecondary to inflam-mations such as uveitis, endophthalmitis and corneal graft infection.
3) Epithelial damage due to mechanical injuries, chemical burns, radiational injuries, thermal
injuries, inflammation and infections.
Clinical features
Initially there occurs stromal haze with reduced vision.
Permanent oedema with epithelial vesicles and bullae formation (bullous keratopathy) - In long-
standing cases with chronic endothelial failure (e.g., in Fuch's dystrophy) there occurs.
This is associated with marked loss of vision, pain, discomfort and photophobia, due to periodic
rupture of bullae.
Treatment
1) Treat the cause wherever possible, e.g., raised 1OP and ocular inflammations.
2) Dehydrate the cornea using:
Hypertonic agents e.g., 5% sodium chloride drops.
Hot forced air from hair dryer.
3) Therapeutic soft contact lenses may be used to get relief from discomfort of bullous keratopathy.
4) Penetrating keratoplasty is required for longstanding cases of corneal oedema, non-responsive to
conservative therapy.

3) Indications of Keratoplasty [11]

a. Indications for Lamellar Keratoplasty [11]
b. Types of Keratoplasty [10]
Ans.
Keratoplasty, also called corneal grafting or corneal transplantation, is a surgery in which the
patient's diseased cornea is replaced by the healthy clear cornea.
Types ofKeratoplasty
A. Autokeratoplasty
1) Rotational keratoplasty, in which patient's own cornea is trephined and rotated to transfer the
pupillary area having a small corneal opacity to the periphery.
2) Contralateral keratoplasty: It is indicated when cornea of one eye of the patient is opaque and
the other eye is blind due to posterior segment disease (e.g., optic atrophy & retinal
detachment, etc.) with clear cornea
B. AllograftingorAllo-keratoplasty In it, patient's diseased cornea is replaced by the donor's healthy
cornea. It can be of following types:
1) Penetrating Keratoplasty (PK) (tull-thickness grafting)- indicated in pseudophakic bullous
keratopathy
2) Lamellar Keratoplasty
(partial-thickness
grafting) which may be
G DALK = Deep Excision of Excision of Fixation of Fioxation af
Excision of
diseased cornea donor's dlear grat
anterior lamellar donor eye donor's cornea donor's clear graft

keratoplasty- Schematic diagram of technique of penetrating keratoplasty

corneal tissue is removed upto Descemet's membrane - indicated in keratoconus.

DSEK = Descemet's stripping endothelial keratoplasty Removal of only endothelium &
Descemet's membrane- indicated after the surgical trauma (Ex: phacoemulsification).
3) Small patch graft (for small defects), which may be full thickness or partial thickness.
Indications of Keratoplasty PKP DALK

1) Optical, i.e., to improve vision in-corneal opacity,

bullous keratopathy, corneal dystrophies, advanced
keratoconus. DSAEK

2) Therapeutic, i.e., to replace inflamed cornea not

responding to conventional therapy.
3) Tectonic graft, i.e., to restore integrity of eyeball e.g.,
after corneal perforation and in marked corneal thinning.
4) Cosmetic, i.e., to improve the appearance of the eye
Donor tissue: The donor eye should be removed as early as possible (within 6 hours of death). It
should be stored under sterile conditions.
Complications of Keratoplasty
Earlycomplications: flat anterior chamber, iris prolapse, infection, secondary glaucoma, etc.
Latecomplications - graft rejection, recurrence of disease and astigmatism.

4) Keratoconus [09, 01]

Ans.
Keratoconus (conical cornea) is a non-inflammatory ectatic condition of cornea.

Etiopathogenesis: It is still not clear. starts at puberty and progresses

It usually
slowly with thinning and ectasia which occur as a result of defective synthesis of
mucopolysaccharide and collagen tissue.
 Clinical features 12 of 18
Symptoms Signs
1) Window reflex is distorted.
2) Placido disc examination shows irregularity ofthe circles
3) Slit-lamp examination thinning and ectasia of central cornea, opacity atthe
Patient apex and Fleischer's ring at the base of cone, folds in Descemet's and Bowman's
presents with membranes.
a defective
Very fine, vertical, deep stromal striae (Vogt lines) which disappearwith
vision due to external pressure on the globe are peculiar feature.
progressive 4) Retinoscopy reveals a yawning reflex (scissor reflex) and irregular astigmatism.
myopia and 5) On distant direct ophthalmoscopy an annular dark shadow (due to total internal
irregular reflection of light) is seen which separates the central and
astigmatism, peripheral areas of cornea (oil droplet reflex).
which does 6) Munson's sign bulging of lower lid when patient looks down.
-

not improve 7) Keratometric values are increased {Normal value is 45 D) and

fully despite based on it the severity of keratoconus is graded as: mild (< 48 D),
Munson's sign

full correction
moderate (48-54 D), and severe (>54 D).
with glasses 8) Corneal topography, i.e., study of shape of corneal surface, is the most sensitive
method for detecting early keratoconus, Forme fruste refers to the earliest
subclinical form of keratoconus detected on topography
Morphological classification: Depending upon the size & shape of the cone, the keratoconus is of 3 types:
1) Nipple cone has a small size (<5 mm) and steep curvature.
2) Oval cone is larger (5-6 mm) and ellipsoid in shape.
3) Globus cone is very large (>6 mm) and globe like.
Complications: Rupture of Descemet's membrane Acute
Rizautis sign=
hydropssuddencorneal oedema, marked defective Arrouhead pattern of light ove
nasal imbus
vision, pain, photophobia and lacrimation
Associations ofKeratoconus:
Ocular conditions e.g, ectopia lentis, congenital cataract, aniridia, retinitis pigmentosa, and vernal
keratoconjunctivitis (VKC)
Systemic conditions e.s., Marfan's syndrome, atopy, Down's syndrome, Ehlers-Danlos syndrome,
osteogenesis imperfecta and mitral valve prolapse.
Treatment options:
1. Spectacle correction may improve vision in early cases.
2. Contact lenses (rigid gas permeable) also improve the vision in early cases.
GIn early to moderate cases a specially designed scleral contact lens (Rose-K) may be useful.
3. Intacs, the intracorneal ring segments, are also useful in early to moderate cases.
4. C3R-Corneal collagen cross linking with riboflavin and UV-A rays-to slow the progression ofdisease.
5. Keratoplasty is required in later stages.

5) Staphyloma [07]
a. Types of Staphylomas [03]
Ans.
Staphyloma refers to a localised bulging of weak and thin outer tunic of the eyebal (cornea or sclera),
lined by uveal tissue which shines through the thinned out fibrous coat.
Iypes: Anatomically, it can be divided into anterior, intercalary, ciliary, equatorial and posterior
staphyloma.
1) Anterior staphyloma: An ectasia of pseudocornea (the scar formed
from organised exudates and fibrous tissue covered with epithelium) which results
after total sloughing of cornea, with iris plastered behind it is
called anterior staphyloma.
2) Intercalary staphyloma: It refers to the localised bulge in limbal
area lined internally by the root of iris and the anterior most part
of ciliary body. It results due to ectasia of weak scar tissue
formed at the limbus, following healing of a perforating injury or
a peripheral corneal ulcer.
3) Ciliary staphyloma: As the name implies, it is the bulge of weak
sclera lined by the ciliary body.
Its common causes are thinning of sclera after a perforating Staphylomas (diagrammatic depiction) A,
Intercalary B. Cillary C, Equatorlal; D, Posterior
injury, scleritis, developmental glaucoma and end stage
primary or secondary glaucoma.
4) Equatorial staphyloma: it results due to bulge of sclera lined by the choroid in the equatorial
region.
Its causes are scleritis and degeneration of sclera in pathological myopia and chronic
uncontrolled glaucoma.
5) Posterior staphyloma. It refers to bulge of weak sclera lined by the choroid behind the equator.
Here again the common causes are pathological myopia (most common cause), posterior
scleritis and perforating injuries. It is diagnosed on ophthalmoscopy

6) Fungal Keratitis [O5]

Ans.
Etiology
Causative Organisms:
G Filamentous fungi: e.g
Septate fungi: Aspergillus, Fusarium, Alternaria, Penicilium etc.
Non-septate fungi: Mucor and Rhizopus.
G Yeasts e.g., Candida and Cryptococcus.
G Dimorphic fungi- histoplasma, coccidioides and Blastomyces
GFungi responsible for mycotic corneal ulcers: Aspergillus (most common), Candida & Fusarium.
Modes of infection
Injury by vegetative material such as crop leaf, branch of a tree etc.- seen in field workers
especially during harvesting season.
Injury by animal tail
Secondary fungal ulcers are common in patients who are immunosuppressed system all or
locally such as patients suffering from dry eye, herpetic keratitis, bullous keratopathy or
postoperative cases of keratoplasty.
Role of antibiotics and steroids: Antibiotics disturb the symbiosis between bacteria and fungi; and
the steroids make the fungi facultative pathogens which are otherwise symbiotic saprophytes.
Hence, excessive use of these drugs predisposes the patients to fungal infections.
Clinical features
symptoms are similar to the central bacterial corneal ulcer (refer 2nd LO), but in general they are less
marked than the equal-sized bacterial ulcer and the overall course is slow.
Signs.
 Corneal ulcer is dry-looking, greyish white, with elevated rolled out margins.
Pigmented ulcer (brownish) can be seen in some species of fungi, e.g., dermatiaceous fungi.
Feathery finger-like extensions are present into the surrounding stroma under the intact epithelium.
Sterile immune ring (yellow line of demarcation) present where fungal antigen & host antibodies meet.
Multiple, small satellite lesions may be present around the ulcer.
Usually, a big hypopyon is present even if the ulcer is very smal. Unlike bacterial ulcer, the hypopyon may
not be sterile as the fungi can penetrate into the anterior chamber without perforation.
Endothelial plaque, composed of fibrin and leucocytes, may be located under the stromal lesion.
Perforation in mycotic ulcer is rare but can occur.
Corneal vascularization is conspicuously absent in pure mycotic ulcer.
Satelite esions
Diagnosis
1. Typical clinical manifestations associated with history of injury by
omea
vegetative material are highly suspicious of a mycotic corneal ulcer lcer

2. Chronic ulcer worsening inspite of most efficient treatment should

arouse suspicion of mycotic involvement. HYpopyon

Lab investigations: include examination of wet KOH, Gram's and Fungal comeal ulcer

Giemsa-stained films for fungal hyphae and culture on Sabouraud's agar medium.
4. PCR for rapid results.
Treatment
Specific treatment with Antifungals
>Topical antifungal eyedrops should be used for a long period (6 to 8 weeks).
Ex: Natamycin (5%), Amphotericin B (01 to 0.3%), Fluconazole (0.2 etc.
Nystatin (3.5%) eye ointment, five times a day is effective against Candida.

Intracorneal administration of voriconazole in cases with intraocular extension or anterior

chamber involvement.
Systemic antifungal drugs in severe cases of deeper furngal keratitis Tablet fluconazole or
-

ketoconazole or voriconazole may be given for 2-3 weeks

Non-specific treatment-similar to that of bacterial corneal ulcer (refer 2d LO).
Therapeutic penetrating keratoplasty is done non-responsive cases.

7) Exposure keratitis (05, 98]

Ans.
occurs when eyes are covered jnsufficiently by the lids (Lagophthalmos).
It
Causes:
1. Extreme proptosis due to any cause will allow inadequate closure of lids.
2. Symblepharon caúsing lagophthalmos
3. Bell's palsy or any other cause of facial palsy.
4. Ectropion of severe degree.
5. Deep coma a/w inadequate closure of lids.
6. Physiological lagophthalmos: Lagophthalmos during sleep may occur in healthy individuals
Pathogenesis: Due to exposure the corneal epithelium dries up desiccation. After the epithelium is
cast off, invasion by infective organisms may occur.
Clinical features
Symptoms and signs of the causative disease are evident.
Ocular irritation, burning, foreign body sensation and redness. Symptoms are gets worse in the morning.
Signs of exposure keratopathy are:
Drying ofcornea
G There is absence of reflex blinking and defective closure of lids during sleep
S Punctate epithelial defects develop in the cornea
Corneal ulceration may develop soon due to necrosis followed by bacterial superinfection.
Treatment
1) Prophylaxis: Once lagophthalmos is diagnosed following measures should be taken
to prevent
exposure keratitis.
Artificial tears should be instilled frequently.
Instillation of ointment and closure of lids by a tape during sleep.
Soft bandage contact lens with frequent instillation of artificial tears
Treatment of cause of exposure: e.g., proptosis, ectropion, symblepharon should be taken up.
2) Treatment of the corneal ulcer once developed.
3) Tarsorrhaphy is required when it is not possible to treat the cause.

8) Neuroparalytic keratitis [2000]

Ans.
There is loss of corneal sensation which results in the formation of corneal ulcer
Etiology: There is 5th nerve (trigeminal nerve) paralysisIt occurstypicallyas a result ofinjecting
alcohol in gasserian ganglion in cases of trigeminal neuralgia.
Symptom: painless condition due to corneal anaesthesia.
It is a
Signs: The characteristic feature is desquamation of corneal epithelium.
Large corneal ulcers are seen due to peeling of the epithelium.
There is corneal anaesthesia
The stroma is cloudy and yellowoften associated with hypopyon.
GCiliary congestion is marked.
Treatment options
Treat the corneal ulcer on usual line of treatment. Special careistaken to protect the eye with an eye shield.
Artificial tears and eye ointment are applied to lubricate the cornea.
Closure of the lacrimal puncta may be done to conserve moisture.
Paramedian or lateral tarsorrhaphy is indicated in these cases.

9) Keratomalacia [94]
Ans.
Keratomalacia refers to corneal necrosis due to vitamin A deficiency> non-healing corneal ulcer
In this condition, there is no inflammatory reaction
 VSQs
1. Corneal endothelium [10]
Ans.
It isthe innermost layer of cornea
It consists of single layer of flattened hexagonal cells.
Epithelium
It helps to maintain corneal transparency by
Bowman's
G Active Sodium-Potassium-ATPase pump to maintain membrane
corneal dehydration
Tight junctions between adjacent endothelial cells-
to prevent aqueous humour from entering cornea
Stroma
Investigation done forendothelial cell count
Specular microscopy.
Normal endothelialcellcount: 2400-3000 cells/ mm2
Ifendothelial cells are between 500-2400 per mm, Descemet's
cornea adapts by Polymegathism and Polymorphism. membrane

If endothelial cells are < 500 per mm, it leads to corneal Ooeeooroooood Endothelium
Structure of cornea
decompensation (hazy, edematous cornea)
 Diseases of Vitreous
sQs
1. Vitreous hemorrhage -causes, c/F & fate [16, 12, 06]
Ans.
Vitreous haemorrhage occurs from the retinal vessels and may present as preretinal (subhyaloid) or an
intragel haemorrhage.
Causes
1. Retinal
tear, PVD (posterior vitreous detachment) and RD.
2. Trauma to eye.
3. Inflammatory diseases - Acute chorioretinitis, Eales' disease, or secondary to uveitis.
4. Vascular disorders, e.8, hypertensive retinopathy, and central retinal vein occlusion.
5. Metabolic diseases- ex: diabetic retinopathy.
6. Exudative age-related macular degeneration.
7. Blood dyscrasias, e.g., retinopathy of anaemia, leukaemias, polycythemia and sickle-cel
8. Bleeding disorders, eg., purpura, haemophilia and scurvy.
9. Neoplasms- rupture of vessels due to acute necrosis in tumours like retinoblastoma and malignant
melanoma of choroid.
10.Other causes -Coat's diseases, radiation retinopathy, retinal capillary aneurysm.
Clinical features

Symptoms Signs
1) Distant direct ophthalmoscopy reveals black shadows against the
Floaters of sudden red glow in small haemorrhages and no red glow in a large
onset (if vitreous haemorrhage.
&
haemorrhage is small).2) Direct indirectophthalmos.copy-show blood in the vitreous
cavity in small vitreous haemorrhage and non-visualization of
Sudden painless loss of
vision occurs in fundus in large vitreous haemorrhage.
3) Slit-lamp examination shows a reddish mass in the vitreous.
massive vitreous
haemorrhage 4) Ultrasonography with B-scan is helpful in diagnosing vitreous
haemorrhage

Fateofvitreous haemorrhage
1. Complete absorption may occur without organization
2. Organization of haemorrhage with formation of a yellowish-white debris occurs in persistent or
recurrent bleeding.
3. Complications like vitreous liquefaction, degeneration & khaki cell glaucoma (in aphakia) may
occur.
4. Retinitis proliferans may occur which may be complicated by tractional retinal detachment.
Treatment
1) Conservative treatment: bed rest & elevation of patient's head-(to allowblood to settle down).
2) Treatment of the cause: Once the blood settles down, indirect ophthalmoscopy should be
performed to locate and manage the causative lesion.
3) Vitrectomy by pars plana route should be considered to clear the vitreous, if the haemorrhage is
not absorbed after 3 months.
 VSQS 18 of 18
1. At macula [05]
Ans.
The macula is situated at the posterior pole with its centre (foveola) being lateral to temporal margin
of disc. Normal macula is slightly darker than the surrounding retina. Its centre imparts a bright reflex
(foveal reflex).
Following abnormalities may be seen at the macula:
1 Macular hole It looks red in colour with punched-out margins.
2) Macular haemorthage is red and round.
3) Cherry red spot is seen in central retinal artery occlusion, Tay-Sach's disease, Niemann-Pick's
disease, Gaucher's disease and Berlin's oedema.
4) Macular oedema may occur due to trauma, intraocular operations, uveitís & diabetic maculopathy.
5) Pigmentary disturbances may be seen after trauma, solar burn, age-related macular degeneration
(ARMD), central chorioretinitis and chloroquine toxicity.
6) Bull's eye macular lesions are seen in ARMD, Stargardt disease, chloroquine retinopathy and cone
dystrophy.
7 Hard exudates may be seen in hypertensive retinopathy, exudative diabetic maculopathy, Coat's
disease, CNVM.
8) Macular scarring-It may occur following trauma and disciform macular degeneration.

Right eye
2. Paracentesis {incl it's indications} [05, 03]
Ans.
Aqueous is slowly released from the anterior chamber by an incision
Temporal Nasa
on cornea via paracentesis needle. This improves the nutrition of the
cornea
Paracentesis
Indications needle

Hypopyon ulcer orhyphaema with raised tension. Paracentesis

Impending perforation of corneal ulcer (descemetocele).

 CONTENTS

Diseases of Sclera..
SQs. =mu3

Diseases of Uveal Tract..

LQS 6
SQs. 10
VSQs.. *** 12
 Diseases of Sclera
sQs
1) Episcleritis [14, 04]
a. Clinical features and treatment of Episcleritis [17]
Ans.
Episcleritis is benign, recurrent, inflammation of the episclera, involving the overlying Tenon's capsule
but not the underlying sclera.
Etiology
1. Idiopathic.
2. Can be a/w-
Systemic diseases like gout, rosacea, psoriasis and connective tissue diseases.
Infections like herpes zoster virus, syphilis, Lyme disease and TB
Pathology Lymphocytic infiltration of episcleral tissue oedema & congestion of Tenon's capsule and
conjunctiva.
Cinical features
Symptoms Signs
Redness, mild ocular discomfort On examination 2 clinical types of episcleritis may be recognised.
(foreign body sensation). 1. Simple episcleritis is sectorial inflammation of episclera.
2. Nodular episcleritis is characterised by a pink or purple
Rarely, photophobia & nodule which is firm, tender, can be moved separately from
lacrimation may occur the sclera and the overlying conjunctiva also moves freely
Differential diagnosis
G Simple episcleritis may be confused rarely with conjunctivitis.
Nodular episcleritis may be confused with inflamed pinguecula, foreign body lodged in bulbar
conjunctiva and, very rarely with scleritis.
Treatment o Nodular
episcierits
1. Topical NSAIDS, e.g., ketorolac 0.3%.
2. Topical mild corticosteroid eye drops, e.g., fluorometholone instilled 2-3 hourly
3. Topical artificial tears, e.g., 0.5% carboxy methyl cellulose have soothing effect.
4. Cold compresses applied to the closed lids may offer symptomatic relief.
5. Systemic NSAIDS e.g., indomethacin (25 mg t.i.d.)-for recurrent cases.
**********
2) Scleritis [99, 97]
Ans.
Scleritis refers to inflammation of the sclera proper.
Etiology
1) ldiopathic
2) Almost 50% cases of scleritis are associated with systemic diseases like:
a. Autoimmune collagen disorders - rheumatoid arthritis (MC), Wegener's granulomatosis, SLE etc.
b. Metabolic disorders- gout & thyrotoxicosis
C. Infections herpes zoster ophthalmicus, staphylococcal and streptococcal infection.
d. Granulomatous diseasesTB, syphilis, sarcoidosis, leprosy.
e. Miscellaneous conditions like irradiation, chemical burns, Bechet's disease and rosacea.
f. Surgically induced scleritis (SIS) is a rare complication of ocular surgery.
Pathology: It is a chronic granulomatous disorder characterised by fibrinoid necrosis, destruction of of 12
collagen with infiltration by PMNs, lymphocytes, plasma cells and macrophages. The granuloma is
Surrounded by multinucleated epithelioid giant cells & some of them may show evidence of vasculitis.
Classification of Scleritis
A. Non- I. Anterior a. Non-necrotizing scleritis (85%)- can be diffuse or nodular
infectious scleritis (98%) b. Necrotizing scleritis (13%) t Inflammation
scleritis II. Posterior scleritis (2%)

B. Infectious scleritis- 5-10% of all cases

Clinical features
Symptoms
Ocular Pain: moderate to severe and often wakes the patient early in the Necrotizing scleritis

morning. Radiates to the jaw and temple.

Redness may be localized or diffuse.
Photophobia and lacrimation.
Diminution of vision may occur occasionally.
Sians of Infectious scleritis
Purulent exudates, painful nodules, Formation of fistulae, conjunctival &scleral ulcers
Sians ofNon-infectious scleritis
Non 1) Non-necrotizing anterior diffuse scleritis -widespread inflammation of
necrotizing the anterior sclera.
anterior 2) Non-necrotizing anterior nodular scleritis-1or 2 hard, purplish,
scleritis immovable scleral noduls, usually situated near the limbus.

Anterior 1. Necrotizing Anterior scleritis with inflammation - intense localised

scleritis inflammation a/w areas of infarction sclera becomes transparent&
Necrotizing8
uveal tissue shine through it.
anterior
Necrotizing Anterior scleritis without inflammation (scleromalacia
scleritis
perforans)-typically occurs in elderly females with longstanding
rheumatoid arthritis.
It is an inflammation of the sclera behind
the equator.
Posterior scleritis /w inflammation of adjacent structures like exudative retinal detachment,
macular oedema etc.

Complications: These are common with necrotizing scleritis and include sclerosing keratitis,
keratolysis, complicated cataract and secondary glaucoma. Involvement of comea

Investigations-Following laboratory studies may be helpful in identifying associated

systemic diseases:
1. TLC, DLC and ESR. Sclerosing keratitis

2. Serum levels of complement (C3), immune complexes, rheumatoid factor, antinuclear antibodies
and L.E cells for an immunological survey.
3. FTA-ABs, VDRL for syphilis.
4. Serum uric acid for gout.
5. Urine analysis.
6. Mantoux test.
7. X-rays of chest, paranasal sinuses, sacroiliac joint and orbit (to rule out foreign body especially in
patients with nodular scleritis).
Treatment
1. Non a. Topical steroid eyedrops
necrotizing b. Systemic indomethacin 75 mg BD
scleritis
1) Topical steroids
A. Non-
2) Oral steroids on heavy doses, tapered slowly.
infectious
3) Immunosuppressive agents like methotrexate or
scleritis 2. Necrotizing
cyclophosphamide may be required in nonresponsive cases.
scleritis
4) Surgical treatment, in the form of scleral patch graft may be
required to preserve integrity of the globe in extensive scleral
melt and thinning.
Most of the time diagnosis is delayed and patients are put on topical and oral steroids
which worsen the infective scleritis.

B. Infectious scleritis G Topical+ oral Abx is required in an aggressive manner.

G Surgical debridement by debulking the infected scleral
-

tissue. It also facilitates the effect of antibiotics.

 Diseases of Uveal Tract
LQs
1. Anterior uveitis- Etiology, clinical features, complications & management [15, 05]
a. Seclusio Pupillae [15]; Festooned pupil [14]
b. Keratic precipitates [14, 11, 09]
c. Aqueous flare [14); Flare j07, 04]
d. Acute iridocyclitis-etiology, clinical picture, Management & complications [13, 10]
e. Granulomatous uveitis etiology, signs, symptoms and management [02]
-

f. Iris nodules [02]

Ans
Anterior uveitis: It is inflammation of the uveal tissue from iris up to pars plicata of ciliary body. It
may be subdivided into:
Iritis-Inflammation predominantly affects the iris.
Iridocyclitis Iris & pars plicata part of ciliary body are equally involved, and
Anterior cyclitis pars plicata part of ciliary body is predominantly affected.

Etiology- lproposed by Duke Eiderl

exogenous, secondary or endogenous.
1) Infective uveitis: Uveal infections may be
Exogenous infection ex: from penetrating injuries, perforation of corneal ulcer etc.
Secondary infection-from neighbouring structures, eg, acute conjunctivitis, keratitis, scleritis, etc.
Endogenous infections are caused by the organisms situated elsewhere in the body.
Types of infectious uveitis:
a. Bacterial -
These may be granulomatous, e.g, TB, leprosy, syphilitic, brucellosis or pyogenic such as streptococci,
staphylococci, pneumococci and gonococcus.
Viral-herpes simplex, herpes zoster and CMV.
b.
c. Fungal-aspergillosis, candidiasis, blastomycosis
d. Parasitic- toxoplasmosis, toxocariasis, onchocerciasis and amoebiasis.
e. Rickettsial-scrub typhus & epidemic typhus
2) Immune related uveitis: It may be caused by Microbial allergy (TB, streptococci etc.), anaphylactic
uveitis, Atopic uveitis, autoimmune uveitis & HLA-associated uveitis.
3) Toxic uveitis:
Endotoxins produced inside the body as in pneumococcal or gonococcal infections
-

Endocular toxins Ex; in patients with blind eyes, intraocular haemorrhage

Exogenous toxins Ex: chemical substances of inorganic, animal or vegetative origin.
4) Traumatic uveitis-seen in accidental or operative injuries to the uveal tissue.
5) Uveitis associated with systemic diseases like DM, gout, Sarocoidosis, PAN, rheumatoid arthritis etc.
6) Idiopathic uveitis - Ex: Fuchs' heterochromic iridocyclitis.

Clinical Features
Symptoms
1) Pain- dull aching throbbing sensation which is typically worse at night; referred along the distribution of 5h nerve,
especially towards forehead and scalp.
2) Redness - occurs due to circumcorneal congestion
3) Photophobia and blepharospasm occurs due to a reflex between sensory fibres of 5th nerve (which are irritated)
-

and motor fibres of the 7th nerve, supplying the orbicularis oculi muscle.
4) Lacrimation occurs due to lacrimatory reflex mediated by 5th nerve (afferent) and secretomotor fibres of the 7th nerve
(efferent).
5) Defective vision - it can be because of induced myopia due to ciliary spasm,
corneal haze (due to oedema & KPs), pupillary block
due to exudates, complicated cataract, vitreous haze, etc.
Signs-Slit-amp examination reveals:
1. Lid oedema
2. Circumconeal congestion is marked in acute cases and minimal
in chronic cases.
3. Corneal signs: Corneal oedema, KPs & posterior corneal
opacities
Keratie preciptates. Mutlon fat KP's at the botlom, small and medium KPs abov

Keratic precipitates (KPs) are proteinaceous cellular deposits

occurring at the back of cornea. The composition and morphology of KPs varies with the type of
uveitis. Types of KPs:
Types of KPS Seen in Composed of Description
1) Mutton fat Granulomatous uveitis Epithelioid cells and They are large, thick,
KPs macrophages fluffy, lardaceous KPs,
having a greasy or waxy
appearance
2) Small & Non-granulomatous Lymphocytes These small, discrete, dirty
medium uveitis white KPs are arranged
KPs irregularly
3) Old KPs Sign of healed uveitis
4) Fine KPs, aka Fuch's heterochromic iridocyclitis, Ihey cover entire corneal endothelium
'stellate'KPs Herpetic iritis and CMV retinitis (Endothelial dusting)
4. Anterior chamber signs
GAqueous cells should be counted in an oblique slit-lamp beam
Aqueous flare earliest sign of acute anterior uveitis -occurs due to leakage of protein into the aqueous
-

humour from damaged blood vessels.

Hypopyon-When exudates are heavy and thick, they settle down in lower part of the anterior chamber as hypopyon (sterile
pus in the anterior chamber)
GHaemorrhagic hypopyon is a feature of uveitis a/w herpetic infection, trauma & rubeosis iridis.
GChanges in depth & shape of anterior chamber- occur due to synechiae formation. Ex: Funnel-
shaped in annular synechiae with iris bombe.
G Changes in the angle of anterior chamber are observed with gonioscopic examination. In active stage, cellular
deposits and in chronic stage peripheral Ciliary congestion

anterior synechiae may be seen. ueous flare

Festooned pupil Busacca's nodule
5. Iris signs Koeppe's nodule Complicated cataract
Busacca's nodule
Loss of normal pattern-occurs ypopyon
Pup
Posterior synechiae
OCCuSiO

Busaccs nodule

due to oedema of iris in active

phase and due to atrophic Sgns of anterior uveiis

changes in chronic phase. Iris

atrophy is typically observed in Fuchs' heterochromic iridocyclitis.
Changes in iris colour - Iris becomes muddy in colour during active phase no Koeppe

Iris nodules- seen typically in granulomatous uveitis.

Koeppe's nodules are situated at the pupillary border and may initiate posterior synechia.
Busacca's nodules are larger and located away from the pupil.
 Posterior synechiae- between the posterior surface of iris and anterior capsule of crystalline lens
» Annular (ring) posterior synechiae are 360" adhesions of pupillary margin to anterior capsule
of lens funnel-shaped Anterior chamber impair circulation of
ins bombe
aqueous humour from posterior chamber to anterior chamber (seclusio Funnel shaped
anterior chamber
pupillae/ Festooned pupil). Thus, aqueous collects behind the iris and
pushes it anteriorly (leading to iris-bombe' formation) 10P
Neovascularisation of iris (rubeosis iridis) seen in chronic cases & in Fuch's heterochromic iridocyclitis.
-

6. Pupillary signs
Narrow pupil occurs due to Iris oedema & iritation of sphincter pupillae by toxins.
-

Irregularpupil shape-(Festooned pupil)- occurs due to posterior

synechiae. Dilatation of pupil with mydriatics (e.g., atropine) looks like Festooned
pup
festive paper decoration
Ectropion pupillae (eversion of pupillary margin).
SluggishPupillary reaction -due to oedema and hyperaemia of iris which hamper pupil
movements.
Occlusio pupillae - occurs if the pupil is completely occluded due to
organisation of exudates across the entire pupillary area.
7. Changes in the lens Oclusio-pupillae
Pigment dispersal on the anterior capsule of lens
Exudates deposit on the lens in cases with acute plastic iridocyclitiscyclitic membrane
Changes in the vitreous and retina
GExudates & inflammatory cells seen in the anterior vitreous
GCystoid macular oedema (CME) may occur in chronic cases.
Complications
1. Complicated cataract- 'polychromatic lustre' & 'bread-crumb' appearance
2. Secondary glaucoma.
Early glaucoma (hypertensive uveitis}-occurs due to clogging of trabecular meshwork because
of exudates and inflammatory cells in the anterior chamber
» Late glaucoma (post-inflammatory elaucoma) is the result of pupil block (seclusio pupillae due to ring
synechiae formation, or occdusio pupilae due to organised exudates) not allowing the aqueous to flow from
posterior to anterior chamber.
3. Cyclitic membrane- occurs due to deposition of exudates on the lens.
Choroiditis.
Ycltic membrane
5. Retinal complications: CME, macular scar, macular hole,
epiretinal membrane, exudative retinal detachment, retinal scars and sub-retinal fibrosis.
6. Papillitis (inflammation of the optic disc) - seen in severe cases
7. Band-shaped keratopathy-seen in chronic cases, especially in children with Still's disease.
8. Phthisis bulbi- end result of any form of chronic uveitis in which the eye becomes soft, shrink and
atrophic.
Investigations
Haematological investigations: TLC, DLC, ESR, Blood sugar levels, Blood uric acid. Serological tests
for syphilis, toxoplasmosis, antinuclear antibodies, Rh factor, LE cells, C-reactive proteins, ACE (for
sarcoidosis).
Urine examination for WBCs, pus cells, RBCs and culture to rule out UT
 Stool examination for cyst and ova to rule out parasitic infestations.
Radiologicalinvestigations:
G X-rays of chest, paranasal sinuses, sacroiliac joints and lumbar spine
G CT scan of thorax should be considered for suspected sarcoidosis cases.
G MRI scan of head for suspected sarcoidosis, demyelination and lymphomas.
Skin tests: tuberculin test, Kveim's test for sarcoidosis, lepromin test and pathergy test for Behcet's
disease.
Treatment
Specific treatment of the cause-for Ex: antitubercular drugs for TB etc.
Nonspecific treatment
1. Cycloplegic drugs -Ex: 1% atropine sulfate eye ointment or drops-t relleves the
spasm of iris sphincter, prevents the formation of synechiae & increases the blood supply to anterior uvea
Local therapy 2. Corticosteroids-Ex: dexamethasone, betamethasone etc. -anti-inflammatory effect
3. Broad spectrum Abx drops aré usually prescribed with topical steroid preparations to provide an
umbrella cover for them.
1) Corticosteroids esp. non-granulomatous uveitis
in & other cases resistant to
topical therapy. Ex: prednisolone (60-100 mg)
Drawback: Steroids (both topical and systemic) may cause many ocular (e.&, steroid-induced glaucoma and cataract) and
systemic side-effects
2) NSAIDS
Systemic G Aspirin can be used where steroids are contraindicated
therapy G Phenylbutazone - used13if uveitis is a/w rheumatoid disease

3) Immunosuppressive drugs-used in severe cases with imminent danger of

blindness-Ex: cyclophosphamide, chlorambucil, azathioprine and
methotrexate
4) Azithromycin or tetracycline or erythromycin used to treat chlamydial infection in
patients and their sexual partners with Reiters syndrome
Hot fomentation it is very soothing, diminishes pain and increases circulation. As a result, more
Physical
antibodies are brought and toxins are drained.
measures
Dark goggles- used in sunlight to photophobia, lacrimation and blepharospasm
Treatment of complications
Inflammatory glaucoma (hypertensive uveitis): 0.5% timolol maleate eyedrops + usual treatment
of iridocyclitis. Pilocarpine and latanoprost eye drops are contraindicated in inflammatory glaucoma.
Post-inflammatory glaucoma due to ring synechiae is treated by laser iridotomy
Complicated cataract requires lens extraction
Exudative Retinal detachment usually settles itself if uveitis is treated aggressively. A tractional
detachment requires vitrectomy
Phthisis bulbi especially when painful, requires removal by enucleation operation.
--* -------mmwmo--***-----m-----*--*--**---------*---****--*--*
2. Describe the aetiology, clinical features and management of red eye [11, 071
a. Differential diagnosis and treatment for Red Eye [05]
Ans.
 Acute conjunctivitis Acute iridocyclitis Acute congestive glaucoma
Feature
1. Onset Gradual Usually gradual Sudden

2. Pain Mild discomfort Moderate in eye and Severe in eye and the entire
along the first divisiontrigeminal area
of trigeminal nerve

3. Discharge Mucopurulent Watery Watery

Coloured halos May be present Absent Present

4
Good Slightly impaired Markedly impaired
5 Vision
Congestion Superficial conjunctival Deep cillary Deep ciliary
7. Tenderness Absent Marked Marked

Pupil Normal Small and irregular Large and vertically oval

8.
9. Media Clear Hazy due to KPs, Hazy due to oedematous
aqueous flare and Cornea
pupillary exudates
Normal May be deep Very shallow
10. Anterior chamber
11. Iris Normal Muddy Oedematous
12. Intraocular pressure Normal Usually normal Raised

13. Constitutional symptoms Absent Little Prostration and vomíting

SQs
1) Endophthalmitis [13]
Ans.
Endophthalmitis is defined as an inflammation of the inner structures of the eyeball, ie, uveal tissue
and retina a/w pouring of exudates in the vitreous cavity, anterior chamber & posterior chamber.
Etiology
Infective endophthalmitis
Modes of infection
1) Exogenous infections from perforating injuries, perforation of corneal ulcers etc.
2) Secondary infection from neighbouring structures -Ex: orbital cellitis, infected corneal ulkcerse
3) Endogenous infections are caused by the organisms situated elsewhere in the body
Causative oraanisms
1. Bacterial-MC is Gram +ve cocci, i.e., Staphylococcus epidermidis and Staphylococcus aureus.
Others: Streptococi, Pseudomonas, Pneumococci, Corynebacterium, Propionibacterium
acnes and Actinomyces
2. Fungalendophthalmitis (rare)- is caused by Aspergillus, Fusarium, Candida, etc.
Non-infective (sterle) endophthalmitis-Results from toxins released in following situations:
1) Postoperative-Ex: Chemicals adherent to intraocular lens (1OL) or instruments.
2) Post-traumatic Ex: retained intraocular foreign body.
-

3) Phacoanaphylactic - induced by lens proteins in patients with Morgagnid cat:taract.

4) Intraocular tumour necrosis may present as sterile endophthalmitis (masquerade syndrome).

Clinical feature of bacterial endophthalmitis - Onset may be acute or delayed

Acute onset between 1-7 days of operation.
-

Delayed onset- a week to month after surgery. Fungi are the most common cause
Symptoms: severe ocular pain, redness, lacrimation, photophobia and loss of vision.
 Signs: 11 of 12
1. Lids become red and swollen.
2. Conjunctiva shows chemosis and marked circumcorneal congestion.
3. Cornea is oedematous, cloudy and ring infiltration may be formed.
4. In exogenous form, Edges of wound become yellow and necrotic.
5. Anterior chamber shows hypopyon- iris and pupil details are not seen.
6. Iris, when visible, is oedematous Treatment
and muddy. Ases Vienl Acuity

7. Pupil shows yellow reflex due to

No Perception of Light fperception of light only. I Hand motion or better vision
purulent exudation in vitreous. Prill Excislon
or Evisceration mmediate pars plana vitrectomy Vitreous ta
8. Vitreous exudation: vitreous
Intravitreal antibiotics
Culhure
cavity is flled with exudation and
pus. Soon a yellowish white mass fntravitreal antibiotics
Antibiotic of cholce-Vancomycin (1 m/0.1mj+Ceftazidime
is seen through fixed dilated pupil. (2.25mein m
01
UE3 Fungal endophthaimitis-voniconazole, Amphotericin CEpOUn 5,

This sign is called amaurotic cat's-

eye reflex.
9. raised in early stages, but in severe cases, the ciliary processes are destroyed, and a fall
1OP is in

OP may ultimately result in shrinkage of the globe

2) Iris bombe [12, 11, 91]

Ans. The iris bow forwards due to collection of aqueous in the posterior chamber.
Physiological iris bombe-on dilatation of the pupil there is crowding of
the iris in the angle of anterior chamber causing obstruction to the flow of
Iris bombe
aqueous from the posterior to the anterior chamber Funnel shaped
Pathological causes: as a complication of Anterior Uveitis anterior chamber

Complications: Post-inflammatory glaucoma

DDx: Cyst of posterior epithelium
Treatment: YAG laser iridotomy is the treatment of choice to prevent secondary glaucoma
***
********
3) Panophthalmitis (04]
Ans. It is an intense purulent inflammation of the whole eyeball including the Tenon's capsule.
Etiology
Panophthalmitis is an acute bacterial infection.
Mode of infection and causative organisms are same as described for bacterial endophthalmitis
Clinical features
Symptoms Signs
Severe ocular pain and 1) Lids show a marked oedema and hyperaemia.
headache, 2) Eyeball is slightly proptosed, ocular movements are limited and
Complete loss of vision, painful
Profuse watering, 3) Conjunctiva shows marked chemosis and
ciliary as well as conjunctival congestion.
Purulent discharge,
4) Cornea is cloudy and oedematous.
Marked redness and
Swelling of the eyes, and Anterior chamber is full of pus. Panophthalmitis
6) Vision is completely lost and perception of
light is absent.
7) JOP is markedly raised.
 Constitutional 8) Globe perforation may occur at limbus, pus comes out and
symptoms like malaise intraocular pressure falls.
and fever.
Complications: Orbital cellulitis, cavernous sinus thrombosis, and Meningitis or encephalitis
Treatment
1) Anti-inflammatory and analgesics should be started immediately to relieve paín.
2) Broad spectrum antibiotics should be administered to prevent further spread of infection in the
surrounding structures
3) Evisceration operation should be performed to avoid intracranial dissemination of infection.
*****

VSQs
1. Hyphema [14]
Ans
Causes of Hyphema -HOTS
Collection of blood in the anterior chamber is called Hyphema. Herpetic uveitis
Treatment O phthalmia nodosa
Trauma
Most hyphaemas absorb spontaneously and thus need no treatment. Syphilis
Acetazolamide and hyperosmotic agents can be given to 1OP
If the blood does not get absorbed in a week's time, then a paracentesis should be done to drain
the blood.

2. Circulus arteriosus iridis major& minor [13]

Ans.
Anterior ciliary arteries pierce the sclera near the limbus to enter the ciliary muscle; where they
anastomose with the two long posterior ciliary arteries to form the circulus arteriosus major, near
the root of iris.
Branches arise from the circulus arteriosus major to supply the ciliary processes (1 branch for each
process)& form circulus arteriosus minor which supply the pupillary margins & some central part of iris

***** ******************************************

3. Hard Exudates [05

Ans. Hard exudates are lipid deposits in the outer plexiform layer of retina which occur following leaky
capillaries in severe hypertensive retinopathy.
They appear as yellowish waxy spots with sharp margins. They are generally seen in posterior pole
and may be arranged as macular-fan or macular-star.
They are temporary and may disappear in 3-6 weeks
**************em=**********

4. Nodule at the Limbus [04]

Ans. A limbal nodule is any nodular lesion at the limbus (junction of the cornea & sclera) of the eye.
DDx for a limbal nodule can include
Early Pterygium
Foreign body/ foreign body granuloma
Phlycten, an inflamed nodule of lymphoid tissue
Episcleritis &Scleritis
Granuloma
Limbal dermoid, Malignant melanoma, naevus etc.
**************
 CONTENTS

Diseases of Lens...
LQs
SQs...
.8
VSQs

GLAUCOMA.
.11
LOs. .. 11
SQs 17
VsQs 19

Neuro-ophthalmology
*20
LOS .. 20
SQs.
. 21
 Diseases of Lens
LQs
1) Congenital cataract-Classification, clinical features, Dx and management [07, 03]
a. Zonular cataract [16
b. Lamellar cataract [15, 02]
Ans.
Congenital cataracts occur due to some disturbance in the normal growth of the lens before birth.
ETIOLOGY
1 ldiopathic About one-third cases
-

2 Hereditary- About one-third cases

E.g, of familial cataracts: Zonular cataract, Coronary cataract, Cataracta pulverulenta etc.
Can occur with/without systemic disorders like cerebro-oculo-facial syndrome, Lowe's synd rome, Stickler syndrome etc.
3. Matermal factors
Malnutrition during pregnancyzonular cataract
Maternal infections like rubella are associated with
cataract in 50% of cases
Ingestion of thalidomide, corticosteroids during Membranous Corbical amellar Nuciear
mpie
pregnancy cataract catarac ataract ataract ataract
Exposure to radiation during pregnancy
Foetal factors
1) Anoxia due to placental haemorrhage.
2) Birth trauma, may cause cataract.
3) Metabolic disorders -galactosemia, galactokinase
deficiency and neonatal hypoglycemia.
4) Congenital anomalies e.g, as seen in Lowe's
Syndrome etc.
000
Postenor
subcapsular
Posterior polar
cataract

Classification of Congenital Cataract

Antenor polar
catarect
pinsped
cataract

ne vanous presentabons or congenita cataract

Postenor
enbconus

A. Congenital capsular 1 Anterior capsular cataract

cataracts 2. Posterior capsular cataract
1) Anterior polar cataract
B. Polar Cataracts
2) Posterior polarcataract
Cataracta pulverulenta
2. Lamellar cataract
C. Congenital Nuclear
Sutural and axial cataracts: Floriform cataract, Coralliform cataract, Anterior
cataracts
axial embryonic cataract & Dendritic suture cataract
4. Total nuclear cataract
1) Coronary cataract
2) Blue dot cataract
D. Generalized cataracts 3) Total congenital cataract
4) Congenital membranous cataract
CLINICAL FEATURES

A. Congenital capsular cataracts

G Anterior capsular cataracts are nonaxial, stationary and visually insignificant.
G Posterior capsular cataracts are rare and can be a/w persistent hyaloid artery remnants
Polar Cataracts- involve the poles of the lens
1. Anterior polar cataract: It arise either due to delayed development of anterior chamber or due to corneal
perforation.
2. Posterior polar cataract: It is a very common lens anomaly & maybe a/w Persistent hyaloid artery
remnants, Posterior lenticonus, and Persistent hyperplastic primary vitreous (PHPV)
C. Congenital Nuclear cataracts
a) Cataracta centralis pulverulenta - it is B/L & is characterised by a small rounded opacity ying in the
centre of the lens. The opacity has a powdery appearance (pulverulenta) and usualy does not affect the vision.
b) Lamellar (Zonular) cataract- it refers to the developmental cataract in which the opacity
occupies a discrete zone in the lens. It is the MC type of congenital cataract presenting with visual
impairment
Etiology: It may be either genetic (autosomal dominant) or environmental (vit D deficiency,
hypocalcaemia, maternal rubella infection).
Riders
Characteristic features:
Two rings
Typically, this cataract occurs in a zone of foetal nucleus surrounding
Zonular cataract
the embryonic nucleus
Smallinear opacities like spokes ofa wheel (riders) may be seen towards the equator.
It is usually B/L and causes severe visual defects
c) Sutural and axial cataracts:
They are punctate opacities scattered around the Y-sutures and do not have much effect on the vision
vary in size and shape and have different pattern and thus are named accordingly as
They -

1. Floriform cataract the opacities are arranged like the petals of a flower
2. Coralliform cataract- spindle- shaped opacity with off shoots resembling a coral
3. Anterior axial embryonic cataract occurs as fine dot near the anterior Y-suture
4. Dendritic sutural cataract occurs as fine dots along the dendritic sutures.
d) Total nuclear cataract: It involves the embryonic and fetal nucleus and sometimes infantile nucleusas
well. It is characterized by B/L, dense chalky white central opacity seriously impairing vision.
D. Generalized cataracts
1. Coronary cataract
around pubertyy
Occur
The opacities are many hundreds in number and have a regular radial distribution in the
Coronary cataract
periphery of lens
2. Blue dot cataract: this is the MC type of congenital cataract. It usually forms in the first two decades of life.
The opacities are in the form of rounded bluish dots situated in the periphery
3. Total congenital cataract-it can be due to heredity or rubella. In rubell, the child is born with a progressive 'pearly white'
nuclear cataract
4. Congenital membranous cataract: Sometimes there may occur total or partial absorption of congenital
cataract, leaving behind thin membranous cataract. This is a/w Hallermann-Streiff-Francois Syndrome
DIEFERENTIAL DIAGNOSIS Congenital cataracts presenting with leukocoria need be to diferentiated
from other conditions presenting with leukocoria such as retinoblastoma, retinopathy of prematurity,
persistent hyperplastic primary vitreous (PHPV), etc.
MANAGEMENT
1) Clinico-investigative work up:
Ocular examination - done to know Density and morphology of cataract, assess visual function
is
& note any associated ocular defects like microphthalmos, glaucoma, PHPV,
optic nerve
hypoplasia etc.
Laboratory investigations- is done to detect:
GIntrauterine infections by TORCH test
GGalactosemia by urine test
G Lowe's syndrome by urine chromatography for amino acids.
GHyperglycemia by blood sugar level
GHypocalcemia by serum calcium and phosphate levels and X-ray skull
 5of 25
2) Prognostic factors - Density of cataract, U/L or B/L, time of presentation & associated ocular or systemic defects
3) Indications and timing of paediatric cataract surgery
Partial cataracts & small central cataracts which are visually insignificant can safely be ignored
Bilateral dense cataracts should be removed within 6 weeks of birth to prevent amblyopia
Unilateral dense cataract should be removed as early as possible (within days) after birth
4) Surgical Technique-extra capsular cataract extraction involving anterior capsulorrhexis and lens
aspiration or lensectomy is used.
5) Correction of paediatric aphakia
Children>2 years - Implant during surgery.
PCIOL
O Children below 2 yrs- treated by extended wear contact lens. Later on,secondary i0L implantation may be done.
6) Correction of amblyopia- It can be done via occlusion therapy, Penalization, Pleoptic exercises etc.
--------

2) Senile Cortical Cataract-C/F & management [04, 03]

a. Local anaesthesia for cataract surgery [13]
b. Morgagnian hypermature cataract [13]
C. Four complications of cataract surgery [12
d. Different etiology for cataract [07]
Ans.
Age-related cataract' also called as senile cataract is the commonest type of acquired cataract
affecting equally persons of either sex usually above the age of 50 years.
Morphologically, the senile cataract occurs in 2 forms: the cortical (soft cataract) and the nuclear
(hard cataract). With increasing age
Risk Factors: (senility)

1 Age-usually occurs after the age of S0 years.

Decreases in the function Reduced oxidative
2. Heredity-can predispose to pre-senile cataract of actve transport pump reactionss
mechanism of lens
3. Exposure to UV radiations from sunlight.
4. Diet deficient in proteins, amino acids, vitamins (riboflavin, Vit E, Vit C) ReversalIof Decreased level of
Na Kratio amino acids
5. Dehydrational crisis - (due to diarrhoea, cholera, etc.)
6. Smoking. Hydration of lens Decreased synthesis of
ndres proteins in lens fibress
Causes of pre-senile cataract: (before 50 years of age)Heredity, DM,
Myotonic dystrophy & Atopic dermatitis Denaturation of lens proteins
Mechanism of loss of transparency of Lens: Opacification of cortical lens fibres

Stages of Maturation of Senile Cortical Cataract:

1. Stage of lamellar separationearliest change is separation of cortical fibres by fluid.
2. Stage of incipient cataract-2 types of senile cortical cataracts can be recognised at this stage:
a) Cuneiform senile cortical cataract It is characterised by wedge-shaped opacities which starts
-

at periphery and extends centrally radial spoke-like pattern of

greyish white opacities.
b) Cupuliform senile cortical cataract-it is a saucer-shaped opacity
develops just below the capsule in the posterior cortex (posterior
subcapsular cataract), which gradually extends outwards
3. Immature senile cataract (ISC): opacification becomes more diffuse DHagramamatic dopiction or immaturo sonile
alaroct (curneom bpe)EA, as
seon by oblique iuminabon:
and irregular. Iris shadow is visible. In some patients, at this stage, lens 6, in opbcal secbon with the beam of the sit-lamp

may become swollen due to continued hydration. This condition is called

Shallow anterior
intumescent cataract'. Due to swollen lens anterior chamber becomes Swollen lens Charmoer
E
shallow.
Intumescent cataraci
4. Mature senile cataract (MSC): In this stage, opacification becomes complete, i.e., whole of the
cortex is involved. Lens becomes pearly white in colour. It is aka 'ripe cataract'
5. Hypermature senile cataract (HMSC): it may occur in any of the two forms:
a. Morgagnian hypermature cataract: here, whole cortex juefies & the lens is converted into a bag
of milky fluid. The smal brownish nucleus settles at the bottom. Morgagniahypermature senile cataract

b. Sclerotic type hypermature cataract: here, cortex becomes

disintegrated and the lens shrink due to leakage of water anterior
chamber becomes deep & iris becomes tremulous (iridodonesis).
Clinical features
Svmptoms
1) Glare -
intolerance of bright light; such as direct sunlight or the headlights of an oncoming motor vehicle.
2) Uniocular polyopia: It occurs due to irregular refraction by the lens
3) Coloured halos: they form because of breaking of white light into coloured spectrum due to presence of water droplets
in the lens.
4) Black spots in front of eyes.
5) Image blur & distortion of images
6) Deterioration of vision: It is painless and gradually progressive in nature
GPatients with central Signs of senile cataract
opacities (e.g, Examination Nuclear cataract ISC MSC HMSC (M) HMSC(S)
cupuliform cataract 1.Visual acuity 6/9 to PL+ 6/9 to CF+ HM+ to PLt PL+ PL+
2.Colour of lens Grey, amber, Greyish white Pearly white with Milky white Dirty white with
i.e., posterior brown, Dlack or sinking brownish hyper white spots
subcapsular cataract) red nucleus

have early loss of 3. Iris shadow Not seen seen Not seen Not Seen Not seen
4. Distant direct Central dark Multiple dark No red glow No red glow No red glow
vision. These patients see ophthalmoscopy area against red areasagainst red but white pupil milky white dirty white pupil
better when pupil is dilated with dilated fundal glow fundal glow due to complete pupil
due to dim light in the evening pupil cataract
(Day blindness). 5. Slit-lamnp Nuclear opacity Areas of normal Complete cortex Milky white Shrunken
xamination cortex clear with
cataractous cataractous
is cortex with cataractous lens
GPatients with cortex sunken brown with thickened
peripheral opacities ish nucleus anterior capsule
ISC: Immature senile cataract, MSC: Mature senile cataract, HMSC (M) Hypermature senile cataract (Morgagnian),
(e.g, cuneiform HMSC (S): Hypermature senile cataract (Sclerotic), PL: Perception of light, HM: Hand movements, CF: Counting finger
cataract) visual loss is
delayed and the vision improves in bright light when pupil is
ISC Nuclear sclerosis
contracted. 1, Painless progressive loss 1. Painless progressive loss
of vision of vision
Differential diagnosis 2. Greyish colour of lens 2.Greyish colour of lens
on oblique illumination
1 Immature senile cataract (ISC) can be differentiated from the nuclear sclerosis
examination
2. Mature senile cataract can be differentiated from retrolental causes of white 3. Iris shadow is present 3. Iris shadowis absent
pupillary reflex (leukocoria) 4. Black spots against 4. No black spots are seen
red glow are observed against red glow
Complications on distant direct
1) Phacoanaphylactic uveitis - Lens proteins leak into the anterior ophthalmoscopy
5. Slit-lamp examination
5. Slit-lamp examination
chamber in hypermature cataractmay act as antigen and induce reveals area ot
reveals clear lens with
antigen-antibody reaction Phacoanaphylactic uveitis. cataractous cortex
nuclear sclerosis
6Visual acuity usually
6. Visual acuity does not
2) Lens-induced glaucoma: improves on pin-hole
improve on pin-hole
a. Phacomorphic glaucoma (MC)-it is caused by intumescent esting k estng
(swollen) lens. It is a type of 2' angle closure glaucoma.
b. Phacolytic glaucoma: Lens proteins are leaked into the anterior chamber in hypermature cataract> proteins
are engulfed by the macrophages > The swollen macrophages clog the trabecular meshwork > Phacolytic
Glaucoma. t is a type of 2" open angle glaucoma.
Phacotopic glaucoma: Hypermature cataractous lens may subluxate/dislocate and cause glaucoma by blocking
the pupil or angle of anterior chamber.
3) Subluxation or dislocation of lens- occur due to degeneration of zonules in hypermature stage
MANAGEMENT OF CATARACT IN ADULTS:
Non-Sugical measures
Treatment of cause of cataract Ex: control of DM, stop cataractogenic drugs (corticosteroids, miotics etc.)
Measures to improve vision- Ex: Prescription of glasses
Types of Cataract Surgeries:
1 Intra-Capsular Cataract Extraction (ICCE) - Complete lens with the capsule is removed
Not done now
Onlycurrent indication: Subluxation of lens due to >180 zonular dehiscence
2) Extra-Capsular Cataract Extraction (ECCE) - Lens is removed but not the capsule.
G Techniques: Site of incision Si2e of inckion
aConventional ecce Limbus 8-Omm
G Latest Technique Femtosecond Laser Assisted
Cataract Surgery (FLACS) b.Small neision Cataract Sclera
Local anaesthesia for cataract surgery: Surgery sics S-7mm

Peribulbar injection: Bupivacaine + Lignocaine + Phacoemulsitcafion Cornea aa-3a mm

1:200000 Adrenaline+ Hyaluronidase.

Complications of Cataract Surgery:
Acute Post-op
Intra-op Complications Late Post-op Complications
Complications
1) Posterior Capsular PCO Posterior Capsular Opacification:
rupture aka After Cataract/secondary cataract
2) UGH Syndrome Displacement of IOL
Shallow anterior
(Uveitis, Glaucoma, Hyphema)
1) Superior 1OL Dislocation -Sunrise Syndrome
3) Expulsive Choroidal chamber 2) Inferior 1OL Dislocation Sunset Syndrome
-

hemorrhage Endophthalmitis 3) Complete Subluxation of Lens Lost Lens -

Descemet's Syndrome
Irvin Gas Syndrome
ae
membrane ens

detachment Anterior Capsular Phimosis Sublacation of lens

3) Discuss the signs, symptoms, diagnosis and management of nuclear cataract [02]
Ans. It is a type of Senile Cataract (Refer 2nd LQ) it occurs due to sclerosis, it causes hard cataract

Aka central cataract

Inerease in refractive index of lens
Pathogenesis:
Main Clinical Features: Inerease in pouer (converging o lens)
»Loss of vision in daytime: (pupils constrict in daytime=> light is
Index myopla - loss of tar vision or rnear sightecness
blocked by the cataractous nucleus => LOv)
leads to second sight
»Improvement of vision in dim light /night
»Second sightImprovement of near vision due to nuclear cataract in a patient who is alreacly presbyopic
Grading of Nuclear Cataract: 4 Grades
1. Grade
1-
yellow due to deposition of urochrome pigment /F yellow coloured vision (xanthopsia)
2. Grade 2-Amber
Cortex
3. Grade 3-Brown called as cataracta brunescens
4. Grade 4- Black called as cataracta nigra Nucleus
Fron vie Side view
Management of Nuclear Cataract- (Refer 2d LQ) Senile nuclear cataract
 sQs
1) Aetiology and clinical features of complicated cataract [14]
Ans.
Complicated cataract refers to opacification of the lens 2" to some other intraocular disease
Aetiology UMAR
»Chronic Anterior Uveitis (MCC) Breadcrumb's
appearance
»High Myopia
»Angle Closure Glaucoma
Complicated cataract
»Fundus dystrophies like Retinitis Pigmentosa
Clinical features
G Typicaly, the complicated cataract starts as posterior subcapsular cortical cataract (PSC).
G The opacity is irregular in outline and variable in density.
In the beam of slit-lamp the opacities have:
Breadcrumb' appearance.
Polychromatic lustre' i.e., appearance of iridescent coloured particles of reds, greens and blue
is a very characteristic sign (Rainbow cataract).
Diffuse yellow-haze is seen in the adjoining cortex
Slowly the opacity spreads in the rest of the cortex, and finally the entire lens becomes opaque,
giving dirty white or chalky white appearance.
Deposition of calcium is common in the later stages

2) Traumatic Cataract [08]

Ans.
OAka Concussion cataract: It occurs mainly due to imbibition of aqueous and partly due to direct
mechanical effects of the injury on lens fibres.
It may assume any of the following shapes: Clear zone
GDiscrete subepithelial opacities (MC
GBlunt Trauma causes Rosette Shaped Cataract Small opacities
Early rosette cataract (punctate)-It appears as feathery
lines of opacities along the star-shaped suturelines; usually
in the posterior cortex Punctate subcapsular cataract
Late rosette cataract; It develops in the posterior cortex 1 to 2 years after the injury. Its
sutural extensions are shorter and more compact than the early rosette cataract.
GInfrared Rays cause- glassblower's cataract occurs due
to true exfoliation of lens capsule.
GLightning/electric shock causes anterior capsular opacities Feathery lines of
radiating opacities
GTraumatic zonular cataract, extend along sutures
GDiffuse (total) concussion cataract.
G Early maturation of senile cataract may follow blunt Early rosette cataract

trauma.
Treatment of traumatic cataract: (Refer 2nd LQ)

3) Intraocular lens [03, 98]

a. Types of Intraocular lenses [16]
Ans.
Types of lOL:
Based on the 1) ACIOL (Angle supported 1OLs) -
made of PMMA (poly-methyl meth acrylate): Drawback: bullous keratopathy
method of Iris-supported lenses: These lenses are fixed on the iris with the help of sutures. These lenses are also
not used due to high Incidence of postoperative complications. Example of iris supported lens is Singh &
fixation in the Worst's iris claw lens
eye 3) PCIOL- rest entirely behind the iris: made of Silicone or Acrylic-Ex: C-Shaped Haptic
Based on the Rigid 10Ls made of PMMA
material of Foldable lOLs made of Silicone or Acrylic
manufacturing Rollable IOL made of hydrogel
Unifocal 1OLs - Depending upon the power of 1OLs implanted, these can make
the patient emmetropic, myopic or hypermetropic. ght condtlors

Based on the Multifocal lOLS These are of 2 types, either refractive or diffractive optics drving

|focussing types. These are also called pseudoaccommodative 1OLs.

ability Accommodative IOLS exhibit some anterior movement of optic to improve onditions

the near vision. Ex: Crystalens ntermeda

1) Toric 1OL-in pre-existing astigmatism

Special
2) Square edged 1OL-To occurrence of Posterior capsular opacification (PCO).
function 10LS
3) Aniridia10Ls: These are devised to cosmetically coverthe defectsof aniridia
Calculation of 1OL Power is known as Biometry ollid haptiG

Formulae to Calculate 1OL power: SRK-T, Holladay, Hoffer Q & Haigis-L

Indications of 1OL implantation: All cases being operated for cataract

Best Site for 1OL implantation - in the Capsular Bag8 ne plece PMMA lens Slcone ens

4) After cataract [2000]

Ans.
PCO Posterior Capsular Opacification: aka After Cataract/secondary cataract
It is the MC late complication of Cataract Surgery; Elschnig's pearts

Occur 6-12 months after surgerY

Types of PCO:
a. Elsching Pearls (90% cases): forms due to posterior migration of residual epithelial cell
b. Sommering's Pearls (10% cases)
Treatment of PCO: Nd: YAG laser posterior capsulotomy;
Nd: YAG 1064 nm; MOA- Photodisruption

vsQs
1. Lenticonus [14]
Ans.
Lenticonus is a bulging of the lens capsule
and the underlying cortex.
It results in Myopia
It is typically seen in Alport's syndrome
Lenticonus PosS
Lenticonus Ante
Diagnosis of lenticonus is made by
biomicroscopic examination
---------------------*--=-***==****=****

2. Snow Blindness [09]

Ans.
Snow blindness occur due to exposure to reflected UV rays of sun from snow surface. It can lead to
Photophthalmia.
Symptoms: extreme burning pain, photophobia, lacrimation and blepharospasm due to desquamation
of corneal epithelium
Signs: multiple epithelial erosions a/w blepharospasm & swelling of the palpebral conjunctiva
Treatment
Cold compresses, astringent lotions and atropine ointment are effective.
Bandage both eyes for 24 hours. This helps in regeneration of the epithelium.
Prophylaxis: Wearing of dark glasses (Crooke's glasses) to block UV rays when such exposure is
anticipated.
----------------- *********
 Glaucomma
LQs
1. Discussthe aetiology, clinical features and management of acute congestive glaucoma [15, 14, 12]
a. Mention stages of primary narrow angle glaucoma [14]
b. Describe aetiology, signs, symptoms & treatment of various stages of congestive glaucoma (97]
Ans.
PRIMARY ANGLE-CLOsURE GLAUCOMA: It is characterised by apposition of iris against the trabecular
meshwork (TM) obstruction of aqueous outflow by closure of an already narrow angle of the anterior chamber.
Etiopathogenesis:
Risk Factors:
Demographic risk factors
Small and hypermetropic eye
Age: it is more common in elderly:-50-70 years
Gender: Female > Male (3:1)
Race: it is more common in South-East Asians, Chinese & Eskimos
Normal eye
Anatomical and ocular risk factors
Hypermetropic eyes with shallow anterior chamber & short axial length
G Eyes with narrow angle of anterior chamber - Ex: small eyeball Mechanism of closed angle glaucoma

GPlateau iris configuration

Heredity-some anatomical factors like shallow anterior chamber & narrow angles are common in 1st degree relatives of
patients
Pathomechanisms of IOP:3 mechanisms
1) Pupillary block
T
mechanism- Evident in almost 70% cases
Precipitating Factors: mydriasis (ex: atropine), miosis (pilocarpine), Valsalva manoeuvre etc.
Precipitating factors mid dilatation of the pupil apposition between iris and lens
relative pupil block aqueous collects in the posterior chamber & pushes the iris anteriorly
(lIris bombe) iridocorneal contactperipheral anterior synechiae > angle closure TIOP
2) Plateau iris configuration- Evident in 10 % Cases = Angle Closure Glaucoma without pupillary block.
»Anterior positioned ciliary processes push the peripheral iris forward > closure of anterior chamber angle
»Iridotomy is sufficient to control 1OP in such patients.
3) Phacomorphic mechanism: Abnormal lens may either cause pupillary block or push the peripheral
iris forward into the angle structures.
Semidilated pupil Iris bombe Relative pupil block

Closed angle of
anterior chamoer
Lens Lens

Lens
1, Pupillary block due to semidilated pupil 2. Physiological iris bombe

Classification: based on natural history (IOP, gonioscopy, disc and visual field evaluation):
1. Primary Angle Closure Suspect (PACS),
2. Primary Angle Closure (PAC), and
3. Primary Angle Closure Glaucoma (PACG).
2

UL UU A
Absolute PACG: PACG, if untreated, gradually passes into the final phase of absolute glaucoma.
Clinical features: Painful blind eye, Perilimbal reddish blue zone, Caput medusae, bullous
keratopathy, Shallow Anterior chamber; Iris becomes atrophic; Pupil becomes fixed and dilated
and gives a greenish hue;
Optic disc shows glaucomatous optic atrophy.
OP is high; eyeball becomes stony hard.

Management of absolute glaucoma

1. Retrobulbar alcohol injection to relieve pain. It destroys the ciliary ganglion.
2. Cyclocryotherapy or Cyclodiathermy or Cyclophotocoagulation- to destroy secretory ciliary epithelium 1OP
3. Enucleation of eyebal- if pain is not relieved by conservative methods.
Complications of absolute glaucoma (due to prolonged high 10P):
Corneal ulceration
Staphyloma formation: As a resut of continued high 1OP, sclera becomes very thin and atrophic and ultimately
bulges out either in the ciliary region (ciliary staphyloma) or equatorial region (equatorial staphyloma).
GAtrophic bulbi.

2. Describe the clinical features, pathology, Dx and Mx of primary open angle glaucoma [08, 2000]
a. Optic nerve head changes in Open Angle Glaucoma [17]
b. Field changes in Primary Open Angle Glaucoma [10, 03, 02]
C. Field defects in Chronic Simple Glaucoma [07

d. Describe the aetiology, clinical features, and treatment of chronic simple glaucoma [95, 91, 90]
Ans.
Primary open-angle glaucoma (POAG), also known as chronic simple glaucoma of adult onset, is
characterised by slowly progressive 10P (>21 mm Hg) associated with:
Open normal appearing anterior chamber angle,
Characteristic optic disc, cupping, and
Specific visual field defects.
ETIOPATHOGENESIS:
A.Predisposingfactors:
1) Age: elders between 5th and 7th decades.
2) Race: black> whites
3) Family history: POAG has a polygenic inheritance Myocilin C, Optineurin & wD repeat domain 36 genes
4) Ocular Factors: Myopes; Low Central corneal thickness (CCT) & T IOP
5) DM, smoking
6) Blood Pressure: Diastolic perfusion pressure (DBP 1OP) of <55 mm Hg.
7) Graves' ophthalmic disease
8) Corticosteroid responsiveness.
B. Pathogenesis of rise in IOP: Trabecular meshwork stiffening & apposition of Schlemm's canalFailure
ofaqueous outflow pump mechanism in the aqueous outflow 1OP
Such changes are caused by age-related:
G Sclerosis of trabecular meshwork with faulty collagen tissue
GNarrowing of intertrabecular spaces.
G Deposition of amorphous material in the juxtacanalicular space.
G Collapse of Schlemm's canal
.Pathogenmesis of glaucomatous optieneuropathys ll glaucomas are characterized by a progressive optic
neuropathy which occurs due to death of retinal ganglion cells (RGCs) which results in characteristic optic disc
appearance and specific visual field defects.
Mechanical effect of T lOP push the lamina cribrosa and squeezes the nerve fibres within it's
meshes to disturb axoplasmic flow.
CLINICAL FEATURES

Symptoms
1) Asymptomatic POAG is insidious. Hence, periodic eye examination
-
is required after middle age.
2) Headache and eye ache.
3) Scotoma (defect in the visual field)
4Increasing difficulty in reading and close work - occurs due to accommodative failure as a resut of constant pressure
on the ciiary muscle and its nerve supply. Patients complain of, frequent changes in presbyopic glasses.
5) Delayed dark adaptation
6) Blindness is the end result of untreated cases of POAG.
Signs of POAG
1. Anterior a Slit-lamp examination may reveal normal anterior segment.
segment b) In late stages, pupil reflex becomes sluggish and cornea may show slight haze
signs c) Alow (<555 mm) central corneal thickness is arisk factorfor POAG.
In the initial stages, the IOP may not be raised permanently
2. 1OP changes GDiurnal variation in IOP of s 5 mm Hg is suspicious and > 8 mm Hg is diagnostic of glaucoma
G In later stages, 1OP is permanently raised above 21 mm of Hg
1) Vertically oval cup due to selective loss of neural rim Glaucamatous

tissue in the inferior and superior poles.

2) Asymmetry of the cups of twoeyes.
Early Changes
es
3) Large cup size 2 0.6 (normal cup size is 0.3 to 0.4). ertcaliy Oval cup

4) Splinter haemorrhages on or near the optic disc margin.

5) Pallorareas on the disc
a) Marked cupping (cup size 0.7 to 0.9)
b) Thinning of neuroretinal rim is seen as a crescentric shadow
adjacent to the
3. Optic disc disc margin.
Splinter
haemorhage

changes c) Notching of the shuftbing

blood of vessels
(Detected on rim specially up to essels
hin neur
fundus Advanced disc margin is bending
of blood vesseis

examination) changes pathognomic.

Laminar dol sign Bayoneting ign
d) Nasal shifting of
retinal vessels wich have the appearance of being broken offat the margin is Bayonetting sign.
e) Pulsations of the retinal arterioles may be seen at the disc
margin (a pathognomic sign of glaucoma if 1OP is very high.
f Laminar dot sign: the pores in the lamina cribrosa are slit
shaped and are visible up to the margin of the disc.
As the damage progresses, all the neural tissue of the disc is
Glaucomatous destroyed and the optic nerve head appears white and deeply
optic atrophy
excavated
 1) Isopter contraction -mild constriction of visual field.
2) Baring of blind spot - t means exclusion of the blind spot from the central field due to inward curve of the
4. Visual field outer boundary of 30" central field
defects (in 3) Small wing-shaped paracentral scotoma - It is the earliest clinically significant field defect.
sequence) 4) Seide's scotoma-
paracentral scotoma joins the Localised
constriction
blind spot to form a sickle-
shaped scotoma known as
Seidel's scotoma
5) Arcuate or Bjerrum's
SCotoma - formed by the Baring of the blind spot
1.

extension of Seidel's scotoma either above or

2. Small scolomatous areas 3. Seidef's sign

below the fixation point to reach the horizontal

line.
6) Ring or double arcuate scotoma. It
develops when the two arcuate scotomas join 4. Bjerrum's arcuate scoloma 5. Double arcuate scotoma or
together. annuiar Scoloma
7) Roenne's central nasal step. It is created when the two arcuate Roenne's.
nasal sioPX
scotomas run in different arcs and meet to form a sharp right-angled
defect at the horizontal meridian.
8) Advanced glaucomatous field defects. The visual field
Tubular vision loss gradually spreads centrally as well as peripherally, and
eventuallyonly a small island of central vision (tubular vision)] and an accompanying temporal
islandare left.
5. Ocular POAG may be associated with high myopia, Fuchs' endothelial dystrophy, retinitis
associations pigmentosa, central retinal vein occlusion and primary retinal detachment.

INVESTIGATIONS
1. Tonometry Applanation tonometry should be preferred over Schiotz tonometry to measure 1OP
2. Central corneal thickness (CCT) measurement
3. Diurnal 1OP variation test is useful in detection of early cases
4. Gonioscopy -It reveals a wide-open angle of anterior chamber- rule out other forms of glaucoma.
5. Documentation of optic disc changes
6. Slit-lamp examination of anterior segment to rule out causes of secondary open-angle glaucoma.
7. Perimetry to detect the visual field defects.
8. Nerve fibre layer analyzer (NFLA) is a device which helps in detecting the glaucomatous damage to
the retinal nerve fibres before the appearance of actual visual field changes
9. Provocative tests are required in border-line cases. The test commonly performed is water drinking test.
GWater drinking test. Itis based on the theory that glaucomatous eyes have a greater response to water drinking. In it
after 8 hours fast, baseline lOP is noted and the patient is asked to drink one litre of water, following which 1OP is noted
every 15 minutes for 1 hour. A rise of 8 mm of Hg or more is said to be diagnostic of POAG.
DIAGNOSIS: Depending upon the level of lOP, glaucomatous cupping of the optic disc and the
visual field changes, the patients are assigned to one of the following diagnostic entities:
A. Primar open-angle glaucoma: POAG is labelled when raised 1OP (>21 mm of Hg) is a/w definite
glaucomatous optic disc cupping and visual field changes
B. Ocular hypertension -patient has an 1OP constantly > 21 mm of Hg but no optic disc and visual field
changes.
C. Normaltension glaucoma (NTG)l or low-tension glaucoma (LTG): Here, typical glaucomatous disc
cuppingt visual field changes is associated with an 1OP <21 mm of Hg
 MANAGEMENT
Baseline evaluation- done to monitor future progress.
It includes: visual acuity, slit-lamp examination of anterior segment, tonometry; measurement of
CCT, optic disc evaluation (preferably with fundus photography), gonioscopy and visual field
charting. Degree Description
Mild Characteristic optic-nerve abnormalities
Grading: American Academy of Ophthalmology (AAO) are consistent with glaucoma but with
normal visual field.
grades glaucoma damage into mild, moderate & severe. Moderate Visual-field abnormalities in one hemi-
field and not within 5 degrees of fixation.
Therapeutic choices. Severe Visual-field abnormalities in both hem
Medical therapy with Antiglaucoma drugs fields and within 5 degrees of flixation.

»ldentify a target pressure from the baseline evaluation data

»Based on your target, Anti-Glaucoma Drugs ( 1OP)
prescribe a Pilocarpine (miotics)
Single/Combination of Drugs to 1 trabecular outflow Dipivefrine
antiglaucoma drugs Bimatoprost
Dipivefrine
»Monitorthe patient for Drugs to t uveoscleral outflow Latanoprost
disc changes and field CA inhibitors (ex: acetazolamide)
changes-tonometry is Drugs to aqueous
production a agonist (ex: dipivefrine, epinephrine)
most essential on Bblockers (ex: timolol)
regular follow-up. Hyperosmotic agents Ex: Mannitol

Laser trabeculoplasty can

be done using argon laser (ALT), or diode laser (DLT) and selective laser trabeculoplasty (SLT). It
should be considered in patients where 1OP is uncontrolled despite maximal tolerated medical
therapy.
Surgical therapy - Filtration surgery Ex: Trabeculectomy
Indications of Surgery
a) Uncontrolled glaucoma despite maximal medical therapy and laser trabeculoplasty.
b) Noncompliance of medical therapy and nonavailability of ALT/SLT.
c)Eyes with advanced disease, i.e., having very high 1OP, advanced cupping and advanced field loss.

3. Enumerate the causes of Secondary Glaucoma. Add a note on its treatment [98, 94]
a. Phacomorphic Glaucoma [15]
Ans.
Depending upon the causative primary disease, secondary glaucomas are named as follows:
Secondary Glaucoma Treatment
therapy to lower the 1OP
Medical
1) Lens-induced
Cataract extraction with implantation of PCIOL (in quiet eyes)
(phacogenic) glaucomas
Laser iridotomy-for Phacomorphic Glaucoma
Irrigation-aspiration of the lens particles from the anterior
chamber-in Lens Particle Glaucoma & Phacoantigenic Glaucoma
Treat iridocyclitis + Medical therapy to lower 1OP
Inflammatory glaucoma Trahe
Trabeculectomy-can be done if medical treatment fails
3) Pigmentary glaucoma. behaves like POAG andisthus managed on the same lines.
4) Pseudoexfoliative behaves like POAG and is thus managed on the same lines.
glaucoma.
 5) Neovascular glaucoma. »Panretinal photocoagulation - to prevent further
neovascularization
Glaucoma drainage device, i.e., artificial filtration shunt (Seton
Hbrovescular operation) may control the lOP.
membrane
CFAAS
Lens
Medical therapy and conventional filtration surgery are usually not
Neovasouar giauconma effective in controlling the lOP.
»Glaucoma drainage device, i.e., artificial filtration shunt (Seton
6) Glaucomas a/w
operation) may control the 1OP.
iridocorneal endothelial
»Medical therapy and conventional filtration surgery are usually not
syndromes.
efective in controlling the 1OP.
7) Glaucomas a/w Examples are: Red cell glaucoma, Haemolytic glaucoma, Ghost cell
intraocular haemorrhage. glaucoma & Hemosiderotic glaucoma
Examples are:
8) Glaucoma-in-aphakia. Steroid-induced glaucoma: Discontinue steroids+ Medical therapy to 10P
Traumaticglaucoma: Treat the cause+ Medical therapy to 10P+ Surgery
9) Glaucoma a/w Enucleation of the eyeball should be carried out as early as possible
intraocular tumours
Lens induced glaucoma can be classified as below:
G Lens-induced secondary angle closure glaucoma:
Phacomorphic glaucoma (due to swollen lens)
.Phacotopic glaucoma (due to anterior lens displacement).
open angle glaucoma: Phacolytic glaucoma, Lens particle glaucoma &
Lens-induced secondary
Phacoanaphylactic glaucoma

Phacomorphic Glaucoma
Causes: Phacomorphic glaucoma is an acute secondary angle-closure glaucoma caused by:
Intumescent lens i.e., swollen cataractous lens due to rapid maturation of cataract
Anterior subluxation or dislocation of the lens and spherophakia (congenital small spherical
lens) are causes of Phacotopic (a variant of Phacomorphic) glaucoma.
Pathogenesis: The swollen lens pushes the iris forward and obliterates the angle secondary
acute angle closure glaucoma.
Clinical presentation: Phacomorphic glaucoma presents as acute congestive glaucoma with
features almost similar to Acute PAC (refer 1st LQ) except that the lens is always cataractous and
swollen.
Treatment should be immediate and consists of:
GMedical treatment to control 1OP by IV mannitol, systemic acetazolamide & topical B-blockers.
G Laser iridotomy may be effective in breaking the angle-closure attack.
GCataract extraction with implantation of PCIOL should be performed once the eye becomes quiet.

SQs
1) Trabeculectomy [15, 02]
Ans.
It isthe most frequently performed external Filtration Surgery till date
In this Surgery, a new channel (fistula) is created around the margin of sclera, through which
aqueous flows from anterior chamber into the subconjunctival space
 Surglcal technique
A fistula is created between Peripheral
Conunctival Superfical iridectomy
ap scleral flap
anterior chamber and Deep
Sclera
subtenon's space, window

MCC of failure fibrosis of 1. Conjunctival flap 2. Scleral fap 3. Trabeculectomy 4. Conjunctival suture
fistula
To prevent fibrosis, use antimetabolites (mitomycin, 5-FU)
Indications
1. Primary angle-closure glaucoma with peripheral anterior synechiae involving> 270° angle.
2. Primary open-angle glaucoma not controlled with medical treatment.
3. Congenital and developmental glaucomas where trabeculotomy and goniotomy fail.
4. Secondary glaucomas where medical therapy is not effective.
Complications: postoperative shallow anterior chamber, hyphaema, iritis, cataract due to
accidental injury to the lens, and endophthalmitis.
Sutureless trabeculectomy is also available nowadays

2) Buphthalmos [10, 05, 02]

Ans.
defined as Congenital Glaucoma occurring prior to age of 3 years.
It is

As it results due to retention of aqueous humour (watery solution) it is also termed as

"hydrophthalmos'
Etiology: It occurs due to congenital abnormality at the angle of anterior chamber (Ex: Absence of
canal of Schlemm, incomplete separation of iris from cornea). It is transmitted as an autosomal
recessive trait.
Symptoms: Lacrimation, Photophobia, defective vision & enlargement of cornea and the eye as a
whole.
Signs
G Corneal enlargement occurs along with the enlargement of the globe-Buphthalmos (Bull-like eyes)
G There is corneal oedema & opacities due to endothelium damage and rupture of Descemet's membrane
(Haabs' striae)
Corneal Diameter > 13 mm
GLens is flattened and displaced backwards due to stretching of the zonule of Zinn
GDeep anterior chamber due to backward displacement of the lens.
GSclera becomes thin and bluish as the uveal tissue shines through it
G OP is Raised (due to retention of Aqueous humour)
Treatment: it is primarily surgical
Medical treatment: not very effective; iOP by anti-glaucoma drugs {ar agonist (brimonidine)
causes CNS depression in children and is contraindicated
>Surgical procedures:
Incisional angle surgery, which can be performed by the internal approach (goniotomy) or
by external approach (trabeculotomy).
Filteration surgery- Ex: Trabeculectomy
Glaucoma drainage devices (GDD) are required in incalcitrant cases
 VSQs
1. Classify Glaucoma [04, 03]
Ans.
Glaucoma is not a single disease process buta group of disorders characterized by a progressive optic
neuropathy resulting in a characteristic appearance of the optic disc and a specific pattern of
irreversible visual field defects that are associated frequently but not invariably with 1OP
Classification: Clinico-etiologically glaucoma may be classified as followS:
A. Congenital/developmental glaucomas
1. Primary congenital glaucoma (without associated anomalies).
2. Developmental glaucoma (with associated anomalies).
B. Primary adultglaucomas Glaucoma

1) Primary open-angle glaucomas (POAG) Congential Acquired

(Buphthalmos or infantile glaucoma)
2) Primary angle-closure glaucoma (PACG)
3) Primary mixed mechanism glaucoma Primary Seconday

C. Secondary glaucomas Open-angle Angle-clousure

2. Indications& types of iridectomy [06, 05]

Ans.
Iridectomy consists of the abscission or cutting of a portion of the iris
Indications:
1) Prolapsed iris
2) Treatment of all stages of primary angle-closure glaucoma.
3) Prophylaxis in the fellow eye
4) Foreign body in the iris
5) Optical iridectomy-In central leucomatous corneal opacity, temporal Peripheral
iridectomy
(for distant vision, e.g. farmers) or nasal (for near work, e.g. clerk,
goldsmith) iridectomy is done according to the requirement and job of the patient
Broad Peripheral Peripheral Sphincterotomy
based basal button hole
B C D

Optical iridectomy Iridodialysis

Types of Iridectomy
 Neuro-ophthalmology
LQs
Discuss Optic Neuritis-CF, DDx and treatment [11)
a. Acute Retrobulbar neuritis [16]
b. Papillitis [05, 03]
Ans.
Optic neuritis refers to inflammatory & demyelinating disorders of the optic nerve.
Etiology
1. Demyelinating disorders (MCc) -
neuromyelitis optica (Devic's disease) etc.
Ex: MS,
2. Hereditary optic neuritis (Leber's disease)
3. Parainfectious optic neuritis -
a/w viral infections- Ex: measles, mumps, chickenpox, whooping
cough and glandular fever. Cotton wool
exudates
4. Infectious optic neuritis may be sinus related Pervascular
sheathing
Hyperaemic
(with acute ethmoiditis) or a/w cat scratch fever, disc with blurred
Blurred
margin
margin
Pgmentation
syphilis, TB, Lyme disease and cryptococcal meningitis Dilated and tortuous
retnal veins
in patients with AIDS.
Early changes Late changes
5. Autoimmune disorders a/w optic neuritis Papiliis

include sarcoidosis, SLE, PAN, GBS &Wegener's granulomatosis

6. Idiopathic
7. Toxic optic neuritis (refer 3rd sa)
-

Anatomical types: Optic neuritis can be classified into 3 anatomical types:

1. Papilitis-It refers to involvement of the optic disc. This is usually Un but sometimes may be B/L.
2. Neuroretinitis refers to combined involvement of optic disc & surrounding retina in the macular area.
3. Retrobulbar neuritis refers to the involvement of optic nerve behind the eyeball. linical features of
acute retrobulbar neuritis are similar to that of acute papillitis except for the fundus changes and ocular changes
Clinical features
Symptoms Signs
1) Visual acuity.
Visual loss Monocular, 2) Impairment of colour vision & Contrast sensitivity.
sudden, progressive 3) Marcus Gunn pupil-itindicates RAPD
Dark adaptation 4) Ophthalmoscopic features:
Visual obscuration in bright Papillitis is characterised by hyperaemia & edema of the disc
light. and blurring of the margins. Physiological cup is obliterated.
Impairment of colour Retinal veins are congested and tortuous. Splinter
vision. haemorrhages & fine exudates are seen on the disc
Movement phosphenes Neuroretinitis = Papillitis + macular star formation
and sound induced In retrobulbar neuritis fundus appears
phosphenes may be normal and the condition is typically defined
perceived by patients as a disease where neither the
Depth perception, ophthalmologist nor the patient sees
particularly for the moving anything. Occasionally, temporal pallor of
the disc may be seen
object may be impaired
(Pulfrich's phenomenon). 5) Visual field-central scotoma (MC defect)
Pain aggravated by ocular 6) Visually evoked response (VER) shows
movements. amplitude delay in the transmission time.
& Visual feld dhanges

7) Fundus fluorescein angiography reveals mild to moderate leak.

DIfferential diagnosis
»Papillitis should be differentiated from papilloedema, ischaemic optic neuropathy, anterior orbital
compressive neuropathy and pseudopapilloedema
»Acute retrobulbar neuritis must be differentiated from malingering, hysterical blindness, cortical
blindness and indirect optic neuropathy.
Treatment
1) Identify & treat the cause.
2) Corticosteroid therapy:
G Ifbrain MRI scan shows lesions of MS > i.v. methylprednisolone (1 gm daily) for 3 days followed by
oral prednisolone (1 mg/kg/day) for 11 days. Then taper prednisolone over 4 days.
GThis therapy willdelay conversion to clinical MS over the next 2 years.
3) Interferon therapy:
It reduces the recurrences in patients with MS.
But this is very expensive and with unknown long-term benefits.
=*** ***********

SQs
1. Optic atrophy Classification, Aetiology, pathology
a. Primary optic atrophy [07, 02]]
& C/F [16, 14, 12, 08]
Y Opression
fumour

b. Consecutive Optic Atrophy [05, 02] aneuryam

Ans.
Optic atrophy refers to degeneration of the optic nerve, which occurs as
an end result of any process that damages axons in the anterior visual nyennal
Ooacce
system, i.e., from retinal ganglion cells to lateral geniculate body Arteosis
teritis Glioma (Children)

Common causes of optic atrophy

Classification & Etiopathogenesis-based on its ophthalmoscopic appearance:

Type of optic atrophy Occurs due to Seen in
retrobulbar neuritis, toxic amblyopias, tabes
MS,
1) Primary (simple) Lesions proximal
dorsalis, intracranial tumours pressing directly on the
optic atrophy: to the optic disc
anterior visual pathway(e.g, pituitary tumour) etc.
2) Consecutive optic Destruction of Diffuse chorioretinitis, retinitis pigmentosa,
atrophy: ganglion cells pathological myopia and CRAO
3) Post-neuritic optic
Occurs due to longstanding papilloedema or papillitis
atrophy
4) Glaucomatous
Occurs due to the effect of long-standing iOP
optic atrophy
5) Vascular
Giant cell arteritis, severe haemorrhage, severe
(ischaemic) optic Disc ischaemia
anaemia and quinine poisoning
atrophy
Pathological features
1. Degeneration gliosis - astrocytes arrange themselves in longitudinal columns replacing the nerve fibres (columnar gliosis)
seen in primary optic atrophy
2. Degeneration of the nerve fibres excessive gliosis (regeneration) seen in consecutive and
post-neuritic optic atrophy.
3. Degeneration of the nerve fibres with negligible gliosisseen in glaucomatous & ischaemic
(vascular) optic atrophy.
Clinical features of optic atrophy
1. Loss of vision, may be of sudden or gradual onset (depending upon the cause of optic atrophy)
2. Pupil is semi-dilated and direct light reflex is very sluggish or absent.
3. Swinging flash light test depicts Marcus Gunn pupil (RAPD).
4. Visual field loss.
5. Ophthalmoscopic appearance:
Type of optic atrophy Ophthalmoscopic appearance
1) Primary (simple) optic Disc appear chalky white.
atrophy: Disc Edges are sharply outlined
Lamina cribrosa is clearly seen at the bottom of the
amine
ribrosa physiological cup.
Retinal vessels and surrounding retina are normal
2) Consecutive optic atrophy Disc appears yellow waxy.
Attenuated
d vessors

Retinal vessels are attenuated

w
Yellow
OSC

3) Post-neuritic optic atrophy appears dirty white in colour

»Disc
Due to gliosis, its edges are blurred
Perivascular
Sneatning Physiological cup is obliterated and lamina cribrosa is
Surred
iscmargin
Macular sippling not visible
Pigmentation
»Retinalvessels are attenuated +Perivascular sheathing
4) Glaucomatous optic atrophy Wide cupping of the optic disc & nasal shift of blood vessels
5) Vascular (ischaemic) optic atrophy Pallor of the optic disc + marked attenuation of the vessels

Treatment of underlying cause may help in preserving some vision in patients with partial optic
atrophy. But, once complete atrophy has set in, the vision cannot be recovered

2. Papilledema {15, 12, 08, 05}

Ans.
Papilloedema is a non-inflammatory oedema of optic disc which occurs 2" to intracranial pressure

Causes of papilloedema
1) Congenital conditions: aqueductal stenosis and craniosynostosis.
2) Intracranial infections such as meningitis and encephalitis.
3) Diffuse cerebral oedema from blunt head trauma
4) Intracranial haemorrhages &Cerebral venous sinus thrombosis
s) Obstruction of CSF absorption via arachnoid villi which have been damaged previously.
6) Intracranial space-occupying lesions (ICSOLS) & Tumours of spinal cord.
7) Idiopathic intracranial hypertension (1IH) also known as pseudotumour cerebri
8) Systemic conditions: malignant hypertension, PIH, cardiopulmonary insufficiency, blood dyscrasias
and nephritis. Flame-shaped
haemorrhages

Clinical features Elevated

opticdisc

General features of ICPheadache, nausea, projectile vomiting

and diplopia. Dilated veins
Cotton wool
Ocular features exudates
Eary changes
 Signs
Stage of
Symptoms Pupillary
Papilledema Ophthalmoscopic Features Visual Field
Reaction
Obscuration of the disc margins
Absence of spontaneous
1) Early venous pulsation at the disc
Absent Normal Normal
(incipient) Blurring of peripapillary
nerve fibre layer
Hyperaemia of the disc
Blurring of the disc margin
Engorged & tortuous veins
Physiological cup is obliterated
2) Established Transient Disc becomes markedly
Enlargement
(fully visuall Normal hyperaemic
Paton's lines i.e., circumferential of Blind Spot
developed) obscurations
greyish white folds may develop
due to separation of nerve fibres
by the oedema.
Optic disc appears as dome of a
3) Chronic or Enlargement of
champagne cork.
Blind Spot+
long-standing Visual acuity Normal The central
Visual fields
240
(vintage) cup remains Mushroom or begin to constrict
obliterated dome shaped

Severely Greyish white discolouration of

Concentric
Light reflex is the disc
4) Atrophic impaired contraction of
impaired Prominence of the disc peripheral fields
visual acuity Retinal arterioles are narrowed
Treatment and prognosis
Urgent neuroimaging (CT scan or MRI with a gadolinium Perivascular
heathing9
enhancement) to reveal the cause. Blurred
disc margin
As a rule, unless the causative disease is treatable or cerebral Pigmentation
decompression is done, the course of papilloedema is chronic and
visual prognosis is bad

3. Toxic Amblyopia [09]

a. Amblyopia [10]
b. Tobacco Amblyopia [90]
Ans.
Amblyopia means partial loss of sight in one or both eyes, in the absence of obvious defect in the eye.
It may be either congenital or acquired.
Acquired amblyopia may be organic (toxic amblyopia) or Functional.

Functional amblyopia occurs due to psychical suppression of the retinal image. It may be
anisometropic, strabismic or due to stimulus deprivation
Toxic amblyopia aka Toxic/nutritional optic neuropathy, is basically chronic retrobulbar neuritis.
Poisons (exo/endogenous) > damage the optic nerve > visual loss
It is frequently bilateral and has a chronic course with permanent visual deterioration.
Some Varieties of toxic amblyopia are: Tobacco amblyopia, Ethyl alcohol amblyopia, Methyl
alcohol amblyopia, Quinine amblyopia & Ethambutol amblyopia
 Tobacco amblyopia Excessive tabacco
smoking
Decreased cyanide
detoxification due to0
alcoholic's dietery
G Seen in in men (40-60 years) who are pipe smokers, heavy deficiency of sulphu
rich proteins
drinkers and have a diet deficient in proteins and vitaminB
complex; and hence also labelled as 'tobacco-alcohol Excessive cyanide in blood

amblyopia'. Degeneration of ganglion cells

particulary of the macular reglon
GPathogenesis Deg
Degeneration of papillo-macular
pune
GSymptoms: B/L, progressive Impairment of central vision. "nerve
Toxic amblyopia
Patients complain of fogginess and difficulty in doing near
work.
G Signs
Visual field: bilateral centrocaecal scotomas with diffuse margins
Fundus examination is
almost normal
GTreatment. 32010 Central caecal scotoma Scotoma extending
to fixation point

Complete cessation of
tobacco and alcohol
consumption
Hydroxocobalamin 1000 mg IM injections weekly for 10 weeks
Care of general health and nutrition.
GPrognosis: It is good, if complete abstinence from tobacco and alcohol is maintained. Visual
recovery is slow and may take several weeks to months

4. Colour Vision [09]

a. Mention any four commonly employed colour vision tests [16]
b. Trichromatic theory of color vision [15]
Ans.
Colour Vision is the ability of the eye to discriminate between different colours excited by light of
different wavelengths.
Colour vision is a function of the cones and thus better appreciated in photopic vision
Theories ofcolour vision: Mnemonic
1) Young-Helmholtz's trichromatic theory: Ram RED PROTA Pehla Naam
Gopal
SIt postulates the existence of 3 inds of cones, Berma-
GREEN DEUTRA
O Doosra Naam
BLUE TRITAN Teesra naam
each containing a different photopigment
which is maximally sensitive to one of the three primary colours viz. red, green and blue.
G The sensation of any given colour is determined by the relative frequency of the impulse
from each of the three cone systems.
2) Hering's Opponent colour theory-it points out that some colours appear to be 'mutually exclusive' colour opponency
occurs at ganglion cell onwards
Commonly employed colour vision tests are:
1. Pseudoisochromatic charts (MC) - Ex: Ishihara's chart-for red-green defects
2. City university colour vision test
3. Edridge-Green lantern test
4. Farnsworth-Munsell 100 hue test- It is the most sensitive test for colour vision defects
5. Farnsworth D15 hue discrimination test
6. Nagel's anomaloscope
7. Holmgren's wools test
5. Snellen's chart for vision testing [90]
Ans. H
Snellen's chart is used to record the visual acuity (Normal distant visual acuity is 6/6)
Snellen's chart consists of a series of letters arranged in lines each diminishing AV
in size.
The lines from above downwards should be read at 60, 36, 24, 18, 12, 9, 6, 5 LTJ
m, respectively. VÖA
At these distances the letters subtend a visual angle of 5' at the nodal point. TXAL
It is kept at a distance of 6 m so that the rays of light are parallel for practical OANVZ
purpose. HZNVTUE

NOHXEZAU
 CONTENTS

Disorders of Ocular Motility.. 3

SQs.
VsQs 4

Disorders of Eyelids.
eccesressceseoetsseaccssssssssse
sQs. .. 6
VSQs .. 15

Diseases of Lacrimal Apparatus.s

17S
LQs. 17

Sas... 19

VSQs. 19
 Disorders of Ocular Motility
SQs
1) Heterophoria [10, 97
Ans. Heterophoria also known as 'latent strabismus', is a condition in which the tendency of the eyes
to deviate is kept latent by fusion. Therefore, when the influence of fusion is removed the visual axis of
one eye deviates away.
Types of heterophoria
1. Esophoria or latent convergent squint refers to tendency of eyeballs to deviate inward.
2. Exophoria or latent divergent squint refers to tendency of the eyebals to deviate outwards
3. Hyperphoria is a tendency of the eyeball to deviate upwards, while hypophoría is a tendency to
deviate downwards.
4. Cyclophoria or torsional deviation is a tendency of the eyebail to rotate around the anteroposterior
axis. When the 12 0'clock meridian of cornea rotates nasally, it is called incyclophoria and when it
rotates temporally it is called encyclophoria.
Etiology
Anatomical factors Physiological factors
1 Orbital asymmetry. 1) Age: Esophoria is more common in younger age
2. Abnormal interpupillary distance (IPD): group as compared to exophoria which is often
A wide IPD is a/w exophoria and small seen in elderly.
with esophoria. 2) Role of accommodation: accommodation is
3Weakness or Faulty insertion of associated with esophoria (as seen in hypermetropes and
extraocular muscle. individuals doing excessive near work) and
4 Anomalous central distribution of the accommodation with exophoria (as seen in simple
tonic innervation of the two eyes. myopes).
S. Variation in the position of the macula Dissoclation factor such as prolonged constant use
in relation to the optical axis of the of one eye may result in exophoria (seen in individuals
eye. using uniocular microscope and watch makers using uniocular
magnifying glass).
Symptoms: Depending upon the symptoms heterophoria can be divided into compensated&
decompensated types
Compensated heterophoria: It is a/w no subjective symptoms. Compensation of heterophoria depends upon
the reserve neuromuscular power to overcome the muscular imbalance.
Decompensated heterophoria: It is a/w multiple symptoms which may be grouped as under:
1. Symptoms of muscular fatigue: Headache and eyeache, Difficulty in changing the focus from
near to distant objects, Photophobia due to muscular ftigue s not rellved by using dark glasses, but relieved by closing one eye.
2. Symptoms of failure to maintain binocular single vision: Blurring of words while reading,
Intermittent diplopia &Intermittent squint
3. Symptoms of defective postural sensations cause
problems in judging distances and positions especially of Right eye Left oye
h oyo Let eye
the moving objects. This difficulty may be experienced
orthophora Orthophoria
by cricketers, tennis players and pilots during landing.
Examination ofa case of heterophorla Enophona Hypophor

1. Testing for vision

and refractive error
Esophoria Ryperphonia
2. Special Tests: Cover-uncover test; Prism cover test;
Maddox rod lest lor horuontal and vertical helerophorias
Maddox rod test & Maddox wing test Maddax rod lest
Treatment
1. Correction of refractive error
2. Orthoptic Exercises will improve the convergence insufficiency. They can be done with synoptophore.
Prescription of prism in glasses Prism is prescribed with apex towards the direction of phoria to
-

correct only; or at the most of heterophoria.

Surgical treatment: It is opted if symptoms are not relieved by other measures. Aim of the surgical
management is to strengthen the weak muscle or weaken the strong muscle.

2) Diplopia [96, 91]

Ans.
Diplopia refers to simultaneous perception of two images of a single object.Diplopia may be binocular
or uniocular.
Binocular diplopia: Occurs due to formation of image on dissimilar points of the two retinae.
Causes of binocular diplopia:
Paralysis or paresis of the extraocular muscles (commonest cause)
Displacement of one eyeball-seen in space occupying lesion in the orbit, & fractures of the orbital wall
Mechanical restriction of ocular movements -Ex: by thick pterveium, symblepharon and thyroid ophthalmopathy
Deviation of ray of light in one eye as caused by decentred spectacles
Anisometropia i.e., disparity of image size between two eyes (eg. uniocular aphakia with spectacle correction).

2 Types of Binocular diplopia:

Definition Seen in
1. Uncrossed (harmonious) False image is on the same Convergent squint as in lateral
diplopia: side as deviation rectus paralysis
2. Crossed (unharmonious)False image is seen on the Divergent squint as in medial
diplopia: opposite side rectus paralysis
Uniocular diplopia: Here, object appears double from the affected eye even when the normal eye is

closed. Causes of uniocular diplopia are:

GSubluxated lens (pupillary area is partially phakic and partially aphakic).
GSubluxated intraocular lens (pupillary area is partially aphakic and partially pseudophakic).
GDouble pupil due to congenital anomaly, or large peripheral iridectomy or iridodialysis.
Incipient cataract.
GKeratoconus.
Treatment of diplopia: Treat the causative disease.
Temporary relief from annoying diplopia can be obtained by occluding the affected eye.

VSas
1. Insertion of extra ocular muscles [16 Righteye Superior rectus
Ans.
The recti muscles are inserted into the sclera by flat tendons at Lateral rectus Medial rectus

various distances from the limbus

Superior oblique gets inserted into the upper and outer Inferior rectus

part of the sclera behind the equator. Insertionof recti muscie tendons in sclera

Inferior oblique It is inserted into the outer part of the sclera behind the equator.
2. Clinical features of concomitant squint [15] Classification of squint
Apparent souint Manifest squnt
Latent squint
Ans.
Heterophoria Heteropia
1. Ocular deviation
Gonicomiant Paralytic
»Unilateral (monocular squint) or alternating (alternate squint SUint

squint). Unicocula AJterma

»Inward deviation (esotropia) or outward deviation Convergent Divergent Convergent Dvergent

(exotropia) or vertical deviation (hypertropia).

Primary deviation (of squinting eye) is equal to secondary deviation (deviation of normal eye
under cover when patient fixes with squinting eye).
»Ocular deviation is equal in all the directions of gaze.
2. Ocular movements are not limited in any direction.
Refractive error may or may not be associated.
Suppression and amblyopia may develop as sensory adaptation to strabismus.
5. A-V patterns may be observed in horizontal strabismus.

3. Cardinal positions of gaze [15]

Ans.
These are the positions which allow Dextroelevation Laevoelevaton

examination of each of the 12

extraocular muscles in their main field D»
Dextroversion
Normal OG Laevoversion
of action. There are 6 cardinal
positions of gaze, viz, dextroversion,
levoversion, dextroelevation, Dextrodepression aevodepression
levoelevation, dextrodepression and Six cardinal positions of gaze
levodepression

4. Cover test [09]

Ans.
Direct cover test It confirms the presence of manifest squint. To
perform it, the patient is asked to fixate on a point light. Then,
the normal looking eye is covered while observing the movement
of the uncovered eye, In the presence of squint, the uncovered
eye will move in opposite direction to take fixation, while in
apparent squint there will be no movement.
Alternate cover test: It reveals whether the squint is unilateral or
alternate and also differentiates concomitant squint from
paralytic squint (where secondary deviation is greater than
primary) 14.17 Dvect cover test depctng lat axoropia
 Disorders of Eyelids
sQs
1. Ptosis-types, etiology, C/F & Mx [17, 12, 10]
a. Myogenic Ptosis [16
Ans.
Abnormal drooping of the upper eyelid is Narrow palpebral aperture

Normal eye Ptosis

called ptosis
Types of Ptosis Etiology&C/F
due to congenital weakness of the LPS.
1 Congenital ptosis It is

a. Neurogenic Occurs due to innervational defects like: Third nerve palsy, Horners
ptosis syndrome & Multiple sclerosis
Occurs due to acquired disorders of the LPS muscle or of the
Myogenic myoneural junction as seen in myasthenia gravis, dystrophia
ptosis myotonica, ocular myopathy, muscular dystrophy, following trauma
to LPS, thyrotoxicosis, and Lambert-Eaton myasthenia syndrome
It develops due to defects of the levator aponeurosis in the
2 Acquired presence of a normal functioning muscle. It includes:
ptosis C. Aponeurotic
ptosis
Involutional (senile) ptosis,
Postoperative ptosis (after cataract & retinal detachment surgery),
Traumatic dehiscence of the aponeurosis.
It may result due to excessive weight on the upper lid as seen in
d. Mechanical patients with lid tumours, multiple chalazia and lid oedema.
ptosis S Itmay also occur due to scarring (cicatricial ptosis) as seen in
patients with ocular pemphigoid and trachoma
Clinical Evaluation:
1. History: age of onset, family history, history of trauma, eye surgery & variability in degree of ptosis.
2. Examination
1) Exclude pseudoptosis on inspection
2) Observe the following points in each case:
Whether ptosis is unilateral or bilateral. Causes of bilateral ptosis congenital ptosis, myasthenia
gravis, myotonic dystrophy, Lambert-Eaton myasthenic syndrome etc.
Function of orbicularjs oculi muscle.
Eyelid crease is present or absent.
Jaw-winking phenomenon is present or not.
Associated weakness of any extraocular muscle.
Bell's phenomenon (up and outrolling of eyeball during forceful
closure) is present or absent, leasurement of degree of plosis

3) Measurement of amount ldegreelof ptosis: Mild (2 mm) or Moderate (3 mm) or Severe ptosis (4 mm)
4) Margin reflex distance (MRD): It is the distance between the upper lid margins and corneal light
reflex. Normal value of MRD is 4-5 mm.
5) Assessment of levator function (Burke's method)
6) Special investigations:
a. Tensilon test: ptosis improve with iv. injection of edrophonium (Tensilon) in myasthenia.
 b. Phenylephrine test is done if Horner's syndrome is suspected.
c. Neurological investigations done to find out the cause in patient with neurogenic ptosis.
7) Photographic record of the patient should be maintained for comparison.
Treatment
Treatment of Congenital ptosis:
In severe ptosis, surgery should be performed at the earliest to prevent amblyopia.
In mild and moderate ptosis, surgery should be delayed until the age of 34 years, when accurate
measurements are possible
Surgical Techniques:
Tarso-conjunctivo-Mullerectomy (Fasanella-Servat operation): for mild ptosis (1.5-2 mm)
2 Levator resection for moderate and severe grades of ptosis. Levator muscle can be resected by
-

either Conjunctival (Blaskowics' operation) or Skin approach (Everbusch's operation)

Frontalis sling operation (Brow suspension) - for severe ptosis with no levator function.
Treatment of acquired ptosis
Treat the underlying cause wherever possible.
Conservative treatment should be done & surgery deferred at least for 6 months in neurogenic
ptosis.
Surgical procedures for acquired ptosis are same as described for congenital ptosis.

2. Aetiology and complications of Trichiasis [17, 14]

Ans.
Itrefers to inward misdirection of cilia (which rub against the eyeball) with normal
position of the lid margin.
Etiology: cicatrising trachoma, ulcerative blepharitis, healed membranous
conjunctivitis, hordeolum externum, mechanical injuries, burns, and operative scar
on the lid margin.
CLINICAL FEATURES

Symptomns Signs
Foreign body sensation & photophobia. 21 Misdirected cilia touching the cornea.
Reflex blepharospasm and photophobia occur.
Patient may feel irritation, pain and Conjunctiva may be congested.
lacrimation Signs of causative disease viz. trachoma, blepharitis,
etc. may be present
Complications: recurrent corneal abrasions, superficial corneal opacities, corneal vascularisation and
non-healing corneal ulcer.
Treatment
1. Epilation (mechanical removal with forceps)- recurrence occurs within 3-4 weeks.
2. Electrolysis -lash follicles are destroyed by electric current loosened cilia are then removed with
epilation forceps.
Cryoepilation: Its main disadvantage is depigmentation of the skin.
Surgical correction-if many cilia are misdirected, surgical correction similar to cicatricial entropion
should be used.
-=====m====
****
3. Chalazion [15, 13, 11, 10, 07, 06)
Ans.
Chalazion
Chalazion, also called a tarsal or meibomian cyst, is a chronic non
infective (non-suppurative) lipogranulomatous inflammation of the
meibomian gland. This is the commonest of allid lumps. Etiopathogenesis
»Predisposing factors are similar to hordeolum externum.
Mild infection of the meibomian gland by very low virulent organisms- proliferation of the
epithelium and infiltration of the duct walls, which are blockedretention of secretions (sebum)
in the gland > enlargement of the blocked meibomian glands and surrounding tissue.
Clinical features
Symptoms:
Painless swelling in the eyelid, gradually increasing in size.
Mild heaviness in the lid may be felt.
Large chalazion > press on the cornea- induce astigmatism Blurred vision.
Large chalazion of lower eyelid eversion of lower punctum Watering (epiphora)
Signs:
Nodule-present slightly away from lid margin, firm to hard and non-tender on palpatíon.
Upper lid is involved more commonly than the lower lid tuper lid contains more melbom.an gands than the lower id
Reddish purple area is seen on the palpebral conjunctiva after eversion of the lid.
Marginal chalazion, occurring occasionally, may present as small reddish grey nodule on lid margin.
Clinical course and complications
Slow increase in size is often seen.
G If the lesion bursts on the conjunctival side Fungating mass of granulation tissue may be formed.
GSecondary infection may lead to formation of hordeolum internum.
G Calcification may occur.
G Malignant change into meibomian gland adenocarcinoma (sebaceous cell carcinoma) may be seen
occasionally in elderly people. In recurrent chalazion malignancy should be ruled out
Complete spontaneous resolution may occur rarely
Treatment
1. Conservative treatment- In small, soft and recent chalazion, self-resolution may be helped by
conservative treatment in the form of hot fomentation, topical antibiotic eyedrops and oral anti-
inflammatory drugs
2. Intralesional iniection of long-acting steroid (triamcinolone)- resolution in about 50% cases
3. Incision and curettage It is the conventional and effective treatment for chalazion.
4. Diathermy.- Better option for marginal chalazion.
5. Oral tetracycline should be given as prophylaxis in recurrent chalazia, especially if associated with
acne rosacea or seborrhoeic dermatitis.

4. Lagophthalmos [12, 99]

Ans.
It is characterised by inability to close the eyelids voluntarily Norm Incompleto ckosure of
palpebral fssure
on closing e oyes
Etiology
It occurs in patients with paralysis of orbicularis oculi muscle, cicatricial contraction of the lids,
symblepharon, severe ectropion, proptosis, following over-resection of the levator muscle for
ptosis, and in comatosed patients.
Physiologically some people sleep with their eyes open (nocturnal lagophthalmos).
Clinical featurest in complete closure of the palpebral aperture a/w features of the causative disease.
Complications: conjunctival and corneal xerosis and exposure keratitis.
Treatment:
1) Measures to prevent exposure keratitis
Artificial tear drops & antibiotic eye ointment (esp. during sleep and in comatosed patients).
Soft bandage contact lens.
Tarsorrhaphy may be performed to cover the exposed cornea when indicated.
2) Measures to treat the cause of lagophthalmos, wherever possible should be taken.

5. Ectropion [12] Ectropion lower eyelid

Ans.

Out rolling or outward turning of the lid margin is called ectropion

Healthy eye Ectropion

Types of Ectropions Etiopathogenesis

1. Congenital Seen in Down syndrome and blepharophimosis syndrome & is due to
ectropion congenital shortage of the skin
Cicatricial Itoccurs due to scarring of the skin as seen in thermal burns, chemical burns,
ectropion lacerating injuries and skin ulcers
Affects only the lower lid in elder people. Factors which contribute for its
3. Senile development are:
Horizontal laxity of the lid due to weakening of orbicularis muscle.
(involutional)
Medial canthal tendon laxity
ectropion
Lateral canthal tendon laxity
Disinsertion of lower lid retractors.
4. Mechanical Itoccurs in conditions where either the lower lid is pulled down (as in tumours) or
ectropion pushed out and down (as in proptosis and chemosis of conjunctiva).
It mainlyoccurs in the lower lids & is due to paralysis of the seventh nerve as
5. Paralytic
seen in Bell's palsy, head injury, infections of the middle ear and operations
ectropion
on parotid gland
Clinical features
Symptoms
Epiphora the main symptom in ectropion of the lower lid.
is
Symptoms due to associated chronic conjunctivitis: irritation, discomfort and mild photophobia.
Signs
Lid margin is outrolled- Depending upon degree of outrolling, ectropion can be divided into 3
grades:
»Grade I: In it only punctum is everted.
»Grade l: Lid margin is everted and palpebral conjunctiva is visible.
Grade l: The fornix is also visible.
Signs of the etiological condition such as:
Skin scars in cicatricial ectropion and
7h nerve palsy in paralytic ectropion may also be seen.
In involutional ectropion, the following signs can be elicited:
Horizontal lid laxity positive snap test, i.e., lid can be easily pulled away from the globe but fails
to snap back to the normal position on release.
G Medial .canthal tendon laxity: Normally on puling the lid laterally the inferior punctum moves by
1-2 mm only: while it can the moved upto limbus in medial tendon laxity.
GLateral canthal tendon laxity is evidenced by its> 2 mm movement on pulling the lid medially.

Complications
Dryness and thickening of conjunctiva and corneal ulceration (exposure keratitis) may occur due to
prolonged exposure
Eczema and dermatitis of the lower lid skin may occur due to prolonged epiphora.
Treatment
1. Congenital ectropion: Mild ectropion need no treatment. Moderate or severe ectropion is treated
with horizontal lid tightening & full thickness skin graft to vertically lengthen anterior lamella.
2. Cicatricial ectropion: Depending upon the degree it can be corrected by any of the following plastic
operations:
a. V-Y operation -for mild degree ectropion
b. Z-plasty (Elschnig's operation)-for mild to moderate degree of ectropion.
c.Excision of scar tissue and full thickness skin grafting-It is performed in severe cases.
3. Involutional ectropion. Depending upon the severity, following 3 operations are done:
a) Medial conjunctivoplasty-for mild degree of ectropion.
b) Horizontal lid shortening-for moderate degree of ectropion.
c) Byron Smith's modified Kuhnt-Szymanowski operation done in severe degree of ectropion.
d) Lateral tarsal strip technique - useful for generalized ectropion a/w horizontal lid laxity.
4. Paralytic ectropion:
Often resolves spontaneously within 6 months. Therefore, temporary measures are taken initially
which include:
a) Topical lubricants,
b) Taping temporal side of eyelid, and
c) Suture tarsorrhaphy

Permanent surgical treatment is required only in non-resolving cases. This includes:

SHorizontal lid tightening or
Palpebral sling operation
5. Mechanical ectropion. It is corrected by treating underlying mechanical force causing ectropion.
---*--==---=----=-----------***-

6. Entropion [10]
Ans.
Entropion refers to inward rolling and rotation of the lid margin toward
Entropion
globe.
Types of Entropions Etiopathogenesis
Lower eyelid congenital entropion is caused by improper development of
1. Congenital the lower lid retractors.
entropion Upper eyelid congenital etropion is secondary to mechanical effects of
microphthalmos
 2. Cicatricial It is caused by cicatricial contraction of the palpebral conjunctiva as seen in
trachoma, membranous conjunctivitis, chemical burns, pemphigus and
entropion
Stevens-Johnson syndrome
Affects only the lower lid in elder people. Factors which contribute for its
development are:
3. Senile
GHorizontal laxity of the lid due to weakening of orbicularis muscle.
(involutional)
GVertical lid instability due to weakening of lower lid retractor
entropion
Over-riding of pretarsal orbicularis
GLaxity of orbital septum along with prolapse of orbital fat into the lower lid
4. Mechanical It occurs due to lack ofsupport provided by the globe to the lids as seen in
entropion phthisis bulbi, enophthalmos and after enucleation or evisceration operation
Clinical features
Symptoms occur due to rubbing of cilia against the cornea and conjunctiva and are thus similar to
trichiasis. These include foreign body sensation, irritation, lacrimation and photophobia.
>Signs are as follows:
In-turning of lid margins: Depending upon the degree of inturning, it can be divided into 3 grades:
Grade entropion -only the posterior lid border is inrolled,
l
Grade Il entropion- Inturning up to the inter-marginal strip, and
Grade Ill entropion - whole lid margin including the anterior border is inturned.
Signs of causative disease, e.g., scarring of palpebral conjunctiva in cicatricial entropion, and
horizontal lid laxity in involutional entropion may be seen.
Signs of complications: recurrent corneal abrasions, superficial corneal opacities, corneal
vascularization and even corneal ulceration.
Treatment
1. Congenital entropion may resolve with time without need of any intervention or may require
excision of a strip of skin and muscle with plastic reconstruction of the lid crease (Hotz procedure).
2. Cicatricial entropion:
It is treated by a plastic operation, which based on any of the following principles: Altering the
is
direction of lashes, or transplanting the lashes, or straightening the distorted tarsus.
Surgical techniques employed for correcting cicatricial entropion are as follows:
a) Anterior lamellar resection done in mild entropion
b) Tarsal wedge resection.
c) Transposition of tarsoconjunctival wedge. (Modified Ketssey's operation)
d) Posterior lamellar graft- done in severe entropion.
3. Senile entropion: Surgical techniques are as below:
a. Transverse everting suture -for temporary cure in very old patients
b. Wies operation (Transverse lid split and everting sutures)-for long term cure in patients with
little horizontal laxity.
c. Plication of lower lid retractors (Jones operation): It is performed in severe cases or when
recurrence occurs after the above-described operations.
d. Quickert procedure: This is indicated in patients having associated marked horizontal lid laxity.
Quickert procedure basically combines horizontal lid shortening with Weis procedure.
4. Mechanical entropion-It is corrected by treating underlying mechanical force causing entropion
 Hordeolum Internum [09, 04, 02]
Ans.
It is a suppurative inflammation of the meibomian gland associated with blockage of the duct.
Etiology
»Hordeolum internum may occur as: Primary Staphylococcal infection of the meibomian gland or
due to Secondary infection in a chalazion (infected chalazion)
Predisposing factors are similar to hordeolum externum.
Clinical features
Symptoms: similar to hordeolum externum, except that pain is more intense, due to the swelling
being embedded deeply in the dense fibrous tissue.
Signs: a localized, firm, red, tender swelling of the lid associated with marked oedema
Point of maximum tenderness and swelling is away from the lid margin and that pus usually
points on the tarsal conjunctiva (seen as yelowish area on everting the lid)
Treatment: It is similar to hordeolum externum, except that, when pus is formed, it should be drained
by a vertical incision from the tarsal conjunctiva.

8. Blepharitis [08, 05, 01]

a. Squamous blepharitis etioloEy, signs, symptoms& Rx [16]
b. Ulcerative Blepheritis [02]
Ans.
Blepharitis is a subacute or chronic inflammation of the lid margins. It can be clinically divided into:
1 Bacterial blepharitis,
Seborrhoeic or squamous blepharitis,
3 Mixed Bacterial & seborrhoeic blepharitis,
4. Posterior blepharitis or meibomitis, and
5. Parasitic blepharitis

O
Small Crusts Crusts
bleeding
ulcers

Ulcerative blepharitis Squamous blepharitis

Parasitic Blepharitis (Lash Infestation

Etiology: It is seen in persons living in poor hygienic conditions infestations of lashes with lice
Clinical features:
Symptoms: chronic irritation, itching, burning, and mild lacrimation.
Signs:
. margins are red and inflamed.
Lid
Lice anchoring the lashes with their claws may be seen on slit-lamp examination.
Nits (eggs) may be seen as opalescent pearls adherent to the base of cilia.
Treatment- Mechanical removal of the lices and nits with forceps.
Abx eye ointment+ Delousing of the patient & family members is done to prevent recurrences.
 ANTERIOR BLEPHARITIS

BACTERIAL BLEPHARITIS aka chronic SEBORRHOEIC or SQUAMOUS

anteriorblepharitis, or staphylococcal blepharitisBLEPHARITIS
or ulcerative blepharitis
Causative organisms are It is a/w seborrhoea ofscalp (dandruff).
Coagulase+ve Staphylococci (MC). Glands of Zeis secrete abnormal
Etiology Rarely, Streptococci, excess lipids which are split by
Propionibacterium acnes & Corynebacterium acne into irritating
Moraxella. freefatty acids.
Chronic irritation, itching, mild whitish material (soft scales) deposit at
lacrimation, gluing of cilia, and mild the lid margin irritation, occasional
Symptoms photophobia. The symptoms are watering
characteristically worse in the morning H/o falling of eyelashes
Accumulation of white dandruff-like
Yellow crusts are seen at the root of scales is seen on the lid margin,
cilia which glue them together. among the lashes.
Small ulcers, which bleed easily, are The lashes fall out easily but are
seen on removing the crusts. usually replaced quickly without
Signs distortion.
Red, thickened lid margins are seen
with dilated blood vessels (rosettes). Lid margin is thickened and the
Mild papillary conjunctivitis and sharp posterior border tends to be
conjunctival hyperemia. rounded leading to epiphora, in long
standing cases.
a)Lashabnormalities: madarosis (sparseness or absence of cilia), trichiasis (misdirected
cilia), and poliosis (greying of lashes).
b) Tylosis- thicken ing and scarring of lid margin.
Eversion of punctum leading to epiphora.
Complications Eczema of skin and ectropion may develop due to prolonged watering
e) Recurrent styes (external hordeola).
Marginal keratitis & phlyctenulosis
g) Tear film instability, and dry ee.

h) Secondaryinflammatory & mechanicalchangesintheconjunctiva and cornea.

1) Lid hygiene:
Warm compresses for 5-10 minutes
to soften the crusts, 1. Associated seborrhoea of the scalp
Remove Crust & clean lid margin with should be adequately treated.
3% NaHCO
2. Local measures: removal of scales from the
»Avoid rubbing of the eyes lid margin with the help of lukewarm solution of
Treatment 2) Antibiotics: 3% NaHCO

Abx eye drops: 3-4 times/day 3. Antibiotics, as described in bacterial

Oral antibiotics used in unresponsive patients blepharitis, may be required in patients with
mixed seborrhoeic and bacterial blepharitis.
3) Topical steroids (weak) such as
fluorometholone - for patients with papillary
conjunctivitis, marginal keratitis & phlyctenulosis.

|4) Artificial tear drops-for dry eyes

Posterior Blepharitis (Meibomitis) inflammation of Meibomian glands occurs in chronic & acute forms.
Chronic meibomitis:
Seen in middle aged persons, especially those with acne rosacea and/or seborrhoeic dermatitis.
Bacterial lipases play main role in the pathogenesis of chronic meibomitis.
Clinical features
Symptoms: chronic irritation, burning, itching, grittiness, mild lacrimation with remissions and
exacerbations intermittently. Symptoms are characteristically worse in the morning.
Signs:
1. White frothy (foam like) secretions are seen on the eyelid margins and canthi (meibomian
seborrhoea).
2. Opening of meibomian glands become prominent with thick secretions which can be
expressed out by pressure on the lids giving toothpaste appearance.
Vertical yellowish streaks shining through conjunctiva can be seen on eversion of the lids.
These represent the meibomian ducts filled with thick secretion.
4. Oily and foamy tear film with accumulation of froth on the lid margins or inner canthus.
5. Secondary changes: papillary conjunctivitis, and inferior corneal punctate epithelial erosions.
Acute meibomitis: it occurs due to staphylococcal infection. It is characterized by painful swelling
Pressure on it results in expression of pus followed by serosanguinous discharge.
Treatment of meibomitis
1. Lid hygiene: Warm compresses & Expression of accumulated secretions by repeated vertical
massage of lids in the form of milking.
2. Topical antibiotics in the form of eye ointment should be rubbed at the lid margin immediately
after massage, and Eye drops may be used 3-4 times a day.
3. Systemic tetracyclines, e.g, doxycycline 100 mg b.d. for 1 week and then o.d. for 6--12 weeks (to
block staphylococcal lipase production).
4. Erythromycin may be used where tetracyclines are contraindicated.
5. Ocular lubricants artificial tear drops.
6. Topical steroids (weak) such as fluorometholone required in patients with papillary
conjunctivitis.

9. Symblepharon [03]
Ans.
In this condition, lids become adherent with the eyeball as a result of adhesions between the palpebral
and bulbar conjunctiva.
Etiology: It results from healing of the kissing raw surfaces upon the palpebral and bulbar conjunctiva.
Common causes are thermal or chemical burns, membranous conjunctivitis, injuries, conjunctival
ulcerations, ocular pemphigus and Stevens-Johnson syndrome.
Clinical features:
1. Ocular movements become restricted,
2. Diplopia may be experienced due to restricted ocular motility,
3. Lagophthalmos, i.e., inability to close the lids may occur due to adhesions.
4. Cosmetic disfigurement is a common complaint.
5. Types of symblepharon, depending upon the
extent of adhesions, are as below: Anterior symblepharon Poslenor
ypes
symbiepharon
of symblopharon
|
Total symblepharon
 Anterior symblepharon-adhesions present only in the anterior part
>Posterior symblepharon-adhesions present in the fornices.
Total symblepharon-adhesions involving whole of the lid.
Complications: Dryness, thickening and keratinisation of conjunctiva due to prolonged exposure and
corneal ulceration (exposure keratitis).
Treatment
Prophylaxis: During the stage of raw surfaces, the adhesions may be prevented by:
Sweeping a glass rod coated with lubricant around the fornices several times a day
Therapeutic soft contact lens of large size, also helps in preventing the adhesions.
Curative treatment consists of symblepharectomy. The raw area created may be covered by:
Mobilising the surrounding conjunctiva in mild cases.
Conjunctival or buccal mucosal graft is required severe cases.
in
Amniotic membrane transplantation (AMT), also gives good results

VSQS
1) Homer's Syndrome [11]
Ans.
Horner's syndrome, occurring due to oculo-sympathetic paresis, is characterised by classic triad of:
1. Mild ptosis (due to paralysis of Muller's muscles),
Ptosis
2. Miosis (due to paralysis of dilator pupillae), and Small pupil
Nomal response
Reduced ipsilateral sweating (anhydrosis), to light and
convergence
Other features include mild enophthalmos, loss Horner's syndrome

of cilio-spinal reflex, heterochromia, i.e., ipsilateral iris is lighter in color, pupil is slow to dilate, and
there occurs slight elevation of the lower eyelid

2) Indications of Tarsorrhaphy [09]

Ans.

Inthis operation, adhesions are created between a part of the lid margins with the aim to narrow
down or almost close the palpebral aperture

Indications of TEMPORARY Tarsorrhaphy Indications of PERMANENT Tarsorrhaphy

1) To protect the cornea when 7th nerve palsy is 1. Cases of VIl nerve palsy where there is no
expected to recover. chance of recovery; and
2) To assist healing of an indolent corneal ulcer 2. Established cases of neuroparalytic
3) To assist in healing of skin-grafts of the lids in keratitis with severe loss of corneal
the correct position. sensations

3) Hordeolum Externum (stye) [08

Ans.
an acute suppurative inflammation of lash follicle and its associated
It is
stye
glands of Zeis or Moll.
Etiology
Causative organism: Staphylococcus aureus (MC).
Predisposing factors:
Age-more common in children and young adults.
Habitual rubbing of the eyes or fingering of the lids and nose, chronic blepharitis and DM.
Chronic debility, excessive intake of carbohydrates and alcohol
Clinical features
Symptoms: acute pain a/w swelling of lid, mild watering and photophobia.
Signs:
Stage of cellulitis- localised, firm, red, tender swelling at the lid margin.
Stage of abscess formation visible pus point on the lid margin in relation to the affected cilia.
Treatment
1) Hot compresses 2-3 times a day-useful especially in cellulitis stage.
2) Clear the pus by epilating the involved cilia.
3) Surgical incision is required for a large abscess.
4) Antibiotic eye drops, eye ointment & Systemic Abx should be used for early control of infection
5) Systemic anti-inflammatory and analgesics relieve pain and reduce oedema.
6) In recurrent styes, try to find out and treat the associated predisposing condition.
---

4) List the swellings in the lid [07]

Ans.
Oedema (swelling) of the lids is classified as inflammatory, solid and passive oedema:
Inflammatory oedema: It is seen in the following conditions.
1) Inflammations of the lid itself-dermatitis, stye, hordeolum internum, insect bites, cellulitis and
lid abscess.
2) Inflammations of the conjunctivaacute conjunctivitis.
3) Inflammations of the lacrimal sac, i.e., lacrimal abscess.
4) Inflammations of the lacrimal gland, ie., acute dacryoadenitis.
5) Inflammations of the eyeball - acute iridocyclitis, endophthalmitis and panophthalmitis.
6) Inflammations of the orbit orbital cellulitis, orbital abscess and pseudotumour.
7) Inflammations of the paranasal sinuses, e.g, maxillary sinusitis.
Solid oedema of the lids. It is chronic thickening of the lids, which follows recurrent attacks of
erysipelas.
Passive oedema of the lids. It may occur due to local or general causes.
Local causes: cavernous sinus thrombosis, head injury and angioneurotic oedema.
General causes: congestive heart failure, renal failure, hypoproteinaemia and severe anaemia
 Diseases of Lacrimal Apparatus
LQs
1) Chronic Dacryocystitis-etiology, c/F, complications& Mx [17, 10, 03]
a. Indications for Dacryocystorhinostomy (DCR) [08]
b. Indications of dacryocystectomy [07]
c. D.C.R. [96]
Ans.
Chronic Dacryocystitis is a chronic suppurative inflammation of the lacrimal sac due to the obstruction
of the nasolacrimal duct.
Etiology: It occurs due to a vicious cycle of stasis and mild infection of long duration.
Predisposing factors
1. Age more common in elderly (40-60 yrs).
2. Sex: predominantly seen in females (80%) (due to narrow lumen of the bony canal).
3. Heredity.
4. Low Socio-economic status & Poor personal hygiene.
Factors responsible for stasis of tears in lacrimal sac
1. Anatomical factors retard drainage of tears Ex: narrow bony canal of NLD etc.
2. Foreign bodies in the sac block opening of NLD
3. Excessive lacrimation causes stagnation of tears in the sac
4. Mild grade inflammation of lacrimal sac due to recurrent conjunctivitis may block the NLD.
5. Obstruction of lower end of the NLD by nasal polyps, DNS, tumours, atrophic rhinitis etc.
Source of infection: Lacrimal sac may get infected from the conjunctiva, nasal cavity (retrograde
spread), or paranasal sinuses.
Causative organisms: Staphylococci, Streptococci, Pneumococci and Pseudomonas pyocyanea.
Rarely chronic granulomatous infections like TB, syphilis, leprosy and occasionally Rhinosporidiosis.
Clinical features: They can be divided into 4 stages:
1 Stage of chronic catarrhal dacryocystitis: Mild inflammation of lacrimal sacblock NLD.
Watering eye is the only symptom in this stage
On syringing the lacrimal sac, either clear fluid or few fibrinous mucoid flakes regurgitate.
Dacryocystography reveals blockin NLD.
2. Stage of lacrimal mucocele. It follows chronic stagnation causing distension of lacrimal sac.
Here constant epiphora &a swelling is seen just below the inner canthus
Regurgitation test: Milky or gelatinous mucoid fluid regurgitates from the lower punctum on
pressing the swelling.
Dacryocystography at this stage reveals a distended sac with blockage somewhere in the NLD.
Encysted mucocele: Sometimes due to chronic infection, opening of both the canaliculi into the sac are blocked and a

large fluctuant swelling is seen at the inner canthus with a negative regurgitation test. This is called encysted mucocele.
3. Stage of chronic suppurative dacryocystitis: Due to pyogenic infection, the mucoid discharge
becomes purulent, converting the mucocele into 'pyocoele'
Here epiphora, recurrent conjunctivitis & swelling at the inner canthus with mild erythema of
the overlying skin is seen.
Regurgitation test; a frank purulent discharge flows from the lower punctum.
If openings of canaliculi are blocked at this stage the so called encysted pyocoele results.
4. Stage of chronic fibrotic sac: repeated infections thickening of mucosa small fibrotic sac due
to persistent epiphora and discharge. Dacryocystography, at this stage reveals a very small sac with
irregular folds in the mucosa.
Complications
Chronic intractable conjunctivitis; Acute on chronic dacryocystitis.
Ectropion of lower lid; maceration and eczema of lower lid skin due to prolonged watering.
Corneal ulceration.
High risk of developing endophthalmitis if an intraocular surgery is Endonasal DCR External DCR
performed in the presence of dacryocystitis. Advantages Disadvantoges
No external scar Cutaneous scar
Treatment Relatively more
Relatively blood less
Conservatlve treatment by probing & lacrimal syringing. surgery bleeding during surgery
Better visualisation of
Balloon catheter dilation (aka balloon dacryocystoplasty) hasal pathology

done in patients with partial NLD obstruction. Less chances of injury to Potential injury to
ethmoidal vessels and adjacent medial canthus
.Dacryocystorhinostomy (DCR): It is the operation of choice cribriform plate structures
Less time consuming (15- More operating time
as it re-establishes the lacrimal drainage. DCR can be done 30 minutes) since nasal (45-60 minutes)
by external or endoscopic approach. mucosal flaps and sac wall
flaps are not made
d. Dacryocystectomy (DCT): It should be performed only when No postoperative Significant
morbidity postoperative morbidity
DCR is contraindicated.
Disadvantages
Indications of DCT include: More success rate (956)
Less success rate (70-9096)
Too old patient. Requires skilled Easily performed by
ophthalmologist and/or ophthalmologists
Markedly shrunken and fibrosed sac. thinologist
TB, syphilis, leprosy or mycotic infections of saci Expensive equipment Cheap (expensive
equipment not required)
Tumours of sac. Requires reasonable Does not require
Gross nasal diseases like atrophic rhinitis access to middle meatus familiarity with
and familiarty with endoscopic anatomy
Conjunctivodacryocystorhinostomy (CDCR): It is performed endoscopic anatomy
in the presence of blocked canaliculi.

2) Acute Dacryocystitis etiology, C/F, complications & Mx [14, 90]

a. 4 complications of acute dacryocystitis [15]
b. Lacrimal Abscess [01]
Ans.
Acute Dacryocystitis is the acute suppurative inflammation of the lacrimal sac.
Etiology
Causative organisms: Streptococcus haemolyticus, Pneumococcus and Staphylococcus
Acute dacryocystitis may develop in 2 ways:
1. As an acute exacerbation of chronic dacryocystitis.
2. As an acute peridacryocystitis due to neighbouring infected structures such as: paranasal sinuses etc.
Clinical features-can be divided into 3 stages:
1) Stage of cellulitis: It is characterised by a painful swelling in the region of lacrimal sac a/w epiphora,
fever and malaise. The swelling is red, hot, firm and tender. Redness and oedema also spread to the lids & cheek.
2) Stage of lacrimal abscess: Continued inflammation occlusion of the canaliculi due to oedema.
Lacrimal sac is filled with pus, distends and its anterior wall ruptures Lacrimal abscess.
3) Stage of fistula formation: When the lacrimal abscess is left un-treated, it discharges, leaving an
external fistula below the medial palpebral ligament. Rarely, the abscess may open up into the
nasal cavity forming an internal fistula.
 Complications: Acute conjunctivitis, Lid abscess, Osteomyelitis of lacrimal bone, Orbital cellulitis,
Conversion of corneal abrasion into corneal ulceration, Facial cellulitis etc.
Treatment
1. During cellulitis stage -systemic & topical Abx to control infection; Analgesics &hot fomentation
to relieve pain and swelling.
During stage of lacrimal absces, in addition to the above treatment, pus should be should be
gently squeezed out and dressing should be done with betadine-soaked rauze. Later on, either DCT
or DCR operation should be carried out, otherwise recurrence wil occur
3. Treatment of external lacrimal fistula: After controlling the acute infection with systemic Abx,
fistulectomy along with DCT or DCR operation should be performed.
--------
sQs
1. Epiphora [97]
a. Causes of Epiphora [12]
Ans.
Epiphora is the watering of eyes due to inadequate drainage (outflow) of normally secreted tears.
Causes ofepiphora:
1) Physiological cause is lacrimal pump' failure due to lower lid laxity or weakness of orbicularis muscle.
'

2) Mechanical obstruction in lacrimal passages may lie at the level of punctum, canaliculus, lacrimal sac or NLD.
a. Punctal causes:
Eversion of lower punctum: seen in old age (due to laxity of the lids), chronic conjunctivitis etc.
Punctal obstruction:
Congenital absence of puncta
a small foreign body can also block the punctum.
Prolonged use of drugs like idoxuridine and pilocarpine is also a/w punctal stenosis.
b. Canalicular obstruction: It may be congenital or acquired due to FB, trauma, canaliculitis due to actinomyces etc.
C. Causes in the lacrimal sac: congenital mucous membráne folds, traumatic strictures, dacryocystitis,infections like
TB and syphilis, dacryolithiasis and tumours.
d. Causes in the NLD:
GCongenital causes: non-canalization, partial canalization or imperforated membranous valves.
Acquired causes: traumatic strictures, inflammatory strictures, idiopathic stenosis, tumours etc.
Diagnosis: via Dacryocystography. It tells the exact site, nature and extent of block.
Radionucleotide Dacryocystography (lacrimal scintillography): It is a non-invasive technique to assess
the functional efficiency of lacrimal drainage apparatus.

VsQs
1. Causes of dry eye [16)
Ans.
"Dry eye is a multifactorial disease of the ocular surface characterized by loss of homoeostasis of the
tear film, and accompanied by ocular symptoms, in which tear film instability and hyperosmolarity,
ocular surface inflammation and damage, and neurosensory abnormalities play etiological roles".
Holly and Lemp classified dry eye in 1977. It can be clasified as follows

Aqueous deficiency Lipid deficlency Mucin deficiency

Keratoconjunctivitis sicca (KCS) Evaporative dry eye

Causes
SjOgren's syndrome Meibomian gland disease (MGD) Vitamin A deficiency
Non-Sjögren's Posterior blepharitis Pemphigoid
Age-related hyposecretion Rosacea Stevens-Johnson syndrome
Congenital alacrima Atopic keratoconjunctivitis Chemical burns
Lacrimal gland disease Low blink rate (Bell's palsy) Trachoma
Riley day syndrome Contact lens wear

2. Tear film [10]

Ans.
Tear Film consist of 3 layers, which from anterior to posterior are Lipid layer, Aqueous layer & Mucus layer
Lipid Layer Aqueous Layer Mucous layer
Secreted Meibomian, zeis & moll Goblet cells & Gland of
Lacrimal Glands
by glands Manz
Supplies atmospheric O, to Converts hydrophobic
evaporation &
cornea & has antibacterial
Functions corneal surface to
lubricates the eyelids
function hydrophilic
Tearfilm

Lipid layer-a

Aqueous layer-b
Cornea - Mucin layer -c
Microvilli
 CONTENTS
Disease ofOrbit.s60sseeeeessesssesescssss0secessssessessccscsssss 3
SQs. 3
VsQs..
Ocular Injuries.
SQs.
VSQs..

Ocular Pharmacology xwes 10

**** 10
1
VsQs.. ***

Lasers&Cryotherapy in Ophthalmology 5 12
SQs.. 12
VsQs. 13

.14
SystemicOphthalmology 0000oosorocseocereeroessesroessee
LOS. .14
SQs. I .14
VSQs. .16

Community OphthalmologyRxs ss 17
SQss * 17
Clinical Methodsin Ophthalmology.ooa
LOS *****aann 20
SQs "*auumuusmuuuunn20

VSQs. = 21
 Disease of Orbit
sQs
1. Orbital Cellulitis- C/F & Complications [15, 07, 05]
Ans.
Orbital cellulitis refers to an acute infection of the soft tissues of the orbit behind the orbital septum
Etiology
1. Exogenous infection-from penetrating injury, retention of intraorbital foreign body, and following
operations like evisceration, enucleation, dacryocystectomy and orbitotomy.
Extension of infection from neighbouring structures (MC) like paranasal sinuses, teeth, face, lids,
intracranial & intraorbital structures.
3. Endogenous infection: It may rarely develop as metastatic infection from breast abscess, puerperal
sepsis, thrombophlebitis of legs and septicaemia.
Causative organisms: Staphylococcus aureus, Streptococcus pneumoniae, Streptococcus pyogenes &
Haemophilus influenzae.
Pathology-similar to suppurative inflammations in general, except for the following special features:
Infection establishes early due to absence of lymphatics in the orbit.
Damage produced is extensive as orbital infection is associated with raised intraorbital pressure
duetothe tight compartment.
Clinical features of Orbital Cellulitis
Symptoms Signs
Swelling & severe pain (T by 1. Swelling of lids -woody hardness & redness.
movements of the eyeball) 2 Restriction of ocular movements
Associated general symptoms 3. Chemosis of conjunctiva
fever, nausea, vomiting and 4 Axial proptosis of varying degree is present.
prostrations. 5. RAPD may occur.
Vision loss t diplopia may also 6. Fundus examination may show congestion of retinal veins
OCCur and signs of papillitis or papilloedema.
Complications:
1 Ocular complications vision loss due to exposure keratopathy, optic neuritis & CRAO.
2 Orbital complications subperiosteal abscess & orbital abscess diagnosed by CT scan
-

Subperiosteal abscess is a collection of pus between the orbital bony wall and periosteum.
Orbital abscess is collection of pus within the orbital soft tissue.
3. Temporal or parotid abscesses may occur due to spread of infection around the orbit.
4. Intracranial complications > cavernous sinus thrombosis, meningitis & brain abscesses.
5. General septicemia or pyaemia
Investigations
1) Bacterial cultures from nasal swabs, conjunctival swabs & blood samples.
2) CBP may reveal leukocytosis.
3) X-ray PNS to identify associated sinusitis.
4) Orbital ultrasonography to detect intraorbital abscess.
5) CT scan and MRI are useful:
In differentiating preseptal and postseptal cellulitis;
In detecting subperiosteal & orbital abscesses,
 In detecting intracranial extension; and
In deciding when and from where to drain an orbital abscess.
Treatment
Orbital cellulitis is an emergency and so the patient should be hospitalised for aggressive Mx.
1) Intensive Abx therapy: based on susceptibility
For Staphylococcal infections oxacillin + ampicillin.
Cefotaxime, ciprofloxacin or vancomycin may be used alternatively.
To cover H. influenzae esp. in children, chloramphenicol or clavulanic acid should also be added.
To cover anaerobes oral metronidazole 500 mg every 8 hours should be added.
2) NSAIDS are helpful in controlling pain and fever.
3) Topical antibiotic eye ointment- if there is severe proptosis.
4) Nasal decongestants
5) Revaluation, at least 2-3 times daily in the hospital, is required to monitor the response and modify
the treatment accordingly.
6) Surgical intervention: Its indications include unresponsiveness to antibiotics, decrease in vision and
presence of an orbital or subperiosteal abscess.
Immediate canthotomy/cantholysis If the orbit is tight, optic neuropathy is present or T 1OP
-

Subperiosteal abscess is drained by a 2-3 cm curved incision in the upper medial aspect.
In most cases, it is necessary to drain both the orbit as well as the infected paranasal sinuses.

2. Cavernous sinus thrombosis [13]

Ans
Cavernous sinus thrombosis, refers to infected blood clot.
Etiology: It occurs due to the extension of thrombosis from various sources which communicate with
the cavernous sinus
Communications of cavernous sinus and sources of Infection
1) Anteriorly, the superior & inferior ophthalmic veins drain in the sinus. These veins receive blood from face, nose,
para nasal sinuses and orbits.
2) Posteriorly, the superior and inferior petrosal sinuses leave it to join the lateral sinus. Labyrinthine veins opening
into the inferior petrosal sinuses bring infections from the middle ear. Mastoid emissary veins may spread
infection from the mastoid air cells
3) Superiorly, the veins Middle meningeal veinss
Superior ophthalmic vein
of the cerebrum may Lateral sinus

be infected from
Frontal vein +{
JUU FMastoid emissary
ein
meningitis and 1 Superior ptrosal sinus
Angular vein
cerebral abscesses. Labyrinthine vein
4) Inferiorly, the sinus Jugular vein
communicates with Facial vein Inferior ophthalmic vein
pterygoid venous Pterygoid plexus Inferior petrosal sinus
plexus. ***
5) Medially, the two
cavernous sinuses are Communications of cavernous sinus-ateral view
connected with each other by transverse sinuses which account for transfer of infection from one side to the
other
Clinical features: CST starts initially as a unilateral condition, which soon becomes bilateral due to
intercavernous communication.
Hence, appearance of sigrns and symptoms in the opposite eye is diagnostic of cST.
 The condition is
characterised by general and ocular features. of 22
General features - abrupt onset of high-grade fever with chills and rigors, vomiting and headache.
Ocular features
Severe pain in the eye and forehead on the affected side.
Conjunctiva is swollen and congested.
Proptosis develops rapidly.
Oedema in mastoid region is pathognomic sign (ocurs due to back pressure in mastoid emissary vein)
a
Ophthalmoplegia is sequential-6th nerve palsy occurs first as it passes through the cavernous
sinus; 3rd and 4th nerves are involved later as they are related to the lateral wall of cavernous
sinus.
Ipsilateral ptosis, dilated pupil, and absence of direct & consensual pupillary light reflex are signs
of 3rd nerve palsy.
Corneal anaesthesia, i.e., loss of corneal reflex due to paralysis of Ví
In advanced cases, retinal veins show congestion and there may appear papilloedema.
Vision loss may occur in later stages
Investigations
CTscan head and orbit may show involvement of cavernous sinuses and proptosis.
Magnetic resonance venography (angiography) is the investigation of choice which shows an
absence of flow void in thrombosed sinuses.
Blood culture is recommended for sepsis.
Complications: At any stage, Clinical features Cavernous sinus thrombosis Orbital cellulitis
1. Laterality Initially unilateral, but soon Unilateral
hyperpyrexia & signs of meningitis or becomes bilateral
pulmonary infarction may precede death. . Degree of proptosis Moderate Marked
3. Vision Not affected in early stage Not affected in early stage
Differential diagnosis: orbital cellulitis
and panophthalmitis 4. Cornea and anterior Clear in early stages Clear in early stages
chamber
Treatment
5. Ocular movements Complete limitation to palsy Marked limitation
a) Antibiotics Massive doses of
IV
6.Oedema in mastoid Present Absent
modern potent broad-spectrum Abx region
b) Analgesics and anti-inflammatory 7.General symptoms Marked Mild
with fever, and
drugs control pain and fever. prostrations
c) Anticoagulants' role is controversial

VSQs
1. Causes of Enophthalmos [07]
Ans.
Enophthalmos is the inward displacement of the eyeball.
Causes of Enophthalmos:
1. Congenital Microphthalmos and maxillary hypoplasia
2. Traumatic- Blow out fractures of floor of the orbit.
3. Post-inflammatory-Cicatrization of extraocular muscles as in the pseudotumour syndromes.
4. Paralytic enophthalmos: It is seen in Horner's syndrome (due to paralysis of cervical sympathetics).
5. Atrophy of orbital contents due to age & irradiation of malignant tumours following cicatrizing8
metastatic carcinoma and due to scleroderma
 Ocular Injuries
sQs
1) Closed globe injuries [13]
a. Vossius Ring [16]
b. Berlin's Oedema [04]
c. Effect of blunt injury on the eye [96]
Ans.
Closed-globe injury is the one in which eyewall (sclera and cornea) does not have a full thickness
wound but there is intraocular damage. It includes contusion & lamellar laceration.
Contusion refers to the closed-globe injury due to blunt trauma.
GLamellar laceration refers to the closed-globe injury by a sharp object or blunt trauma.
G CAUSES
Direct blow to the eyeball by fist, a tennis or cricket ball or blunt instruments like sticks & big
stones.
Can also occur in roadside accidents, injuries by agricultural and industrial machines etc.
LESIONS OF CLOSED-GLOBE INJURY

1 Cornea.
a)Simple corneal abrasions -These are very painful and diagnosed by fluorescein staining.
b) Recurrent corneal erosions (recurrent keratalgia) occur due to finger nail trauma.
c) Partial corneal tears (lamellar corneal laceration)
d) Tears in Descemet's membrane are known to occur in birth trauma.
e) Acute corneal oedema.
f)Blood staining of cornea
2. Sclera: Partial thickness scleral wounds (lamellar scleral lacerations) may occur
3. Anterior chamber: Traumatic hyphaema (blood in the anterior chamber) & Exudates
4. Iris, pupil and diliary body
a. Traumatic miosis & Traumatic mydriasis (Iridoplegia)
b. Rupture of the pupillary margin.
C. Radiating tears in the iris stroma.

d. Iridodialysis, i.e., detachment of iris from its root at the ciliary body D-shaped pupil
e. Anti-flexion & Retroflexion of the iris
f. Traumatic aniridia or iridemia- iris sinks to the bottom of anterior chamber
8. Inflammatory changes - traumatic iridocyclitis, haemophthalmitis, post-traumatic iris atrophy
and pigmentary changes.
5. Lens:
1) Vossius ring: It is a circular ring of brown pigment seen on the anterior capsule. It occurs due
to striking of the contracted pupillary margin against the crystalline lens. It is always smaller
than the size of the pupil.
2) Concussion (traumatic) cataract Feathery oflines

3) Traumatic absorption of the lens aphakia (esp. in young children) radiating opacitbies
Bxlend aiong sulures

4) Subluxation of the lens occur due to partial tear of zonules.

Early rosete cataract
5) Dislocation of the lens occurs due to complete rupture of the
zonules.
 7 of 22
Vitreous
Detachment of the vitreous
Vitreous haemorrhage.
Vitreous herniation in the anterior chamber may occur with subluxation or dislocation of the lens.
7. Choroid rupture, haemorrhage & detachment
8. Retina
a) Commotio retinae (Berlin's oedema) - milky white cloudiness in the posterior pole with a 'cherry
red spot' in the foveal region. It may disappear after some days
or may be followed by pigmentary changes.
Milky white retina
b) Retinal haemorrhages& Retinal tears. Chery red spot

c)Traumatic proliferative retinopathy (Retinitis proliferans). Berlin's oedema

d) Retinal detachment
e) Traumatic macular oedema > pigmentary degeneration.
9. 1OP changes in closed-globe injury Traumatic glaucoma & Traumatic hypotony.
10.Traumatic changes in the refraction
Myopia may follow ciliary spasm or rupture of zonules or anterior shift of the lens.
Hypermetropia & loss of accommodation may occur from damage to the ciliary body (cycloplegia).

2) Open globe injury C/F & complications [10]

Antenior chamber
Ans.
Open-globe injury refers to a full-thickness wound of eyewall (sclera & cornea).
It includes rupture and laceration of eyewall.
Globe Rupture (inside to outside break) caused by a blunt object. Extraocular

Globe Laceration (outside to inside break)-caused by a sharp object. It trecus Sdera

Onnon Ses lor reenton of

includes penetrating injuries (has entry wound), perforating injuries (has entry
andexit wound) & Intraocular FB.
Open globe injury Clinical Features Treatment
Wounds of the conjunctiva Suture if it is> 3 mm
Pad & bandage with atropine & Abx
Uncomplicated corneal wounds ointments for Small Wounds
Suture for Large wounds
Globe Laceration Complicated corneal wounds (a/w
Suture the wound after abscising the iris
prolapse of iris)
'Corneo-scleral tear & Scleral wounds 1 suture should be applied at limbus.
sdeross bub Kae cer m Lensectomy
Wounds of the lens (Ex: lens ruptures) Small wounds in the anterior capsule may seal
and lead on to traumatic cataract which should
managed accordingly
| Severely wounded eye EXcision
» a/w: Prolapse of uveal tissue, vitreous
It is Repair of tear in the eyewall should be
loss, intraocular haemorrhage & done meticulously under general
dislocation of the lens anaesthesia to save the eyeball whenever
Globe rupture possible
Accompanying signs include irregular
pupil, hyphaema, commotio retinae Post-op Abx, steroids & Atropine
choroidal rupture, and retinal tears Enucleation in badly damaged eye

3) Blow out fracture [09]

 Ans. 8 of 22
Blow-out fractures are isolated comminuted fractures which occur when the orbital walls are pressed
indirectly. These mainly involve orbital floor and medial wall.
Etiology-Trauma to the orbit by tennis ball, cricket ball, human fist or part of an automobile.
Clinical features
1. Periorbital oedema and blood extravasation in and around the orbit (such as subconjunctival ecchymosis)
occur immediately.
2. Emphysema of the eyelids
3. Paraesthesia and anaesthesia in the distribution of infraorbital nerve (lower lid, cheek, side of nose, upper lip
and upper teeth)
4. Ipsilateral epistaxis as a result of bleeding from maxillary sinus into the nose
5. Proptosis - occurs because of associated orbital oedema and haemorrhage.6
6. Enophthalmos (inward displacement of eyeball) and mechanical ptosis.
7. Diplopia.
Orbital imaging
Plain X-rays taken in Water's view revealfragmentation of the orbital floor and herniation of
contents into maxillary antrum (hanging drop or tear drop sign)
CT scan &MRI for detailed visualisation of soft tissues & evaluating the extent of the fracture
-

Management
General measures and medical treatment
a) Cold compresses, immediately after trauma may swelling by causing vasoconstriction
b) Avoid nose blowing, as it may contribute to surgical emphysema and herniation of soft tissue.
c) Systemic antibiotics should be given to prevent secondary infection from the maxillary sinus.
d) Analgesics and anti-inflammatory drugs to decrease pain and swelling.
Surgical repair to restore continuity of the orbital floor.
-

Indications of surgical intervention include:

G Large herniation of tissues into the antrum
Diplopia not resolving significantly.
GEnophthalmos >3 mm.

4) Sympathetic ophthalmitis [09, 99

Ans.
Sympathetic ophthalmitis is a serious bilateral granulomatous panuveitis which follows a penetrating
ocular trauma. The injured eye is called exciting eye and the fellow eye which also develops uveitis is
called sympathizing eye, Very rarely, sympathetic ophthalmitis can also occur following an intraocular surgery.
Predisposing factorsz child, penetrating injury, Wounds in the ciliary region, incarceration of the iris,
lens capsule etc.
Pathogenesis: Allergic theory - it states that the uveal pigment acts as an allergen and excites plastic
uveitis in the sound eye.
Pathology It is characteristic of granulomatous uveitis, i.e., there is:
Aggregation of lymphocytes, plasma cells, epithelioid cells & giant cells throughout the uveal tract.
Dalen-Fuchs' nodules are formed due to proliferation of the pigment epithelium (of the iris, ciliary
body and choroid) associated with invasion by the lymphocytes and epithelioid cels.
Sympathetic perivasculitis: Retina shows perivascular cellular infiltration.
 Clinical features

In Exciting (injured) eye In Sympathizing(sound)eye

Here, Clinical feature can be divided into 2 stages which occur after 4-8
weeks of injury in the other eye:
GFeatures of Prodromal stage
persistent low grade
Symptoms: photophobia & transient indistinctness of near objects
plastic uve itis: ciliary (due to weakening of accommodation)
congestion, lacrimation
Signs:
and tenderness
GKeratic precipitates Presence of retrolental flare and cells
may be present at Presence of KPs on back of cornea.
Mild ciliary congestion, slight tenderness of the globe,
the back of cornea
(dangerous sign) Vitreous haze and disc oedema.
Fully-developed stage - typical signs & symptoms of acute plastic
iridocyclitis are seen
Treatment
Early excision (enucleation) should be done when the injured eye has no useful vision
Conservative treatment:
Corticosteroids should be administered by ll routes, i.e., systemic, periocular injections & frequent instillation of topical drops.

Immunosuppressant drugs should be started in severe cases, without delay.

Atropine should be instilled three times a day in all cases.
Prognosis
»It is good if steroid therapy is commenced early.
»It is bad if the uvea is heavily infiltrated and inflammation has taken firm hold

VSQs
1. Cherry red spot {incl Causes) [16, 15, 09, 05]
-

Ans.
Milky white retina
Differential diagnosis of cherry red spot Cherry red spot
1) Tay-Sachs disease
Attenuated
2) Niemann-Pick disease artenes
3) Myoclonus
Central retinal artery Occlusion
4) Berlin's oedema
5) Macular hole or haemorrhage.
 Ocular Pharmacology
SQs
1) Pilocarpine [16, 11, 08, 02]
Ans.
direct-acting parasympathomimetic drug.
It is a
Ocular Indications
i) Primary open-angle glaucoma;
i) Acute angle closure glaucoma;
(ii) Chronic synechial angle-closure glaucoma
Contraindications: inflammatory glaucoma, malignant glaucoma and known allergy.
Available preparations and dosage are
a. Eye drops are available in 1%, 2% and 4% strengths > Effect last upto 4-6 hours. Hence, it is given
every 6th or 8th hiurly
b. Ocusert are available as pilo-20 and pilo-40. These are changed once in a week.
C. Pilocarpine gel (4%) is a bedtime adjunct to the daytime medication.

2) Timolol maleate [14]

a. Action and adverse effects of Beta blockers [10]
Ans.
MOA: Timolol is a nonselective B-blockerblock Ba receptors in the ciliary processes aqueous
production 1OP.
Indications
O B blockers are useful in all types of glaucomas, viz., developmental, primary and secondary; narrow
as well as open angle.
B-blockers are the 1" choice in POAG & all secondary glaucomas.
Contraindications: bronchial asthma, emphysema, COPD, heart blocks, congestive heart failure or
cardiomyopathy; Known drug allergies etc.
Preparations: Timolol is available as 0.25% and 0.5% eye drops > effects last up to 24 hours. Hence, it
is used once or twice daily.
The drug is very effective, however the phenomenon of 'short-term escape' and long-term drif
are well known.
Adverse-effects:
1. Ocular side-effects: burning, conjunctival hyperaemia, superficial punctate keratopathy & corneal
anaesthesia.
2. Systemic side-effects
cVS effects (due to B, block): bradycardia, arrhythmias, heart failure and syncope
Respiratory effects (due to B, block); bronchospasm & airway obstruction, esp in asthmatics.
CNS effects: depression, anxiety, confusion, drowsiness, disorientation, hallucinations etc.
Miscellaneous effects: nausea, diarrhoea, decreased libido, skin rashes, alopecia & exacerbation
of myasthenia gravis

3) Atropine (incl it's uses in OphthaImology} [12, 11, 09, 071

a. Homatropine [03]
Ans.
Atropine is a parasympatholytic Drug
MOA: It competitively block the Muscarinic effects of Ach (competitive antagonism){refer pharma)
Uses in Ophthalmology: Atropine, homat ropine, cyclopentolate or tropicamide are used topically as
mydriatic & cycloplegic for refraction testing
For fundoscopic examination, short acting agent like Tropicamide is used.
In iridocyclitis atropinic mydriatics are used alternatively with miotics to break adhesions between
iris& lens

4) Anti-Glaucoma drugs [09, 05]

a. Topical drugs for glaucoma [05, 99]
Ans.
Anti-Glaucoma Drugs ( 1OP)
Pilocarpine (miotics)
Drugs to t trabecular outfloww Dipivefrine
Bimatoprost
Dipivefrine
Drugs to t uveoscleral outflow
Latanoprost
CAinhibitors (ex: acetazolamide)
Drugs to J aqueous production a agonist (ex: dipivefrine, epinephrine)
Bblockers (ex: timolol)
Hyperosmotic agents Ex: Mannitol

5) Uses of steroids in Ophthalmology [04, 03]

a. Uses of cortisones in Ophthalmology (97]
Ans.
1 Topical preparations are used in scleritis, uveitis, allergic conjunctivitis, allergic keratitis, cystoid
macular oedema and after intraocular surgery.
2. Systemic preparations are used in scleritis, posterior uveitis, Vogt-Koyanagi-Harada (VKH)
syndrome, papillitis, retrobulbar neuritis, malignant exophthalmos, orbital lymphangioma and
corneal graft rejections.

Vsas
1. Cycloplegic drugs [16
Ans.
cycloplegics are the drugs which cause paralysis of accommodation and dilate the pupil (cycloplegia)
Ex (Pa) Atropine, Homatropine, Cyclopentolate, Tropicamide& Phenylephrine.
Indications: These are used for wet retinoscopy

2. Uses of Acetazolamide in Ophthalmology [13]

Ans.
Alltypes of acute & chronic Glaucomas: to IOP by formation of aqueous humour.
Used either orally or topically.
Oral preparations have many side effects> Paresthesias, Urinary Frequency, electrolyte imbalance, Gl

symptoms etc.
 Lasers and Cryotherapy in Ophthalmology
sQs
1. Uses of laser in Ophthalmology [12, 08]
a. Nd YAG laser [14, 02]
Ans.
LASERis an acronym for 'Light Amplification by Stimulated Emission of Radiation'
LASER EFFECTS THERAPEUTIC APPLICATIONS
Photoradiation Corneal collagen linking with riboflavin
(Photochemicaleffect)

1. Eyelid lesions haemangioma.

2. CorneaTreatment of corneal neovascularisation.
In glaucoma- Ex: Laser iridotomy for narrow-angle glaucoma etc.
Lesions of iris:
Photomydriasis for pathologic miotic pupil,
Laser sphincterotomy.
2) Photocoagulation Lesions of retina and choroid:
Diabetic retinopathy- Pan Retinal Photocoagulation (PRP)
Intraocular tumours retinoblastoma, malignant melanoma and
choroidal haemangioma.
Macular diseasesAge-related macular degeneration (ARMD).
For sealing of holes in retinal detachment.
1) Nd: YAG laser: {wavelength -1064 nm)
Capsulotomy for thickened posterior capsule
Membranectomy for pupillary membranes.
Iridotomy & Vitreolysis.
Phacolysis in phacoemulsification technique of cataract extraction

3) Photodisruption2) Femtosecond laser:

Creation of corneal flap for LASIK
Creation of tunnel for intracorneal rings,
Arcuate incisions to correct corneal astigmatism,
Keratoplasty incisions,
Small incision lenticule extraction (SMILE) for correction of myopia
Femtosecond laser assisted cataract surgery (FLACS).
Excimer (Argon fluoride laser)
Photorefractive keratectomy (PRK)
Laser assisted in situ keratomileusis (LASIK) for correction of refractive
4) Photoablation errors and
Phototherapeutic keratectomy (PTK) for corneal diseases such as band-
shaped keratopathy
 vsQs
1) Uses of cryo in ophthalmology [11]
Ans.
1. Lids: Cryosurgery may be used for following lesions:
(i) Cryolysisfor trichiasis
(i) Cryotherapy for warts and Molluscum contagiosum,
(ii) Cryotherapy for basal cell carcinoma and haemangioma.
2. Conjunctiva: Cryotherapy is used for hypertrophied papillae of vernal catarrh and ocular surface
squamous neoplasia (0sSN).
Cornea: Herpes simplex keratitis may be treated by cryotherapy.
4.
Lens: Cryoextraction of the lens used to be the best intracapsular technique. However, nowadays
intracapsular cataract extraction (ICCE) is no more performed.
5. Ciliary body: Cyclocryopexy for absolute glaucoma and neovascular glaucoma.
6. Retina:
Cryopexy for sealing retinal holes in retinal detachment.
b. Prophylactic cryopexy to prevent retinal detachment in predisposed cases.
Anterior retinal cryopexy (ARC) in retinal ischaemic disease, e.g., retinopathy of prematurity to
prevent neovascularization.
d. Cryo treatment of retinoblastoma.
 SystemicOphthalmology
LQs
1. Describe the various viral infections of the eye and its complications [02]
Ans.
Viral
Ocular Lesions &Complications
Infections
Measles Catarrhal conjunctivitis, Koplik's spots on conjunctiva, corneal ulceration, optic neuritis
andretinitis
Mumps Conjunctivitis, keratitis, acute dacryoadenitis and uveitis
Rubella Congenital microphthalmos, cataract, glaucoma, chorioretinitis and optic atrophy
1. Retinal microvasculopathy develops from vaso-occlusive process. It is
characterised by nonspecific lesions:
a) Multiple 'cotton wool spots' occur in 50% cases,
b) Superficial and deep retinal haemorrhages occur in 15- 40% cases, and
c) Microaneurysms and telangiectasia may also be seen rarely.
2. Usual ocular Infections becomes severe in patients with AIDS. These include:
Herpes zoster ophthalmicus, Herpes simplex infections, Toxoplasmosis
AIDS
(chorioretinitis), and Ocular tuberculosis, syphilis and fúngal corneal ulcers.
Opportunistic infections of the eye: These are caused by micro-organisms which do
not affect normal patients. These include: Cytomegalovirus (CMV) retinitis, Candida
endophthalmitis, Cryptococcal infections, Pneumocystis carini, and Choroiditis.
4. Unusual neoplasms:
Kaposi's sarcoma - on the eyelid or conjunctiva
Burkitt 's lymphoma of the orbit.
5. Neuro-ophthalmic lesions: Cranial nerve palsiesparalysis of eyelids, extraocular
muscles, Loss of sensory supply to the eye, loss of vision etc.

Management:
CMV infections can be treated by zidovudine, ganciclovir and foscarnet.
G Kaposi's sarcoma responds to radiotherapy
Herpes zoster ophthalmicus is treated by acyclovir.

SQs
1) Ocular features of Vitamin A deficiency [16]
a. Vitamin A deficiency [03]
b. Bitot Spot [02]
C. Avitaminosis Vitamin A (Ocular) [2000]

Ans.
Ocular manifestations of vitamin A deficiency arc referred to as xerophthalmia.
Etiology: It occurs either due to dietary deficiency of vitamin A or its defective absorption.
Clinical features
1) Night blindness: It is the earliest symptom of xerophthalmia in children.
2) Conjunctival Xerosis: It consists of one or more patches of dry, lustreless, non-wettable
conjunctiva.
 15 of 22
3) Bitot' s spot: It is an extension of the xerotic process. The Bitot' s spot is a raised, silvery white,
foamy, triangular patch of keratinised epithelium, situated on the bulbar conjunctiva
4) Corneal xerosis: cornea lacks lustre.
5) Cormeal ulceration/keratomalaciastromal defects blindness.
6) Corneal scars: Healing of stromal defects results in corneal scars of different densities and sizes.
7) Xerophthalmic Fundus: It is characterized by typical seed-like, raised, whitish lesions scattered
uniformly over the pan of the fundus at the level of optic disc

Treatment
1. Local ocular therapy:
For conjunctival xerosis: artificial tears (0.7% hydroxypropyl methyl cellulose) should be instilled
every 3-4 hours.
GFor keratomalacia: full-fledged treatment of bacterial corneal ulcer should be instituted.
Vitamin A therapy: The WHO recommended schedule is as given below:
() All patients above the age of 1 year (except women of reproductive age): 200,000 IU of vitamin
A orally or 100,000 IU by IM injection should be given immediately on diagnosis and repeated
the following day and 4 weeks later
(i) Children under the age of 1 year- should be treated with half the doses for patients of more
than 1 year of age.
ii) Women of reproductive age, pregnant or not:
For s
night blindness, conjunctival xerosis and Bitot' spotsDaily dose of 10,000 IU of
vitamin A orally (1 sugar coated tablet) for 2 weeks.
For corneal xerophthalmia same as described for patients above 1 year of age
3. Treatment of underlying conditions such as PEM and other nutritional disorders, diarrhoea,
dehydration and electrolyte imbalance, infections and parasitic conditions should be considered
simultaneously

2) Night blindness [12, 04]

Ans.
Night Blindness (Nyctalopia) occur in patients with rod dysfunction, media opacities & advanced
POAG.
Causes of Night Blindness
Rod dysfunction Media opacities: Advanced POAG
It can be due to
A deficiency,
Here ocular media interfere
Vitamin
Tapetoretinal degenerations with the light rays in dim light In advanced cases of primary
(i.e., with dilated pupils). open angle glaucoma, dark
(e.g, retinitis pigmentosa),
Seen in: adaptation may be so much
Congenital high myopia,
Peripheral Cortical cataract delayed that patient gives
Congenital night blindness, & history of night blindness
and
Corneal opacities
Oguchi's disease

Treatment of Night Blindness: it depends on the cause; hence proper evaluation is the key.
 16 of 22
3) Common causes of Blindness in India [08] RAAB Survey (2006-07)
Ans.
Disease condition Percent
Blindness is defined as, "Visual acuity < 3/60 (Snellen) or counting finger at blindnes
a distance of 3 meters or central visual field < 10 degrees". Cataract
Refractive errors (0.76) .3
aphakia (5.6%)
Glaucoma
Rapid assessment of avoidable blindness (RAAB) survey has been carried
Complications of S.0

out in India to estimate the magnitude & causes of blindness: cataractsurgery

Corneal opacity 5.5
including trachoma
Posterior segment 3.0
disorders (DR, 0.1%+
ARMD 0.7% + others
2.2%)

VsQs
1. Foods rich in Vitamin-A [14]
Ans.
Animal sources: milk, butter, cream, cheese, egg yolk and liver. Fish liver oils (cod liver oil and shark
liver oil)
Vegetable sources: Carrot, Papaya, mango, pumpkins, green leafy vegetables (spinach, amaranth) and
drumsticks

2. WHO classification of Blindness [10]

Ans.
As per WHO, 10th Revision of ICD, the vision impairment Category off visual Level of visual acuity
(maximum vision less than 6/ 18 Snellen in the better eye) has impairment (Snellen)
Normal vision: 0 6/6 to 6/18
been divided into 4 categories: Moderate vision Less than 6/18 to 6/60
impairment
Severe vision Less than 6/60 to 3/60
impairment
Blindness:
Less than 3/60 (FC at 3 m
or visual field <10

3. Preventable blindness [06]

Ans.
Preventable blindness is that which can be easily prevented by attacking the causative factor at an
appropriate time.
Ex: corneal blindness due to vitamin A deficiency and trachoma can be prevented by timely measures.
 Community Ophthalmology
sQs
1. NPCB (National Programme for Control of Blindness) [04, 02]
a. Role of Primary Health Center in NPCB. [11]
b. Mobile Eye Camp [11]
C. Primary Eye Care System [08]

d. Eye Bank [05]

Ans.
National Prosramme for Control of Blindness and Visual Impalrment (NPCB&VD In Indla:
Previously called as NPCB launched in 1976 e 1or Contro
Objectives:
a. Reduction in the backlog of blindness through identification and
treatment of blinds.
b. Development and strengthening of eyecare facilities in every district.
Development of human resources for providing eye care services.
c.
d. Improvement in quality-of-service delivery.
e. Securing participation of voluntary organizations and private practitioners in eye care.
f. Enhancement in community awareness on eye care.
8. Setting up of mechanism for referral, coordination and feedback between organizations
dedicated to prevention, treatment and rehabilitation.
Definition of Blindness (same as definition by WHO):
G Presenting visual acuity «3/60 in better eye
or
GVisual Field limitation to < 10 degrees
Prevalence of Blindness: 1.05%
Main Causes: Cataract (MC)> Refractive errors> Glaucoma
Adoption of vision 2020: Right to Sight in 2001 is the most prestigious major flip for NPCB
Vision 2020 was Launched in 1999 in Geneva but India adopted in 20o1
Aim:
a) To reduce blind people to as million by 2020
b) To eliminate avoidable blindness by 2020
7 diseases covered by Vision 2020 in India: Cataract, Refractive Errors, Glaucoma, Corneal
Blindness, Childhood Blindness, Trachoma & Diabetic Retinopathy
Since 2001, NPCB is being implemented as per guidelines of the initiative Vision 2020".
During 12t five-year plan (2012-2017), from it has been decided to continue the NPCB under the
NCD pool of the recently approved 'National Health Mission'
The contribution of the central government will be 75% and that of state/UT government will be
25% of the total fund requirement for NPCB.
Primaryeye care System: This is defined as the provision of promotive, preventive and therapeutic
measures for eye health to individuals and the community at peripheral level (PHCs & subcentres)
under NPCB.
Promotive and preventive activities focus on health education.
Education is aimed at making the people aware that the majority of blinding diseases are
preventable or curable.
 f 22
Alocally available, willing person is selected and trained as a primary care worker
The health worker is trained to recognize common eye conditions and take appropriate action.
The 'kit' includes a hand torch, vision measuring chart, antibiotics (usually tetracycline eye
ointment), vitamin A capsules, zinc sulphate eye drops, bandages, sticking plaster, epilation
forceps and eye shields
Community ophthalmology practice at primary level

Promotive |Preventive Curative Rehabilitative

Nutrition education Ocular prophylaxis at Vision screening Provision of low vision
Improved maternal birth Treatment for vitamin A services
and ch nutrition Vitamin A doses deficiency Community based
Health education Measles vaccine Referral for surgery rehabilitation
Face washing Perinatal care Emergency management Counselling of the incurable
blind
Good antenatal care Avoid medication in Treatment for trachoma
Safe water pregnancy Treatment for other Certification of blind by eye
surgeon
Improved Avoid hypoxia at birth common eye diseases
environmental Examine neonate's eyes Sensitise about concessions
sanitation Nutrition
supplementation

Mobile Eye Camp:

a team of specialized staff (ophthalmologists, nurses, optometrists and technicians) form a mobile
ophthalmic unit which conducts 'eye camps' in the rural areas, with the assistance of several NGOs.
Facilities: screening for common eye diseases, refraction and prescription of glasses, cataract
surgery, surgery for angle-closure glaucoma, optical iridectomies and referral of complicated cases.
They also provide health education.
These units are supported by the government to deliver basic eye health facilities to communities
who cannot otherwise avail of them
A central body organizes health education,
Primary eye Secondary Tertiary eye
care ye care
training of staff, evaluates and monitors all
activities related to the National programmes
for the prevention of blindness

Eve bank is an organization which deals with Mobile eye

services
the collection, storage and distribution of
cornea for the purpose of corneal grafting, Modkl for aa difecive eye caue delivery snie

research and supply of the eye tissue for other ophthalmic purposes.
GFunctions of an eye bank
1) Promotion of eye donation by 1 awareness about eye donation to the general public.
2) Registration of the pledger for eye donation.
3) Collection of the donated eyes from the deceased.
4) Receiving and processing the donor eyes.
5) Preservation of the tissue.
6) Distribution of the donor tissues to the corneal surgeons.
7) Research activities for improvement of the preservation methodology, corneal substitute and
utilisation of the other components of eye.
Eye Bank Personne
1) Eye bank in-charge - should be an ophthalmologist
 2) Eye bank technician - record data pertaining to donor material and waiting list of patients
3) Clerk-cum-storekeeper - coordinate with other eye banks.
promote voluntary eye donation
4) Medical social worker -
5) Driver- maintain vehicle of the eye bank
G Legal aspect: The collection and use of donated eyes come under the preview of 'The
Transplantation of Human Organs Act, 1994'
GFacts about eve donation
a. The eyes have to be removed within six hours of death.
b. The eyes cannot be removed from a living human being in spite of his/ her consent and wish

REHABILITATION OF THE BLIND: A blind person needs the following types of rehabilitation
1) Medical rehabilitation- By low vision aids (LVA)
2) Training and psychosocial rehabilitation:
blinds should be assured and made to feel that they are equally useful and not inferior to the
sighted persons.
GMobility training with the help of a stick.
Training in daily living skills such as bathing, washing, putting on clothes, shaving, cooking etc.
3) Educational rehabilitation 'Blind Schools' with the facility of Braille system of education.
4) Vocational rehabilitation It will help them to earn their livelihood and live as useful citizens.
Blinds can be trained in making handicrafts, book binding, candle and chalk making, cottage
industries and as telephone operators.

2. Legal Blindness [2000, 98]

Ans.
Vision in better eye <1/60 to perception light is called Legal Blindness.

"Legal blindness" is a definition used by the US government to determine eligibility for vocational
training, rehabilitation, schooling, disability benefits, low vision devices, and tax exemption programs
 Clinical Methods in Ophthalmology
LQs
1) A 45-year-old man, tailor by profession reports to eye O.P.D. with complaints of painless gradual
diminution of vision. Describe DDx and principles of treatment [10]
a. Enumerate causes for painful diminution of vision [15]
b. Enumerate the causes for sudden loss of vision [11, 03]
c. Enumerate the causes for gradual loss of vision [08]
d. Enumerate the causes of Gradual dimension of vision in a person above the age of 50 years and
how will you investigate such a case [97]
e. Sudden loss of vision in one eye etiology&DDx [90
Ans.

Sudden Loss of Vision Gradual Loss of visionn

Painless Painful Painless Painful
1. CRAO0 Mechanical injuries to
1) 1. Corneal degenerations 1) Corneal

2. CRVO eyeball 2. Refractive errors ulcerations

3. Massive Vitreous2) Chemical injuries to 3 Senile cataract 2) Chronic
Hemorrhage eyeball 4. Developmental cataract iridocyclitis
4. Retinal 3) Acute Congestive 5. Optic atrophy
Detachment Glaucoma 6. Diabetic retinopathy
4) Acuteiridocyclitis
Refer to the respective topics for principles.

SQs
1. Fundus Fluorescein Angiography (FFA)-indications, technique and complications [16, 11]
Ans.
FFA is atool which helps to diagnose various fundus disorders by using fluorescein dye along the
vasculature of the retina and choroid.
Indication- Disorders of ocular fundus, viz.,
1. Diabetic retinopathy
2. Vascular occlusions
3. Eales' disease.
4. Central serous retinopathy,
5. Cystoid macular oedema
Contraindications: renal impairment and known allergy to fluorescein.
Technique: Rapidly inject 5 mL of 10% solution of sterile sodium fluorescein dye in the antecubital vein
and take serial photographs (with fundus camera) of the fundus of the patient who is seated with
pupils fully dilated.
Complications: Minor side effects include: discoloration of skin and urine, mild nausea and rarely
vomiting. Anaphylaxis or cardiorespiratory problems are extremely rare.
Phases of Angiogram:
1. Pre-arterial phase
2. Arterial phase
3. Arteriovenous phase
Venous phase
Abnormalities detected by FFA:
Causes of hyperfluorescence CAUSES OF HYPO FLUORESCENCE
LEAKAGE OF DYE FROM THE VESSELS SEEN IN CASES OF -
1. Blockage of background
PROLIFERATIVE DIABETIC RETINOPATHY & IN AGE-RELATED fluorescence due to abnormal
MACULAR DEGENERATION deposits on retina, e.g., as seen
LEAKAGE OF DYE FROM OPTIC NERVE HEAD AS SEEN IN due to the presence of retinal
PAPILLEDEMA haemorrhage, hard exudates
3. WINDoW DEFECT IN RPE DUE TO ATROPHY and pigmented clumps
4. POOLING OF DYE UNDER DETACHED RPE, E.G., ARMD 2. Occlusion of retinal or
5. POOLING OF DYE UNDER SENSORY RETINA AFTER choroidal vasculature, e.g., as
BREAKDOWN OF THE OUTER BLOOD-RETINAL BARRIER ASs seen in centra retinal artery
I

OCcUR IN CENTRAL SEROUS RETINOPATHY (CSR) occlusion and occlusion of

6. STAINING, I.E., LONG RETENTION OF DYE BY SOME TISSUES, capillaries in diabetic
E.G. AS SEEN IN THE PRESENCE OF DRUSEN AND NORMAL retinopathy.
OPTIC DISC 3. Loss of vasculature as occurs in
patients with choroideremia
and myopic degeneration.

VSQs
1) Relative Afferent Pupillary Defect (RAPD) [17]
a. Marcus Gunn pupil [13, 12, 09, O5]

Ans.
Marcus Gunn pupil is the paradoxical response of a pupil to light in the presence of optic nerve lesions
and severe retinal diseases.
Swinging flash light test: a bright flash light is shone on to one pupil & then quickly moved to the
contralateral pupil. This swinging to-and-fro of flash light is repeated several times while observing the
pupillary response. Normally, both pupils constrict equally and the pupil to which light is transferred
remains tightly constricted. In the presence of RAPD in one eye, the affected pupil will dilate when the
flash light is moved from the normal eye to the abnormal eye. This response is called 'Marcus Gunn
pupil' or a relative afferent pupillary defect (RAPD).
Significance: Marcus Gunn pupil is the earliest indication of optic nerve disease even in the presence
of normal visual acuity.
****
2) Applanation Tonometry [16]
Ans. It is based on Timbert-Fick law which states that the pressure inside a sphere (P) is equal to the
force (W) required to flatten its surface divided by the area of flattening (A); i.e., P = W/A.
Commonly used applanation tonometers are:
1. Goldmann tonometer: It is the most popular
and accurate tonometer. It requires slit-lamp.
2. Perkin's applanation tonometer: it is small,
easy to carry and does not require slit-lamp. Too smal: 8, Too large:
Flg. 23.15 End point ol applanalion tonomesry: A, End pont
C.

3. Pneumatic tonometer: In this tonometer,

there is a pneumatic-to-electronic transducer, which converts the air pressure to a recording on a
paper strip, from where 1OP is read.
4. Pulse air tonometer
5. Tono-Pen is a computerised pocket tonometer.
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3) Madarosis [13]
Ans. It refers to partial or complete loss of eyelashes.
Causes:
LOcal causes chronic blepharitis, cicatrizing conjunctivitis, & complication of cryotherapy,
radiotherapy or surgery done for any eyelid lesion.
Svstemic causes alopecia, psoriasis, hypothyroidism and leprosy.

4) Ciliary Vessels [09]

Ans.
BLOODSUPPLY OF UVEAL TRACI
Arterial supply: 3
1. Short posterior ciliary arteries-(br. of ophthalmic artery).

Long posterior ciliary arteries

3. Anterior ciliary arteries (arise from muscular branches of ophthalmic artery).
Venous drainage: A series of small veinsform the vortex veins (4 in number - Superior temporal,
inferior temporal, superior nasal and jnferior nasal) pierce the sclera behind the equator and drain
into superior and inferior ophthalmic veins, which in turn, drain into the cavernous sinus