Preface

Agam is a group of budding medicos, who are currently doing their under graduation in
various Medical Colleges across Tamil Nadu and Pondicherry. The group was initiated on 18th
November 2017, in the vision of uniting medicos for various social and professional causes.
We feel delighted to present you Agam Ophthalmology notes prepared by Agam Divide and
Rule 2020 Team to guide our fellow medicos to prepare for university examinations.

This is a reference work of 2017 batch medical students from various colleges. The team
took effort to refer many books and make them into simple notes. We are not the authors of the
following work. The images used in the documents are not copyrighted by us and is obtained from
various sources.

Dear readers, we request you to use this material as a reference note, or revision note, or
recall notes. Please do not learn the topics for the 1st time from this material, as this contain just the
required points, for revision.
Acknowledgement

On behalf of the team, Agam would like to thank all the doctors who taught us Ophthalmology.
Agam would like to whole heartedly appreciate and thank everyone who contributed towards the
making of this material. A special thanks to Barath Raj R, who took the responsibility of leading the
team. The following are the name list of the team who worked together, to bring out the material in
good form.

 A Anusha Lakshmi
 Hareesh Kumar
 Balaji
 Saahini
 Kiran
 Prathish
 Aishwarya
 Vaishali
 Annal
 Preethi
 Anusha Suresh
 Menaka
 Priyadharsini K
 Ramachandran
 Sri Komali
 Sneha Jenifer
 Udayalakshmi
 Theeraja Padmanaban
 Priyadarshini N
 Mansee
 Preethii S P
 Mano
 Heera
 Vanisri
 Preethi Thiruna
 Puvashree
 Srividhya
 Shreeshivani
 Manigandan A
 Gokulakrishnan
 Arjun  Mruddula
 Jason Thetralavan  Kareeshmaa H C
 Praveena  Madhumetha
 Mruthulagi
 Greeshma
 Raghunandhan
 Shobana
 Vanisri
 Kamesh
 Fahima
 Yogesh
 Sneha
 Shalini
 Pradakshini
 Dharshini
 Jayalakshmi
 Joanna
 Anchitha
 Volume 1

 Anatomy and Physiology of EYE

 Errors of Refraction
 Diseases of Conjunctiva
 Diseases of Cornea
 Diseases of Sclera
 Diseases of Uveal tract
 Diseases of Lens
 Glaucoma
 Anatomy of eye

Eyeball is a cystic structure kept distended by the pressure inside it.

Shape - oblate spheroid.

Wall- dense - imperfectly elastic.

Transparent cornea and opaque sclera.

Dimension of adult eyeball

Anteroposterior diameter 24mm

Horizontal 23.5mm

Vertical 23mm

Circumference 75mm

Volume 6.5 ml

Weight 7 gm

Parts of eyeball

Coat-

I. Outer fibrous coat - dense strong.

 Anterior 1/6th is transparent - cornea.

Posterior 5/6th opaque- sclera.

Junction between the cornea and sclera is called limbus.

Function - protects intraocular contents.

Cornea

Cornea transparent front part of eyeball has different layers:

a. Epithelium

b. Bowman's membrane

c. Stroma ( substantia propria )

d. Dua's layer ( pre descemet's layer)

e. Descemet's membrane

f. Endothelium

Transparency of cornea -
Stromal collagen fibrils at regular diameter arranged as lattice with an interfibrillar spacing of less than wavelength of
light so that longitudinal row of fibres acr as diffraction grating resulting in destructive interference of scattered rays.
 Sclera

Outer surface is covered by conjuctiva.

Beneath it is a loose connective tissue called episcleral.

Inner layer has circular venous sinus broken up into more lumen called canal of schlemm.

Innermost layer has elastic fibres- lamina fusca.

Inner aspect of sclera has uveal tract and retina.

II. Middle vascular layer ( uveal tissue )-

Function- supplies nutrition.

Has 3 parts.

Iris

Composed of stroma containing branched connective tissue.

Stroma is covered by 2 layer of pigmented epithelium on posterior surface.

Anterior layer has flattened cells.

Posterior later has cuboidal cells.

Thinnest at attachment to ciliary body.

Function- control of movement of pupil by - Sphincter pupillae.

Dilator pupillae.

Ciliary body

It is isosceles triangle in shape with base forward..

Unstripped muscle fibre - ciliary muscle.

Inner surface of ciliary body- Para plicata- anteriorly.

Para plana- posteriorly .

Extends backwards as ora serrata at which retina proper begins.

Choroid

Extremely vascular.

Space between sclera and choroid is called epichoroidal/suprachoriodal.

Inner side is made of elastic membrane called lamina vitrea or membrane of bruch.

Beneath the lamina vitrea is capillary plexus called choriocapillaries.

III. Inner nervous coat( retina )

Projects to visual cortex.

Function- concerned with visual function.

Retina

Made up of 10 layers with 2 distinct functional component- pigment epithelium and neurosensory
retina.

Layers

i. pigment epithelium- outer most layer.

Adherent to basal lamina ( bruch's membrane ).

Function - metabolic support to neurosensory retina.

Antireflective layer.

Space between pigment epithelium and neurosensory has interphoto receptor

matrix- it's constituents are

Inter-photoreceptor retinal binding protein (IRBP)

proteoglycan-glycosaminoglycans (sulphated and nonsulphated chondroitin and

hyaluronic acid)
fibronectin, sialoprotein associated with rods and cones (SPARC)

intercellular adhesion molecules

hyaluronic acid receptor (CD44 antigen)

lysosomal enzymes (matrix metalloproteinases and tissue inhibitors of
metalloproteinases, i.e., TIMP).

ii. Layers of rod and cones- aka photoreceptor.

End organ of vision

Rod- subseeve peripheral vision and visslion of low illumination.

Cones- highly discrimatory central vision and colour vision.

iii. External limiting membrane - has fenestrations in it.

iv. Outer nuclear layer- has nuclei of rods and cones.

v. Outer plexiform layer- connection of rod spherules and cone pedicles with dentrites of bipolar
cells of horizontal cells.

vi. Inner nuclear layer- cell bodies of bipolar cells, horizontal, amacrine, Muller cells and capillaries
of Central artery of retina.

vii. Inner plexiform layer- connection between the axons of

bipolar cells, dendrites of ganglionic cells and processes of amacrine cells.

viii. Ganglionic cell layer- cell bodies of ganglionic cells

There are 2 types of ganglionic cells- midget ganglion cell and polysynaptic
ganglionic cells.

ix. Nerve fibre layer ( stratum opticum )- axons of ganglionic cells.

x. Internal limiting membrane- seperates retina from vitreous formed by union of terminal
expansion of Muller's fibres.

At posterior pole about 3 mm to temporal side of optic disc a

differentiated spot found in retina- fovea centralis- it is a depression/ pit with only cones present- it
is most sensitive part of retina.
Fovea centralis- is surrounded by small area of macula lutea.

Segments and chambers-

a. Anterior segment- has lens,

iris, cornea, and 2 aqueous filled lspaces. Anterior chamber-
boundary: anteriorly back of cornea ; posteriorly anterior
surface of iris and part of ciliary body- communicates with
posterior chamber through pupil.

Posterior chamber- triangular- has 0.06ml aqueous humor.

Boundaries: anteriorly- posterior surface of iris, part of ciliary
body; posteriorly- crystalline lens, it's zonules, laterally by
ciliary body.

b. Posterior segment- Structure

posterior to lens- vitreous humour,retina,choroid,optic disc.
 Lens

Biconvex

3main parts- outer capsule- made up of epithelium.

Lens fibres- surface ectoderm.

Nucleus- central denser zone surrounded by cortex has youngest fibres.

Aqueous humour:-

The aqueous humour is a clear watery fluid filling the anterior chamber and the posterior chamber
of the eyeball.

Function- maintains proper intraocular pressure - provides substrates and removes metabolites
from the avascular cornea and the crystalline lens.

Viterous humour:-

Jelly like with few cells and wandering leucocyte- occupies posterior chamber.

Viterous body attached anteriorly to posterior lens surface by ligament of weigert.

Posteriorly to margin of optic disc and macula forming ring around each structure and large blood
vessel.
 Blood supply
Arteries
Ophthalmic artery, a branch of internal carotid artery, constitutes the main source of blood supply
for the eyeball and other orbital structures.

Veins

Veins draining blood from the eyeball include

• Central retinal vein which drains blood from the retina;

• Anterior ciliary veins, short posterior ciliary veins and venae verticosae which drain blood from the
uveal tissue.

Main venous channels which ultimately get tributaries from various orbital structures include :
• Superior ophthalmic vein,
• Inferior ophthalmic vein,
• Middle ophthalmic vein,
•Medial ophthalmic vein,
• Angular vein, and
• Cavernous sinus.

Retinal circulation- The retina is supplied by the central retinal artery, which enters the optic nerve
on its lower surface.

The central artery divides on, or slightly posterior to, the surface of the disc into the main retinal
trunks.

The retinal arteries are end-arteries and have no anastomoses at the ora serrata. The only place
where the retinal system anastomoses with any other is in the neighbourhood of the lamina
cribrosa.

Blood supply of optic nerve-

The blood supply of the optic nerve head in the region of the lamina cribrosa is served by fine
branches from the arterial circle of Zinn but mainly from the branches of the posterior ciliary arteries
.
 The central retinal artery makes no contribution to this region. The prelaminar region is supplied by
centripetal branches from the peripap-illary choroidal vessels with some contribution from the
vessels in the lamina cribrosa region.

Venous drainage of the optic disc is mainly carried out by the central retinal vein. The prelaminar
region also drains into the choroidal veins. There is no venous channel corresponding to the circle of
Zinn.

The central retinal vein communicates with the choroidal circulation in the prelaminar region.

Ciliary circulation-

The uveal tract is supplied by the ciliary arteries, which are divided into three groups—the short
posterior, the long posterior and the anterior.

The ciliary veins also form three groups—the short posterior ciliary, the vortex veins and the anterior
ciliary.

The short posterior ciliary arteries supply the whole of the choroid. The ciliary body and iris are
supplied by the long posterior and anterior ciliary arteries.
 Nerve supply
Sensory nerves
[Link] nerve- Ophthalmic nerve, smallest of the three divisions of trigeminal (5th cranial)
nerve, supplies the various ocular structures through its three branches
a. Lacrimal nerve. It lies in the lateral part of the orbit
and supplies lacrimal gland, conjunctiva and lateral part of upper eyelid.
b. Frontal nerve. It divides into two branches in the middle of orbit:■Supratrochlear
nerve supplies the conjunctiva, middle part of upper eyelid, and skin of the forehead above the root
of nose.

■Supraorbital nerve supplies the conjunctiva, central part of upper eyelid, and part
of the skin of forehead and scalp.
c. Nasociliary nerve. It has following branches:
■Long ciliary nerves, two in number, supply sensory nerves to the ciliary body,
iris and cornea.
■Communicating branchesto ciliary ganglion form its sensory root and their
fibres pass along the short ciliary nerves, to supply the ciliary body, iris and cornea.

■posterior ethmoidal nerve supplies the ethmoidal and sphenoidal air sinuses.
■Anterior ethmoidal nerve is a terminal branch of nasociliary nerve which leaves
the orbit through the anterior ethmoidal foramen.
■Infratrochlear nerve is the other terminal branch of nasociliary nerve. It
supplies the conjunctiva, lacrimal sac, caruncle, and medial part of the eyelids.
Motor nerves
• 3rd, 4th and 6th cranial nerves supply the extraocular muscles, and
• 7th cranial nerve branches supply the orbicularis oculi muscle of the eyelids.

Autonomic nerves

Parasympathetic nerves
Edinger-Westphal nucleus, located in midbrain Postganglionic nerve fibres from
ciliary ganglion travel along the short ciliary nerves to supply the sphincter pupillae muscle and
postganglionic fibres from the accessory ganglion supply the ciliary muscle.
Salivatory nucleus, located in pons sends preganglionic fibres through facial
nerve to the sphenopalatine ganglion. Postganglionic secretomotor fibres finally reach the lacrimal
gland through the lacrimal nerve.
Ciliary ganglion Ciliary ganglion is a peripheral parasympathetic ganglion placed
in the course of oculomotor nerve near the apex of orbit.

Roots of ciliary ganglion include:

■Sensory root,

■Sympathetic root of ciliary ganglion

■Parasympathetic root of ciliary ganglion

Short ciliary nerves, branches of ciliary ganglion

Sympathetic nerves- Preganglionic fibres

Postganglionic fibres

■Orbital arteries receive vasomotor fibres through the plexuses around

ophthalmic artery.
■Dilator pupillae muscle is supplied by the sympathetic fibres from the
carotid plexuses
 ■Palpebral(Muller’s) muscle of the eyelid
is supplied by the postganglionic fibres.

Visual pathway

Components are retina with optic nerve, optic chiasma, optic tract,
lateral geniculate bodies, optic radiation, visual cortex.

Optic nerve- It is II cranial nerve ends up to optic chiasma

Parts:- Intraocular part.

Intraorbital part.

Intracanalicular part.

Intracranial part.

Optic chiasma- flattened structure measuring 12 mm( horizontally ) lies over tuberculin and
diaphragms sellae.

Fibres from nasal half decussate.

Optic tract- cylindrical bundles of nerve fibres running outward and backward from posterolateral
aspect of optic chiasma.

It carries temporal fibres of retina of same eyes and nasal fibres of retina from opposite
side.

Lateral geniculate bodies- oval structure at posterior termination of optic tract.

Consist 6 layers of neurons.

Optic radiation- carries fibres from lateral geniculate bodies to visual cortex.

Visual cortex- medial aspect of occipital lobe above and below the calcarine fissure.

Subdivided into Visuosensory area ( area 17 )

Visuopsychic area ( area 18,19 )

 REFRACTIVE ERRORS AND ACCOMODATION OF EYE

What will we learn here?

• Errors of refraction
Emmetropia
Ametropia
Hypermetropia
Myopia
Astigmatism
Anisometropia
Aniseikonia
Aphakia
Pseudophakia
• Accommodation
• Anomalies of accommodation
Presbyopia
Insufficiency
Paralysis
Spasm
• Determination of refractive
errors
• Modalities for correction of
refractive errors
Spectacles
Contact lenses
Refractive surgeries
 EMMETROPIA

❖ Optically normal eye

❖ Definition:
It is a state of refraction were parallel rays of light coming from infinity are
focused at the sensitive layer of retina with the accommodation being at rest.

❖ Emmetropization:
The series of changes which occur in the eye from birth to about 14 years of
life in order to maintain and achieve emmetropia
• Increasing axial length (18mm -> 24mm)
• Change in power of lens
• Cornea flattens
• Increase in Anterior chamber depth
 AMETROPIA

❖ Definition:
It is a state of refraction, when parallel rays of light coming from infinity, do not
come to focus upon the light sensitive layer of the retina i.e.: they are focused
either in front or behind the sensitive layers of retina, in one or both the meridians.

❖ Ametropia includes
→ Myopia
→ Hypermetropia
→ Astigmatism

Myopia Hypermetropia

Astigmatism
❖ Etiological classification:
→ Axial ametropia – abnormal length of the globe
→ Curvature ametropia – abnormal curvature of refracting surfaces (cornea,
lens)
→ Index ametropia – abnormal refractive indices of the media
→ Abnormal lens position

Ametropia Myopia Hypermetropia

Axial (length) Long Short

Curvature Too strong – more Too weak – flatter

curved – steeper cornea corneas

Index (refractive index R.I. of cornea, aqueous R.I. of cornea, aqueous

– R.I.) or lens – high or lens – low

Vitreous – low Vitreous – high

Abnormal lens Forward displacement Backward displacement
position
 HYPERMETROPIA

❖ Also known as hyperopia or long sightedness

❖ Definition:
It is a Refractive state of the eye wherein parallel rays of light coming from
infinity are focused behind the retina with accommodation being at rest.

❖ Etiological classification:
→ Axial hypermetropia (commonest)
→ Curvatural hypermetropia
→ Index hypermetropia
→ Positional hypermetropia
→ Absence of crystalline lens (Aphakia)
→ Consecutive hypermetropia

→ Axial hypermetropia
▪ Total refractive power of eye is normal but there’s axial shortening of
eyeball.
▪ Maybe developmental or pathological.
▪ High hypermetropia occurs in microphthalmos and nanophthalmos.
→ Curvature Hypermetropia
▪ Curvature of cornea, lens or both is flatter than the normal leading to
Decrease in refractive power
▪ Developmental or rarely pathological
▪ Common factor in astigmatism
→ Index Hypermetropia
▪ Decrease in refractive index due to cortical sclerosis
▪ Common in Old age and diabetes
→ Positional Hypermetropia
▪ Posteriorly placed crystalline lens
→ Aphakia
▪ Absence of crystalline lens – high hypermetropia
▪ Congenital or acquired
→ Consecutive hypermetropia result of
▪ Overcorrected myopia after refractive surgery
▪ Underpowered intraocular lens implantation during cataract surgery
and refractive lens exchange
 ❖ Clinical types of hypermetropia:

Hypermetropia

Physiological Non physiological Functional

Developmental
Congenital
axial

Developmental
Acquired
curvatural

Congenital non physiological Acquired non physiological Functional hypermetropia

conditions: conditions: conditions:

▪ Microphthalmos ▪ Senile ▪ oculomotor nerve

▪ Nanophthalmos ▪ Positional paralysis
▪ Microcornea ▪ Aphakia ▪ internal
▪ Posterior subluxation ▪ Consecutive ophthalmoplegia
of lens ▪ Axial
▪ Aphakia ▪ Curvatural
▪ Pseudophakia

❖ Clinical features:
→ Symptoms
▪ Asymptomatic (when the refractive error is small)
▪ Asthenopenic symptoms (due to sustained accommodative efforts)
 Tiredness of eyes
 Headache
 Watering of eye
▪ Defective vision with Asthenopenic symptoms
▪ Defective vision only.
 → Signs
▪ Size of eyeball – appears small
▪ Corneal – small
▪ Anterior chamber – shallow
▪ Retinoscopy and autorefractometry – hypermetropic refractive error
▪ Fundus examination
• Small optic disc
• Vascular ill-defined margins
• Shot silk appearance
▪ A- scan ultrasonography – short anteroposterior length – axial type

❖ Grading: (according to American Optometric association)

→ Low hypermetropia <=2D
→ Moderate hypermetropia +2D to +5D
→ High hypermetropia >=5D

❖ Complications:
→ Recurrent styes, chalazia, blepharitis
→ Accommodative convergent squint
→ Amblyopia
→ Predisposition to primary narrow angle glaucoma

❖ Treatment:
→ Optical treatment
▪ Convex lens of appropriate power
▪ Preference: Spectacles > Contact lenses
→ Surgical treatment
▪ Cornea based procedures
i. Thermal laser keratoplasty
ii. Conductive keratoplasty
iii. Hyperopic PRK
iv. Hyperopic LASIK
▪ Lens based procedures
i. Phakic refractive lens
ii. Refractive lens exchange
 Hypermetropia and its
correction using convex lens

❖ Nomenclature:

Total
Hypermetropia
TOTAL = LATENT+MANIFEST(F+A)

Latent Manifest
Hypertropia corrected Hypertropia not
by inherent tone of corrected by the tone
ciliary muscle of ciliary muscle

Facultative Absolute
Hypertropia corrected Hypertropia not
by patient's corrected by patient's
accomodative effort accomodative efforts
 MYOPIA

❖ Also known as short-sightedness

❖ Definition:
A type of refractive error in which parallel rays coming from infinity are focused
in front of retina when accommodation is at rest

❖ Etiological classification:
→ Axial myopia
→ Curvatural myopia
→ Positional myopia
→ Index myopia
→ Myopia due to excessive accommodation

→ Axial myopia
▪ Increase in AP length of eyeball
▪ Commonest
→ Curvatural myopia
▪ Increase in curvature of cornea/ lens/ both
→ Index myopia
▪ Increase in refractive index of lens
→ Positional myopia
▪ Anterior placement of lens
 → Myopia due to excessive accommodation
▪ Occurs in patients with spasm of accommodation

❖ Grading: (according to American Optometric Association)

→ Low myopia </=-3D

→ Moderate myopia -3D to -6D
→ High myopia >/= -6D

❖ Clinical classification:

→ Congenital
→ Simple or developmental
→ Pathological or degenerative
→ Acquired or secondary
▪ Post-traumatic
▪ Post-keratitic
▪ Drug induced
▪ Pseudomyopia
▪ Space myopia
▪ Night myopia
▪ Consecutive myopia

Congenital myopia
▪ Present since birth, diagnosed by 2-3 years of age
▪ Anisometropia (usually unilateral) present
▪ High degree error (8-10D)
▪ Convergent squint may develop
▪ Maybe associated with congenital anomalies
→ Cataract
→ Microphthalmos
→ Aniridia
→ Megalocornea
→ Congenital separation of retina
Simple myopia
▪ Commonest
▪ Physiological
▪ Also called school myopia
▪ Normal biological variation

Etiology: Clinical features:

→ Axial type
→ Curvatural type Symptoms
→ Short sightedness
→ Role of diet
→ Asthenopic symptoms
→ Role of genetics
→ Half shutting of eyes
→ Theory of excessive near
Signs
work
→ Prominent eyeballs
→ Limited outdoor activity
→ Anterior chamber deeper
→ Pupils large
→ Fundus Normal, rarely - temporal myopic crescent
→ Magnitude of error - low to moderate

Pathological myopia
→ Rapidly progressive disorder
→ Less common
→ Etiology
▪ Role of heredity
▪ Role of general growth process

Genetic factors
General growth factors

more growth of retina

stretching of sclera

• ↑axial length
• degeneration of choroid,
vitreous and retina
Clinical features:
Symptoms:
→ Defective vision
→ Muscae volitantes – floating black opacities on front of the eye
→ Difficulty in night vision

Signs:
→ Prominent eyeballs (posterior pole elongation)
→ Cornea- large
→ Anterior chamber - deep
→ Pupils - large, react sluggishly
→ Magnitude- high, increase rapidly
→ Fundus examination
Optic disc Degenerative changes Posterior Degenerative
in retina and choroid staphyloma changes in
vitreous
Large and pale Chorioretinal atrophic Ectasia of sclera at Liquefaction
patches at macula posterior pole
Temporal Opacities
crescent Foster-Fuchs' spot at
macula- dark red
PVD - Weiss'
Peripapillary circular patch
reflex
crescent
Cystoid degeneration
Supertraction
crescent - nasal Lattice degeneration/
snail track lesions

Total retinal atrophy

→ Visual field – Contraction and Ring scotoma

→ ERG - Subnormal - Chorioretinal atrophy
❖ Complications:

→ Retinal detachment
→ Complicated cataract
→ Vitreous haemorrhage
→ Choroidal haemorrhage
→ Strabismus fixus convergence

❖ Treatment:

Treatment

optical surgical low vision aids

→ Optical:

▪ Concave lenses
▪ In high myopia - contact lenses preferred to avoid peripheral distortion and
minification
 → Surgical:

Cornea based procedures Lens based procedures

▪ Radial keratotomy ▪ Refractive lens exchange
▪ Laser ablation corneal ▪ Phakic refractive lens
procedures (implantable contact lens)
▪ Refractive lenticule extraction
▪ Intercorneal ring
transplantation
▪ Orthokeratology

→ Low vision aids:

▪ Indicated in patients with progressive myopia having advanced degenerative
changes.
▪ Spectacles and contact lenses are not useful.

❖ Preventive measures:

Therapeutic interventions General measures Genetic counselling

1. Atropine drops 1. Balanced diet Two individuals having

2. Pirenzepine 2. Early management of progressive myopia are
associated advised not to marry – since
debilitating disease it has strong genetic basis
3. Visual hygiene
4. Avoidance of
excessive near work
 ASTIGMATISM

❖ Definition:
A type of refractive error wherein refraction varies in different meridian of eye,
so that the rays of light entering the eye cannot converge to a point focus but form
focal lines.

❖ Broadly astigmatism is divided into:

→ Regular
→ Irregular

REGULAR ASTIGMATISM

❖ When the refractive power uniformly changes from one meridian to another (2
principal meridians present)

❖ Etiological classification:

→ Corneal astigmatism (most common)

▪ Abnormality of curvature of cornea
→ Lenticular astigmatism (rare)
▪ Types:
 Curvatural – abnormalities in curvature of lens
 Positional – subluxation of lens
 Index – variable refractive index of lens
→ Retinal astigmatism
▪ Oblique placement of macula

❖ Optics:

Sturm’s conoid
The configuration of rays refracted through a toric surface is called a sturm’s
conoid.
Point Rays
A Vertical rays converge more than horizontal rays
B Vertical rays are focused while horizontal rays
are still converging
C Divergence of vertical rays < convergence of
horizontal rays Focal
D – circle of least Divergence of vertical rays = convergence of Interval
diffusion horizontal rays Of
E Divergence of vertical rays > convergence of Sturm
horizontal rays
F Horizontal rays are focused, vertical rays are
diverging
G Both horizontal and vertical rays are diverging

❖ Refractive types of astigmatism: depending on position of two focal lines

→ Simple
▪ Simple myopic – only one meridian focused in front of the eye
▪ Simple hypermetropic – only one meridian focused in behind the eye
→ Compound
▪ Compound myopic – both meridian focused in front of eye
▪ Compound hypermetropic – both meridian focused behind the eye
→ Mixed
▪ One meridian eye is myopic and another meridian eye is hypermetropic
❖ Types of astigmatism based on axis:
→ With the rule astigmatism
→ Against the rule astigmatism
→ Oblique astigmatism
→ Bioblique astigmatism
 → With-the-rule astigmatism
▪ The principal meridians are at right angles to one another
▪ Vertical meridian is more curved than the horizontal meridian

→ Against-the-rule astigmatism
▪ Horizontal meridian is more curved than the vertical meridian.

→ Oblique astigmatism
▪ the principal meridians are at right angles to each other, but not horizontal
and vertical (e.g.450 and 1350)

→ Bioblique astigmatism
▪ the principal meridians are not even at right angles to each other

❖ Clinical features:
→ Symptoms:
▪ Asthenopia symptoms
▪ Blurred vision and defective vision
▪ elongation of objects
▪ Keeping the reading material close to the eyes
→ Signs:
▪ Half closure of lids
▪ Head tilt
▪ Oval/tilted optic disc
▪ Different power in two meridians

❖ Investigations:

→ Retinoscopy
→ Keratometry & computerized corneal topography
→ Astigmatic fan test
→ Jackson’s cross cylinder test

❖ Treatment:
→ Optical treatment
→ Surgical treatment
 → Optical treatment
▪ Spectacles – cylindrical lens
▪ Contac lenses

→ Surgical treatment
▪ Astigmatic keratotomy
▪ Limbal relaxing incisions
▪ Corneal relaxing incisions
▪ Photo astigmatic refractive keratotomy
▪ LASIK procedure
▪ SMILE procedure
IRREGULAR ASTIGMATISM

❖ Irregular change of refractive power in different meridians

❖ Etiological classification:
→ Curvatural
→ Index

❖ Clinical features:

→ Symptoms
▪ Defective vision
▪ Distortion of vision
▪ Polyopia

→ Signs
▪ Irregular pupillary reflex
▪ Corneal irregularity or keratoconus
▪ Distorted circles
▪ Irregular corneal curvature

❖ Treatment:
→ Optical treatment - Contact lens
→ Phototherapeutic keratotomy
→ Surgical treatment - penetrating keratoplasty/deep anterior lamellar
keratoplasty

❖ Management of post keratoplasty astigmatism:

→ Selective removal of sutures (the following procedures should be done only
after doing selective removal of sutures)
→ Arcuate relaxing incisions
→ Relaxing incisions combined with compression
→ Corneal wedge resection
→ LASIK procedure
 ANISOMETROPIA

❖ Definition:
→ The total refraction of two eyes is unequal.

❖ Etiology:
→ Congenital and developmental
→ Acquired

❖ Clinical types:

TYPES

SIMPLE COMPOUND
SIMPLE COMPOUND MIXED
ASTIGMATIC ASTIGMATIC

→ Simple
▪ one eye is normal
▪ another eye is either myopic or hypermetropic

→ Compound
▪ both eyes are either myopic or hypermetropic
▪ one eye having higher refractive error than the other

→ Mixed
▪ one is myopic
▪ other being hypermetropic
▪ also called as Antimetropia
 → Simple astigmatic
▪ one eye is normal
▪ other eye has simple myopic or hypermetropic astigmatism

→ Compound astigmatic
▪ when both eyes are astigmatic of unequal degree

❖ Status of binocular vision:

▪ Binocular single vision-in small degree
▪ Uniocular vision-in higher degree
▪ Alternate vision (hypermetropic eye for distant vision, myopic eye for near
vision)

❖ Diagnosis:
▪ Retinoscopy
▪ Autorefractometry

❖ Treatment:
→ Spectacles
→ Contact lenses
→ Aniseikonic glasses
→ Intraocular lens
→ Refractive corneal surgery
→ Phakic refractive lenses
→ Refractive lens exchange
 ANISEIKONIA

❖ Definition:
→ A condition in which the images projected to the visual cortex from two
retinae are abnormally unequal in size and/or shape.

❖ Etiological types:
→ Optical
▪ Due to anisometropia of higher degree
→ Retinal
▪ Due to displacement of retinal elements towards the nodal point in
one eye
→ Cortical
▪ Asymmetrical simultaneous perception, despite normal retinal
images

❖ Clinical types:
 Symmetrical
→ Spherical
▪ Image magnified or minimized equally in both meridians
→ Cylindrical
▪ Image is magnified or minimized symmetrically in one
meridian

 Asymmetrical
→ Prismatic
▪ Distortion increases progressively in one direction
→ Pincushion
▪ Distortion increases progressively in both directions
→ Barrel distortion
▪ Distortion decreases progressively in both directions
→ Oblique distortion
▪ Size of image is same but there is oblique distortion of
shape
❖ Symptoms:
→ Asthenopia
→ Diplopia
→ Difficulty in depth perception

❖ Treatment:
→ Optical aniseikonia – Aniseikonic glasses, Contact lenses, Intraocular lenses and
Refractive surgery
→ Retinal aniseikonia
→ Cortical aniseikonia
 APHAKIA

❖ Definition: absence of crystalline lens

❖ Causes:
→ Congenital absence of lens
→ Surgical aphakia
→ Aphakia due to absorption of lens matter
→ Trauma
→ Posterior dislocation of lens

❖ Optics:
→ Hypermetropia
→ Total power of eye is reduced
→ Anterior focal point is raised
→ Posterior focal point is also raised
→ Accommodation is lost completely

❖ Clinical features:

Symptoms: Signs:
▪ Defective ▪ Corneal scar
vision ▪ Deeper anterior chamber
▪ Erythropsia ▪ Iridodonesis
▪ Cyanopsia ▪ Pupil becomes jet black
▪ Purkinje’s image shows 2 images rather than 4
▪ Fundus examination – hypermetropic small disc
▪ Retinoscopy and autorefractometry – high hypermetropia

❖ Treatment:
→ Spectacles
→ Contact lens
→ Intraocular lens implantation
→ Refractive corneal surgery
 PSEUDOPHAKIA
❖ Also known as artephakia

❖ Definition:
→ The condition where aphakia is corrected by intraocular lens implant is
referred to as pseudophakia
→ Refractive statuses of pseudophakic eye
→ Emmetropia
→ Consecutive myopia
→ Consecutive hypermetropia

❖ Signs of pseudophakia:
→ Surgical scar
→ Slightly deeper anterior chamber
→ Mild Iridodonesis
→ Purkinje image shows 4 images
→ Presence of intraocular lens

❖ Management:
→ Spectacles
→ LASIK
→ Intraocular lens exchange
 ACCOMMODATION

❖ Definition:
Accommodation is a mechanism by which the eyes can focus the diverging rays
coming from a near object on the retina by increasing the curvature of lens to see
clearly

❖ Mechanism of accommodation: according to von Helmholtz’s capsular theory

Unaccommodated eye Accommodated eye

Ciliary muscle Relaxes Contracts
Ciliary ring diameter Large Shortens
Ciliary zonular tension ↑ ↓
Lens Thin Thick
Flatter anterior surface Curved anterior surface

❖ Far point and near point:

Eye Far point Near point

Emmetropic eye Infinity Varies with age

Hypermetropic eye Virtual Lies behind the eye

Myopic eye Real Lies in front of eye

❖ Range of accommodation:
The distance between the near point and the far point is called the range of
accommodation

❖ Amplitude of accommodation (A): A = P - R

The difference between the dioptric power needed to focus at near point(P)
and far point(R).
 ANOMALIES OF ACCOMMODATION

❖ Anomalies of accommodation include:

→ presbyopia
→ Insufficiency of accommodation
→ Paralysis of accommodation
→ Spasm of accommodation

PRESBYOPIA

❖ Definition:
A condition of failing near vision due to age related decrease in amplitude of
accommodation or increase in punctum proximum

❖ Causes:
→ Age -related changes in the lens which include:
▪ Decrease in the elasticity of lens capsule and
▪ Progressive increase in size and hardness (sclerosis) of lens
→ Age- related decline in ciliary muscle power
→ Causes of Premature Presbyopia are:
▪ Uncorrected hypermetropia
▪ Premature sclerosis of the crystalline lens
▪ General debility causing presenile weakness of ciliary muscle
▪ Chronic simple glaucoma

❖ Symptoms:
→ Difficulty in near vision.
→ Asthenopic symptoms due to fatigue of the ciliary muscle
→ Intermittent diplopia

❖ Treatment:

→ Optical treatment
→ Surgical treatment
 → Optical treatment

▪ Convex glasses
▪ Rough guide for providing presbyopic glasses in an emmetrope can be
determined from the age of the patient.
45 years: +1 to +1.25D
50 years: +1.5 to 1.75D
55 years: +2 to +2.25D
60 years: +2.5 to +3D

▪ Exact presbyopic addition required,

Basic principles for presbyopic correction are:

→ Always find out refractive error for distance and first correct it.
→ Find out the presbyopic correction needed in each eye separately and add it to the
distant correction.
→ Near point should be fixed by taking due consideration for profession of the
patient.
→ The weakest convex lens with which an individual can see clearly at the near point
should be prescribed, since overcorrection will also result in Asthenopic
symptoms.
→ Presbyopic spectacles may be unifocal, bifocals or varifocal i.e. progressive

→ Surgical treatment
▪ Cornea based procedures
→ Monovision conductive keratoplasty
→ Monovision LASIK
→ Presbyopic bifocal LASIK or LASIK-PARM
→ Presbyopic multifocal LASIK
→ Presbyond laser blended vision
→ Corneal inlays for presbyopia

▪ Lens based procedures

→ Multifocal or accommodating IOL
→ Monovision with intraocular lenses
 ▪ Sclera based procedures
→ Anterior ciliary sclerotomy
→ Scleral spacing procedures and scleral ablation
→ Scleral expansion

INSUFFICIENCY OF ACCOMMODATION

❖ Definition:
The condition in which the accommodative power is significantly less than the
normal physiological limits for the patients age.

❖ Causes:
→ Premature sclerosis of lens.
→ Weakness of ciliary muscle due to systemic causes of muscle fatigue such as
▪ Debilitating illness
▪ Anaemia
▪ Toxaemia
▪ Malnutrition
▪ Diabetes mellitus
▪ Pregnancy
→ Weakness of ciliary muscle associated with primary open-angle glaucoma

❖ Clinical features:

All the symptoms of presbyopia are present, but those of asthenopia are more
prominent than the blurring of vision.

❖ Treatment:
→ Treatment of underlying cause is essential.
→ Near vision spectacles
→ Accommodation exercises
PARALYSIS OF ACCOMMODATION

❖ Also known as cycloplegia

❖ It refers to complete absence of accommodation

❖ Causes:
→ Drug induced cycloplegia
▪ atropine, homatropine or other parasympatholytic drugs.
→ Paralytic internal Ophthalmoplegia
results from neuritis associated with
▪ Diphtheria
▪ Syphilis
▪ Diabetes
▪ Alcoholism
▪ Cerebral or meningeal diseases.
→ Paralysis of accommodation as a component of complete third nerve
paralysis
▪ Intracranial or orbital causes
▪ The lesions may be traumatic, inflammatory or neoplastic in nature.

❖ Clinical features:
→ Blurring of near vision (previously emmetropic or hypermetropic patients)
→ Photophobia
→ Abnormal receding of near point

❖ Treatment:
→ Self - recovery occurs in drug - induced cycloplegia and in diphtheric cases.
→ Dark glasses
→ Convex lenses
SPASM OF ACCOMMODATION

❖ It refers to exertion of abnormally excessive accommodation

❖ Causes:
→ Drug- induced spasm of accommodation - after use of strong miotics such
as echothiopate and DFP.
→ Spontaneous spasm of accommodation - It usually occurs when the eyes
are used for excessive near work in unfavourable circumstances

❖ Clinical features:
→ Defective vision due to induced myopia
→ Asthenopic symptoms are more marked than the visual symptoms.

❖ Diagnosis:
→ It is made with refraction under atropine cycloplegia.

❖ Treatment:
→ Relaxation of ciliary muscle by atropine for few weeks and prohibition of
near work allow prompt recovery from spasms of accommodation.
→ Correction of associated causative factors prevent recurrence.
→ Assurance and if necessary, psychotherapy should be given.

DETERMINATION OF REFRACTIVE ERRORS

❖ The procedure of determining refractive errors is termed as clinical refraction

❖ Methods of refraction:
→ Objective refraction method includes:
▪ Retinoscopy
▪ Autorefractometry
▪ Photorefraction
→ Subjective refraction steps include:
▪ Monocular subjective refraction
▪ Correction for near vision
▪ Binocular balancing
 MODALITIES OF CORRECTION OF REFRACTIVE ERRORS

❖ Modes of correcting refractive errors include:

→ Spectacles
→ Contact lenses
→ Refractive surgery

SPECTACLES
→ Lenses fitted in a frame constitute the spectacles

→ Lens materials:
▪ Glass lenses
→ Problems with glass lenses are – shatters on impact, thick and heavy
▪ Plastic lenses
→ Light weighted
→ Materials used are
• Resin lenses
 Needs protective coating for scratch resistant
• High index plastic lenses
 Thinner- so preferred for high powered spectacles
 Types: Polyurethane, Co-polymer, allye base
• Polycarbonate
 Thinner, light weight, impact resistant
 Has property of ultraviolet protection

→ Lens shapes:
▪ Meniscus lenses: For moderate degree of refractive errors
▪ Lenticular form lenses: For high and high minus lenses
▪ Aspheric lenses: For high plus aphakic lenses

→ Single versus multiple lenses:

▪ Single vision lens: Have the same corrective power over the entire surface
▪ Bifocal: Have 2 optical corrections (For presbyopia)
 Upper – Distant vision
  Lower- near vision
 Types:
• Two-piece bifocal
• Cemented supplementary wafer
• Inserted wafer
• Fused Bifocals
• Solid bifocals
▪ Trifocal lenses:
Upper-Distant
Lower-near
Strip for-intermediate
▪ Progressive power adds lenses (varifocal): the power increases progressively
from distance to near stimulating accommodation process
 They have different zones
• Distance vision zone
• Near vision zone
• Intermediate zone
• Blending region

→ Tinted lenses: Reduces amount of light they transmit. Prescribed in albinism, high
myopia and glare prone patients. Also absorbs UV and infrared rays
→ Photochromatic lenses: Alter their colour according to UV rays

Centring: The visual axis of the patient and optical centre of the lens should correspond.
Decentring: It is indicated where prismatic effect is required Reading glasses should be
decentred
CONTACT LENSES
→ Prescribed in irregular corneal astigmatism and high myopia
→ It is an artificial device whose front surface substitutes anterior surface of cornea

nomenclature

diameter curves edge power thickness tint

overall
base curve
diameter

optic zone peripheral

diameter curve

central
anterior curve

peripheral
anterior curve

intermediate
anterior curve

❖ Types:
▪ Hard lenses
▪ Rigid gas permeable
▪ Soft lenses
→ Hard lenses: Made from Polymethylmethacrylate
 Advantages:
• High optical quality
• Stability
• Light in weight
• Nontoxic, Desirable and cheap
 Disadvantages:
• PMM is impermeable to O2
• Cause corneal abrasion
• Resists wetting

→ Rigid gas permeable lenses

 Made from silicone acrylate and cellulose acetate pyruvate.
 Permeable to oxygen

→ Soft lenses
 Made of Hydroxyethyl methacrylate
 Advantage – soft and oxygen permeable
 Disadvantage- Proteinaceous deposit corneal infections

❖ Indications:

 Optical indications:
▪ Anisometropia
▪ Unilateral aphakia
▪ High myopia
▪ Keratoconus
▪ Irregular astigmatism
 Therapeutic indications:
▪ Corneal disease
▪ Disease of tris
▪ Glaucoma
▪ Amblyopia
 Preventive indications:
▪ Symblepharon and restoration of fornix after chemical burns
▪ Exposure keratitis
▪ Trichiasis
 Diagnostic indications:
▪ Gonioscopy
▪ Electroretinography
▪ Fundus photography
 Operative indications:
▪ Goniotomy
▪ vitrectomy
Contraindications:
▪ Endocular photocoagulation
 Cosmetic indications: ▪ Mental incompetence
▪ Unsightly corneal scars ▪ Chronic conjunctivitis
▪ Ptosis ▪ Dry eye syndromes
▪ Phthisis bulbi ▪ Corneal dystrophies
 Occupational indications: ▪ Episcleritis, etc.
▪ Sportsmen
▪ Pilots
▪ Actors
 REFRACTIVE SURGERY

❖ REFRACTIVE SURGERY FOR MYOPIA

myopia

cornea based lens based

procedures procedures

radial laser refractive intercorneal refractive lens

lenticule orthokerathology
keratotomy ablation ring implantation exchange
extraction

photorefractive implanatable
keratectomy contact lens

LASIK

→ CORNEA BASED PROCEDURES:

RADIAL KERATOTOMY:
▪ Deep radial incisions in peripheral part of cornea.
▪ The central 4mm of optical zone is left untouched.
▪ Healing → central cornea flattens → reduction in refractive power
▪ Used for low to moderate myopia (2 to 6 D)
▪ Disadvantages
 Weakening of cornea- globe rupture following trauma-high
risk groups (sportsmen, military personnel)
 Uneven healing-astigmatism
 Sensation of glare at night

LASER ABLATION CORNEAL PROCEDURES:

→ Photorefractive keratectomy:
▪ A central optical zone of anterior corneal stroma is photoablated
▪ This results in flattening of cornea

→ Laser in situ keratomileusis:

 a flap of 130 - 160 micron thickness

raised from anterior corneal tissue by

automated microkeratome

midstromal tissue is ablated by excimer

laser

flattening of cornea occurs

▪ Patient selection criteria:

▪ Age above 20 years
▪ Stable refraction - ≥12 months
▪ Motivated patient
▪ Corneal pathology(absent)
▪ Corneal thickness >450micrometres

▪ Advances in LASIK:
▪ Customised LASIK:
→ based on topography and wavefront technology
→ also corrects aberrations in eye –gives vision beyond 6/6
▪ Femto LASIK:(no blade LASIK)
→ flap is made with femtosecond laser - greater precision &
consistency
▪ Custom Femto LASIK:
→ based on topography and wavefront technique
→ flap made with femtosecond laser
▪ Epi LASIK:
→ instead of corneal(stromal) flap- only epithelium is
separated-advanced procedure-no complications
Advantages: Disadvantages:
▪ No postoperative pain ▪ Expensive
▪ Recovery of vision very fast ▪ Requires greater surgical skills
▪ No risk of perforation or rupture ▪ Risk of flap related complications:
▪ No residual haze → intraoperative flap amputation
▪ Effective in correcting myopia of -8D → wrinkling of flap on reposition
→ post-operative flap dislocation
→ epithelization of flap bed
interface
→ astigmatism

REFRACTIVE LENTICULE EXTRACTION

Also known as small incision Lenticule extraction - SMILE

→ A lenticule of corneal stroma extracted with femtosecond laser
→ Used for myopia ± astigmatism up to 10D

INTERCORNEAL RING IMPLANTATION

→ Implantation into the peripheral cornea- approximately 2/3 stromal
depth
→ Vaulting effect thus resulting in flattening of central cornea
→ Advantage – it is reversible
→ Disadvantage – unpredictable results and keratitis

ORTHOKERATOLOGY
→ Non-surgical
→ Reversible method
→ Moulding of cornea by using an overnight wear of rigid gas permeable
contact lens
→ Used for myopia upto-5D
→ can be used for candidates below 18 years
 → LENS BASED PROCEDURES

REFRACTIVE LENS EXCHANGE:

▪ Clear lens extraction + intraocular lens implantation
▪ Used for myopia >12D
▪ Retinal detachment and endophthalmitis after cataract or possible
complications of this procedure
PHAKIC REFRACTIVE LENS:
▪ A special type of intraocular lens-implanted in anterior chamber or
posterior chamber anterior to natural crystalline lens
▪ Cataract formation and secondary glaucoma can be possible
complication

REFRACTIVE SURGERY FOR HYPEROPIA

hyperopia

cornea based lens based

procedures procedures

thermal laser implantable

keratoplasty contact lens

conductive refractive lens

keratoplasty exchange

hyperopic
PRK

hyperopic
LASIK

→ CORNEA BASED PROCEDURE

THERMAL LASER KERATOPLASY:

▪ Used for low degree hyperopia
▪ 8 laser spots- applied in a ring at the periphery –producing central
steeping with mild infrared energy from Thallium-Holmium-
Chromium
 ▪ Regression effect & induced astigmatism(complication)

HYPEROPIC PRK:
▪ Main problem faced is regression effect and prolonged epithelial
healing

HYPEROPIC LASIK:
▪ Used for hypermetropia up to +4D

CONDUCTIVE KERATOPLASTY:
▪ Non ablative and non-incisional procedure
▪ Cornea steeped by collagen shrinkage through radiofrequency
energy
▪ It is applied by fine tip inserted into peripheral corneal stroma in a
ring pattern
▪ Used for hyperopia upto 3D

→ LENS BASED PROCEDURES

PHAKIC REFRACTIVE LENS: used for hyperopia of more than +4D

REFRACTIVE LENS EXCHANGE: for high hyperopia in presbyopic age

❖ REFRACTIVE SURGERY FOR ASTIGMATISM

ASTIGMATIC KERATOTOMY
▪ Transverse cuts are made in mid periphery of steep corneal meridian
▪ This procedure can be performed alone for astigmatism or along with
radical keratotomy for myopia
LIMBAL RELAXING INCISIONS
▪ Astigmatism upto 2D can be corrected
CORNEAL RELAXING INCISIONS
▪ Similar to limbal relaxing incisions
PHOTO- ASTIGMATIC REFRACTIVE KERATOTOMY
LASIK – to correct astigmatism upto 5D
SMILE
MANAGEMENT OF POST KERATOPLASTY ASTIGMATISM
▪ SELECTIVE REMOVAL OF SUTURES:
(the other below mentioned procedures should be performed only after sutures
are out)
▪ ARCUATE RELAXING INCISIONS: used to correct astigmatism upto 4-6 D
▪ RELAXING INCISION COMBINED WITH COMPRESSION: used for astigmatism
upto 10D
▪ CORNEAL WEDGE RESECTION: used for astigmatism > 10D
▪ LASIK

REFRACTIVE SURGERY FOR PRESBYOPIA

→ CORNEAL BASED PROCEDURES:

MONOVISION LASIK
MONOVISION CONDUCTIVE KERATOPLASY
PRESBYOPIC MULTIFOCAL LASIK
PRESBYOND LASER BLENDED VISION
CORNEAL INLAYS FOR PRESBYOPIA
PRESBYOPIC BIFOCAL LASIK (OR) LASIK-PARM Under trial
▪ The shape of cornea is altered to have two concentric vision zones
to help the patients to focus near and far vision

→ LENS BASED PROCEDURES

MULTIFOCAL OR ACCOMMODATIONG IOL
MONOVISION WITH INTRAOCULAR LENSES
▪ Correction of one eye for distant vision and another for near
vision

→ SCLREA BASED PROCEDURES

ANTERIOR CILIARY SCLEROTOMY under trial
SCLERAL SPACING PROCEDURES AND SCLERAL ABLATION under trial
SCLERAL EXPANSION
▪ Insertion of intrascleral segments of collagen or silicone expansion
plugs which helps in improving accommodation
 CONJUNCTIVA

What will we learn here???

Applied anatomy
Inflammation of conjunctiva
▪ Infective conjunctivitis
o Bacterial
o Chlamydial
o Viral
o Ophthalmia neonatorum
o Granulomatous conjunctivitis
▪ Allergic
o Simple allergic
o Vernal
o Atopic
o Giant cell papillary
o Phlyctenular
o Contact dermoconjunctivitis
▪ Cicatricial
▪ Toxic

Degenerative conditions
▪ Pinguecula
▪ Pterygium
▪ Concretions
▪ Amyloid degenerations

Symptomatic conditions of conjunctiva

▪ Hyperemia
▪ Chemosis
▪ Ecchymosis
▪ Xerosis
▪ Discoloration of conjunctiva

Cysts and tumours of conjunctiva

 APPLIED ANATOMY

➢ translucent mucous membrane

➢ lines the posterior surface of the eyelids
and anterior aspect of the eyeball
➢ it joins the eyeball to the lids.
➢ It stretches from the lid margin to the
limbus, and encloses a complex space
called conjunctival sac which is open in
front at the palpebral fissure.

PARTS OF CONJUNCTIVA

marginal
Conjunctiva

palpebral tarsal

bulbar orbital

conjunctival fornix

❖ Palpebral conjunctiva

Marginal conjunctiva
▪ extends from the lid margin to about 2 mm on the back of lid up to a shallow
groove (sulcus subtarsalis)

Tarsal conjunctiva
▪ it is thin, transparent and highly vascular.
 ▪ firmly adherent to the whole tarsal plate – upper lid.
▪ adherent only to half width of the tarsus-lower lid.
▪ The tarsal glands are seen through it as yellow streaks.

Orbital part of palpebral conjunctiva

▪ lies loose between the tarsal plate and fornix.

❖ Bulbar conjunctiva.

▪ thin, transparent and lies loose over the underlying structures.

▪ It is separated from the anterior sclera by episcleral tissue and Tenon’s capsule.
▪ A 3 mm ridge of bulbar conjunctiva around the cornea is called limbal
conjunctiva.

❖ Conjunctival fornix.

▪ continuous circular cul-de-sac

▪ broken only on the medial side by caruncle and the plica semilunaris.
▪ joins the bulbar conjunctiva with the palpebral conjunctiva.
▪ subdivided into superior, inferior, medial and lateral fornices.

HISTOLOGY OF CONJUNCTIVA

The 3 layers of conjunctiva

are:
▪ Epithelium
▪ Adenoid layer
▪ Fibrous layer
 GLANDS OF CONJUNCTIVA

GLANDS
MUCIN SECRETORY GLANDS ACCESSORY LACRIMAL GLANDS
Goblet cells Glands of Krause
Crypts of Henle Glands of Wolfring
Glands of Manz

BLOOD SUPPLY

Arteries
▪ Peripheral arcade of eyelid
▪ Marginal arcade of the eyelid
▪ Anterior ciliary arteries

Veins
▪ Anterior ciliary veins

LYMPHATICS

▪ Lateral side – preauricular lymph nodes

▪ Medial side – submandibular lymph nodes

NERVE SUPPLY
▪ long ciliary nerves
▪ branches from lacrimal, infratrochlear, supratrochlear etc.
 INFLAMMATION OF CONJUNCTIVA

INTRODUCTION
▪ conjunctivitis is conjunctival hyperaemia associated with discharge

CLASSIFICATION

conjunctivitis

infective allergic cicatricial toxic

Infective conjunctivitis

Bacterial conjunctivitis Chlamydial Viral conjunctivitis

• Acute bacterial conjunctivitis • Adenovirus conjunctivitis
conjunctivitis •Trachoma o Epidemic
• Hyperacute bacterial • Adult inclusion keratoconjunctivitis
conjunctivitis conjunctivitis o Pharyngoconjunctival
• Chronic bacterial • Neonatal chlamydial fever
conjunctivitis conjunctivitis • Enterovirus conjunctivitis
• Angular bacterial • Molluscum contagiosum
conjunctivitis conjunctivitis
• Herpes simplex conjunctivitis
Ophthalmia neonatorum Granulomatous
conjunctivitis
• Parinaud
oculoglandular
syndrome
Allergic Conjunctivitis

1. Simplex allergic conjunctivitis

• Hay fever conjunctivitis (rhino conjunctivitis)
• Seasonal allergic conjunctivitis (SAC)
• Perennial allergic conjunctivitis (PAC)
2. Vernal keratoconjunctivitis (VKC)
3. Atopic keratoconjunctivitis
4. Giant papillary conjunctivitis (GPC)
5. Phlyctenular conjunctivitis (PKC)
6. Contact dermo conjunctivitis (drop conjunctivitis)

Cicatricial conjunctivitis

• Ocular mucous membrane pemphigoid (OMMP),

• Stevens Johnson syndrome (SJS),
• Toxic epidermal necrolysis (TeN), and
• Secondary cicatricial conjunctivitis.

Toxic conjunctivitis
 INFECTIVE CONJUNCTIVITIS

BACTERIAL CONJUNCTIVITIS

ETIOLOGY

Predisposing Causative organisms Mode of infection.

factors:
• Staphylococcus aureus-common Exogenous infections
• Flies
• Streptococcus pneumoniae- associated Directly through close
• poor with petechial subconjunctival contact airborne infections,
hygienic hemorrhages waterborne infections,
conditions Vector transmission,
• Streptococcus pyogenes- Material transfer
• hot dry pseudomembranous conjunctivitis.
climate
• Staphylococcus epidermidis
• poor Local spread
sanitation • Hemophilus influenzae – red eye from neighbouring
• dirty • Moraxella lacunata - angular structures such as infected
habits. conjunctivitis lacrimal sac, lids, and
nasopharynx.
• Pseudomonas pyocyanea
• Neisseria gonorrhoeae- ophthalmia Endogenous infections
neonatorum in newborn
may occur very rarely
• Neisseria meningitidis- mucopurulent through blood, e.g.,
conjunctivitis. gonococcal and
• Corynebacterium diphtheriae - acute meningococcal infections.
membranous conjunctivitis.

PATHOLOGY

vascular cellular conjunctival conjunctival

response response response discharge
Vascular response:
o congestion and increased permeability of the conjunctival vessels
o proliferation of capillaries.
Cellular response:
o exudation of polymorphonuclear cells and other inflammatory cells
Conjunctival tissue response:
o edematous.
o superficial epithelial cells degenerate, become loose and even desquamate.
o proliferation of basal layers of conjunctival epithelium
o increase in the number of mucin-secreting goblet cells.
Conjunctival discharge.
o It consists of tears, mucus, inflammatory cells, desquamated epithelial cells,
fibrin and bacteria.
 ACUTE BACTERIAL CONJUNCTIVITIS

Definition:
Acute conjunctivitis is characterized by marked
conjunctival hyperemia and mucopurulent discharge from the
eye.
chemosis

Clinical features:
Signs:

• Flakes of mucopus seen in the fornices and lid margins is a critical sign.
• Chemosis.
• Cilia is matted together with yellow crusts
• Petechial haemorrhages (pneumococcus)
• Congestion - appearance of fiery red eye.
• Eyelids are slightly oedematous.
• Papillae of fine type may be seen.
fiery red eye

Symptoms:

• Discomfort, foreign body, grittiness, blurring and redness of sudden onset

• Coloured halos due to prismatic effect of mucus present on cornea.
• Slight blurring of vision due to mucus flakes in front of cornea.
• Mucopurulent discharge from the eyes.
• Sticking together of lid margins with discharge.

matting of lids mucopurulent discharge

Complications:

• Keratitis.
• Chronic redness, discharge and irritation.
• Blindness.
• Infection with N. gonorrhoeae can precede meningitis.

Management:

General treatment:

• Avoid spreading
• Frequent hand washing.
• Avoid sharing personal care objects such towels, cosmetics, etc.
• Avoid contact with eyes.
• Avoid shaking hands.
• Strict instrument disinfection.

Medical therapy:

Most cases are self-limiting

❖ Antibiotics are the main treatment of acute bacterial conjunctivitis.

o Aminoglycosides like Gentamicin (0.3%), or Tobramycin (0.3%) or Framycetin
0.3% eye drops 3-4 hours a day
o Ciprofloxacin (0.3%), or ofloxacin (0.3%), moxifloxacin (0.5%), or gatifloxacin
(0.3%) eye drops
❖ Topical steroids should be avoided
❖ Irrigation of conjunctival sac with sterile Luke warm water saline once or twice daily
will help to remove the delirious material. Frequent eyewash is contraindicated as it
will wash away the lysozyme and other protective proteins in the tears.
❖ Dark googles must be used to prevent photophobia.
❖ Anti- inflammatory and analgesic drugs like Ibuprofen and Paracetamol may be given
orally for 2-3 days to provide symptomatic relief from mild pain in sensitive patients.
 HYPERACUTE BACTERIAL CONJUNCTIVITIS

Definition:

Hyperacute bacterial conjunctivitis also called as acute purulent conjunctivitis or acute

blennorrhoea is characterized by violent inflammatory response.

Types:

• Adult purulent conjunctivitis.

• Ophthalmia neonatorum. (dealt separately)

Etiology:

• Most common organism - Neisseria gonorrhoea.

preauricular lymph node swelling

Incidence:

• It’s predominant in males

• There may be associated arthritis and urethritis.
• The incubation period is 12 to 24 hrs

Clinical features:

Stages Clinical features

Stage of • painful and tender eyeball
infiltration • Lids are tender and swollen
• Bright red velvety chemosed
conjunctiva.
• Discharge is watery and
sanguineous. conjunctival chemosis

• Pre auricular lymph nodes are

enlarged.

Stage of • Frank purulent, copious thick

blennorrhoea discharge tricking down
• mild photophobia
• moderate to severe pain blurring of
vision.
copius purulent discharge
Stage of slow All the symptoms will start to regress
healing resulting in healing.

Conjunctiva still remains red thickened

and velvety.

Complications:

▪ Corneal involvement is quite frequent. It may

occur in the form of diffuse haze and edema,
central necrosis, cornea ulceration or even
perforation.
▪ Iridocyclitis may also occur
▪ Systemic complications - gonorrhoea arthritis,
endocarditis and septicemia.
iridocyclitis

Treatment:

Systemic therapy
▪ Third generation cephalosporin such as Cefoxitime 1.0 gm or Cefotaxime 500 mg IV
qid or ceftriaxone 1.0 gm IM qid, all for 5 days; should be preferred for treatment.
▪ Quinolones such as Norfloxacin 1.2 gm orally qid for 5 days, or Spectinomycin 2.0 gm
IM for 3 days, may be used alternatively.
▪ All of the above regimes should then be followed by a one-week course of either
doxycycline 100 mg bid or erythromycin 250–500 mg orally qid.

Topical antibiotic therapy

▪ ofloxacin, ciprofloxacin or tobramycin eye drops or bacitracin or erythromycin eye
ointment every 2 hours for the first 2–3 days and then 5 times daily for 7 days.

Irrigation of the eyes frequently with sterile saline

Other general measures are similar to acute mucopurulent conjunctivitis.
Topical atropine 1% eye drops should be instilled once or twice a day if cornea is
involved.
 CHRONIC BACTERIAL CONJUNCTIVITIS

Definition:

Chronic bacterial conjunctivitis also known as Chronic catarrhal conjunctivitis’ or ‘simple

chronic conjunctivitis’ is characterized by mild catarrhal inflammation of the conjunctiva.

Etiology

Predisposing factors:
• Chronic exposure to dust, smoke, and chemical irritants.
• Local cause of irritation
• Eye strain
• Abuse of alcohol, insomnia and metabolic disorders.

Causative organisms
• Staphylococcus aureus is the commonest cause
• Gram negative rods such as Proteus mirabilis, Klebsiella pneumoniae, Escherichia coli
and Moraxella lacunata are other rare causes.

Source and mode of infection

Chronic conjunctivitis may occur:
• As continuation of acute mucopurulent conjunctivitis when untreated or partially
treated.
• As chronic infection from associated chronic dacryocystitis, chronic rhinitis or chronic
upper respiratory catarrh.
• As a mild exogenous infection which results from direct contact, airborne or material
transfer of infection.

Clinical features
Symptoms
• Burning and grittiness in the eyes, especially in
the evening.
• Mild chronic redness in the eyes.
• Feeling of heat and dryness on the lid margins.
• Difficulty in keeping the eyes open.
 • . Mild mucoid discharge especially in the canthi.
• Watering, off and on is often a complaint.
• Feeling of sleepiness and tiredness in the eyes.

Signs

Grossly the eyes look normal but careful congested lid

examination may reveal following signs:
• Congestion of posterior conjunctival
vessels.
• Mild papillary hypertrophy of the
palpebral conjunctiva.
• Sticky look of surface of the conjunctiva.
• Lid margins may be congested.

Treatment:
• Eliminate predisposing factors when associated.
• Topical antibiotics such as chloramphenicol, tobramycin, gentamicin should be
instilled 3–4 times a day for about 2 weeks to eliminate the mild chronic infection.
• Astringent eye drops such as zinc-boric acid drops provide symptomatic relief.
 ANGULAR BACTERIAL CONJUNCTIVITIS

Definition:
It is a type of chronic conjunctivitis characterized by mild grade inflammation confined
to the conjunctiva and lid margins near the angles and associated with maceration of the
surrounding skin.

Etiology
Predisposing factors
▪ Chronic exposure to dust, smoke, and chemical irritants.
▪ Local cause of irritation such as trichiasis, concretions, foreign body and seborrhoeic
scales.
▪ Eye strain due to refractive errors, phorias or convergence insufficiency.
▪ Abuse of alcohol, insomnia and metabolic disorders

Causative organisms
Moraxella Axenfield (MA) is the commonest causative organism. MA bacilli are placed
end to end, so the disease is also called ‘diplobacillary conjunctivitis’. Rarely, staphylococci
may also cause angular conjunctivitis.

Source of infection is usually nasal cavity.

Mode of infection: Infection is transmitted from nasal cavity to the eyes by contaminated
fingers or handkerchief.

Pathology:

MA bacillus enzyme gets

mild grade
produces collected at maceration of vascular and
chronic
proteolytic angle of action epithelium cellular changes
inflammation
enzyme of tears
Clinical features

Symptoms: excoriation of skin

▪ Irritation, burning sensation and feeling of
discomfort in the eyes.
▪ History of collection of dirty-white foamy
discharge at the angles.
▪ Redness in the angles of eyes.

Signs:
▪ Hyperemia of bulbar conjunctiva near the canthi.
▪ Hyperemia of lid margins near the angles.
▪ Excoriation of the skin around the angles.
▪ Foamy mucopurulent discharge at the angles is usually present.

Complications:
▪ Blepharitis.
▪ Shallow marginal catarrhal corneal ulceration.

Treatment:
Prophylaxis includes treatment of associated nasal infection and good personal hygiene.
Curative treatment consists of:
• Oxytetracycline (1%) eye ointment, 2–3 times a day for 9–14 days will eradicate the
infection.
• Zinc lotion instilled in day time and zinc oxide ointment at bed time inhibits the
proteolytic ferment and thus helps in reducing the maceration.
CHLAMYDIAL CONJUNCTIVITIS

LIFECYCLE OF CHLAMYDIA
 TRACHOMA

Introduction

• Other names: Egyptian ophthalmia

• Affects – superficial epithelium of conjunctiva and cornea
• Leading cause of preventable blindness in the world

Causative organism

• Chlamydia trachomatis – serotype A, B, C

• The organism produces intracytoplasmic inclusion bodies known as HALBERSTATER
PROWAZEK (HP) – HP bodies.

Predisposing factors

• Age – infancy to early childhood.

• Sex – female
• Climate – dry and dusty weather
• Environmental factors – contagious in early stages.
• Source of infection – conjunctival discharge of affected person.

Mode of spread

• direct
• vector -> flies
• material transfer
Clinical features:

Phase of active trachoma Phase of cicatricial trachoma

Age Childhood Middle age
Cause Active chlamydial infection Continued mild grade chronic
inflammation
Type 4 hypersensitivity
reaction
Symptoms in absence of secondary infection - mild foreign body sensation,
occasional lacrimation, slight stickiness of lids and scanty mucoid
discharge

in presence of secondary infection – acute mucopurulent

conjunctivitis
Signs
Conjunctival Congestion of upper tarsal and Conjunctival scarring in arlt’s
forniceal conjunctiva line

Conjunctival follicles – Concretions

pathognomic of trachoma – Pseudocyst
consists of multinucleated giant Xerosis
cell known as Leber cells Symblepharon

Papillary hyperplasia
Corneal Superficial keratitis Regressive pannus
Herbert follicles Herbert pits
Progressive pannus Corneal opacity, etc.
Corneal ulcer
Lid Trichiasis
Entropion
Tylosis
Ptosis
Madarosis, etc.
Lacrimal Chronic dacryocystitis
apparatus Chronic adenitis
Grading

McCallan’s classification

Stages Name Features

I Incipient trachoma or stage filtration Hyperemia of palpebral conjunctiva
and immature follicles
II Established trachoma or stage of florid Appearance of mature follicles,
infiltration papillae and progressive corneal
pannus
III Cicatrizing trachoma or stage of Obvious scarring of palpebral
scarring conjunctiva
IV Healed trachoma or stage of sequelae Quiet and cured but sequel due to
Cicatrization produces symptoms

WHO classification

Type Diagnosis
TF – trachomatous inflammation – follicular Follicular inflammation - >= 5 follicles
present in upper tarsal
TI – trachomatous inflammation – intense Inflammatory thickening of upper tarsal
conjunctiva
TS – trachomatous scarring Scarring in tarsal conjunctiva
TT – trachomatous trichiasis One eyelash rubs the eyeball
CO – corneal opacity Visible corneal opacity – the only
complication of trachoma

Diagnosis

Clinically by who classification

Laboratory

• Conjunctival cytology – Leber cells among others in giemsa stained smears

• Detection of inclusion bodies
 • ELISA
• PCR
• Isolation of chlamydia – yolk sac inoculation method
• Serotyping of TRIC agents

Management

Treatment of trachoma
Active trachoma Treatment
TF & TI Topical therapy – tetracycline, sulfacetamide
Systemic antibiotics – tetracycline, doxycycline, azithromycin
orally
Combination of above two

Cicatricial trachoma
TS Concretions – hypodermic needle
Conjunctival xerosis – artificial tears
TI Trichiasis – bilamellar tarsal resection
CO Penetrating keratoplasty
Keratoprosthesis
Punctal occlusion and lateral tarsorrhaphy

Prophylaxis

Safe strategy
S – surgery – tertiary prevention
A – antibiotic use – secondary prevention
F – facial hygiene – primary prevention
E – environmental changes – primordial prevention
 ADULT INCLUSION CONJUNCTIVITIS

Introduction

• Type of acute follicular conjunctivitis associated with mucopurulent discharge.

• Affects sexually active young adults
• Also known as swimming pool conjunctivitis

Etiology

• Serotypes d to k of chlamydia trachomatis

• Primary source of infection – urethritis in males and cervicitis in females
• Transmission occurs to eye due to genital hand eye contact
• Contaminated waters in swimming pool

Clinical features

Incubation period – 5 to 14 days

Symptoms

• Ocular discomfort
• Foreign body sensation
• Mild photophobia
• Mucopurulent discharge from eyes

Signs

• Conjunctival hyperemia
• Acute follicular hypertrophy
• Superficial keratitis
• Pre auricular lymphadenopathy
Complication

• Chronic follicular conjunctivitis

Lab investigations
Similar to trachoma

Treatment

• Topical therapy – tetracycline

• Systemic therapy – azithromycin, tetracycline, erythromycin, doxycycline
• Referral to genitourinary specialist

Prophylaxis

• Improve personal hygiene

• Regular chlorination of swimming pool
• Patients’ sexual partner to be examined and treated
• Abstinence of sexual intercourse until treatment completion
 VIRAL CONJUNCTIVITIS

The most common viral causes are adenovirus such as enterovirus and HSV and occurs in
epidemics. The modes of transmission are due to contact perhaps through contaminated
fingers, swimming pools

ADENOVIRAL CONJUNCTIVITIS (PINK EYE)

Causative organism – adenoviruses

Clinical types

• Epidemic keratoconjunctivitis
• Nonspecific acute follicular conjunctivitis
• Pharyngoconjunctival fever
• Chronic relapsing adenoviral conjunctivitis

Epidemic keratoconjunctivitis

• type of acute follicular conjunctivitis associated with superficial punctate

keratitis
• commonly seen during epidemic

Clinical features

Incubation period – 8 days

 Symptoms Signs

• Redness of eye • Swollen eyelids

• Watering • Conjunctiva – hyperemic, chemosed, presence of
• Mild mucoid follicles
discharge • Petechial subconjunctival hemorrhages are seen
• Ocular discomfort • Pseudomembrane formation
• Foreign body • Cornea – epithelial microcystic, superficial punctate
sensation keratitis, subepithelial infiltrates
• Photophobia • Preauricular lymphadenopathy

Treatment
• Supportive treatment – cold compresses, decongestant, lubricants
• Topical antibiotics
• Topical antiviral drugs
• Topical steroids

Prevention
• Frequent handwashes
• Isolation of infected individual
• Avoid eye rubbing
• Disinfection of ophthalmic instruments

Non-specific acute follicular conjunctivitis

• More common
• Caused by serotypes 1 to 11 and 19
• Clinical features and treatment is similar to epidemic type except corneal
involvement

Pharyngoconjunctival fever

Etiology – adenovirus 3,4,7

Transmission by personal contact, fomites, swimming pools
clinical features – acute follicular conjunctivitis with pharyngitis, fever, preauricular
lymphadenopathy
Treatment – similar to EKC
 Newcastle conjunctivitis

• Rare
• Caused by Newcastle virus
• Similar to pharyngoconjunctival fever

ACUTE HEMORRHAGIC CONJUNCTIVITIS

• Acute hemorrhagic conjunctivitis is associated with enterovirus 70 and group A

coxsackievirus 24.
• Also known as Apollo conjunctivitis
• They have an incubation period of about 1 to 2 days.
• Symptoms – pain, redness, watering photophobia, transient blurring of vision
• Signs – congestion, chemosis, multiple hemorrhages in bulbar conjunctiva
• Treatment – similar to EKC

ACUTE HERPETIC CONJUNCTIVITIS

• When the herpes virus is the cause of conjunctivitis, it is called herpetic
conjunctivitis.
• Seen in children and adolescents
• Clinical feature
▪ Typical form – vesicular lesion on face and lids
▪ Atypical form – resembles EKC, no vesicular lesion on face and lids
 OPTHALMIA NEONATORUM

INTRODUCTION
• Ophthalmia neonatorum is bilateral inflammation of the conjunctiva occurring in an
infant, less than 30 days old.
• It is a preventable disease usually occurring as a result of carelessness at the time of
birth.
• Any discharge or even watering from the eyes in the first week of life should arouse
suspicion of ophthalmia neonatorum, as tears are not formed till then.

ETIOLOGY
• Infection may occur in three ways:
▪ Before birth infection is very rare through infected liquor amnii in mothers with
ruptured membranes.
▪ During birth. It is the most common mode of infection from the infected birth
canal especially when the child is born with face presentation or with forceps.
▪ After birth. Infection may occur during first bath of newborn or from soiled
clothes or fingers with infected lochia.

CAUSATIVE AGENTS
• Chemical conjunctivitis It is caused by silver nitrate or antibiotics used for
prophylaxis.
• Gonococcal infection was considered a serious disease in the past, as it used to be
responsible for 50 per cent of blindness in children.
• Other bacterial infections responsible for ophthalmia neonatorum are
Staphylococcus aureus, Streptococcus hemolyticus, and Streptococcus pneumoniae.
• Neonatal inclusion conjunctivitis caused by serotypes D to K of Chlamydia
trachomatis is the commonest cause of ophthalmia neonatorum in developed
countries.
• Herpes simplex ophthalmia neonatorum is a rare condition caused by herpes
simplex-II virus

Causative agent Incubation period

Chemical 6 hrs
Gonococcal 2 – 5 days
Other bacterial 5 – 8 days
Neonatal inclusion conjunctivitis 5 – 14 days
Herpes simplex 6 – 15 days
CLINICAL FEATURES

1. Pain and tenderness in the eyeball.

2. Conjunctival discharge.
It is purulent in gonococcal ophthalmia neonatorum
mucoid or mucopurulent in other bacterial cases and neonatal inclusion
conjunctivitis.
3. Lids are usually swollen.
4. Conjunctiva may show hyperaemia and chemosis. There might be mild papillary
response in neonatal inclusion conjunctivitis and herpes simplex ophthalmia
neonatorum.
5. Corneal involvement - rare

TREATMENT

Prophylactic
• Antenatal
• Natal
• Postnatal
1. Antenatal measures
▪ Include thorough care of mother and treatment of genital infections when
suspected.

2. Natal measures
▪ It is of utmost importance, as mostly infection occurs during
childbirth. Deliveries should be conducted under hygienic conditions
taking all aseptic measures. The newborn baby's closed lids should be
thoroughly cleansed and dried.

3. Postnatal measures
▪ Use of either 1 percent tetracycline ointment or 0.5 percent
erythromycin ointment or 1 percent silver nitrate solution (Crede's
method) into the eyes of the babies immediately after birth. Single
injection of ceftriaxone 50 mg/kg IM or IV (not to exceed 125 mg) should
be given to infants born to mothers with untreated gonococcal infection.
Curative treatment.
1. Chemical ophthalmia neonatorum is a self-limiting condition, and does not require any
treatment.
2. Gonococcal ophthalmia neonatorum needs prompt treatment to prevent complications.

Topical therapy should include:

• Saline lavage till the discharge is eliminated.
• Bacitracin eye ointment 4 times/day.
• penicillin drops 5000 to 10000 units per ml
• If cornea is involved then atropine sulphate ointment should be applied.

Systemic therapy. Neonates with gonococcal ophthalmia should be treated for 7 days
with one of the following regimes:
• Ceftriaxone 75-100 mg/kg/day IV or IM, QID
• Cefotaxime 100-150 mg/kg/day IV or IM, 12 hourly.
• Ciprofloxacin 10-20 mg/kg/day or Norfloxacin 10 mg/kg/day.
• If the gonococcal isolate is proved to be susceptible to penicillin, crystalline
benzyl penicillin G 50,000 units to full term, normal weight babies and 20,000
units to premature or low weight babies should be given intramuscularly twice
daily for 3 days.

4. Other bacterial ophthalmia neonatorum should be treated by broad spectrum

antibiotic drops and ointments for 2 weeks.

5. Neonatal inclusion conjunctivitis responds well to topical tetracycline 1 per cent or

erythromycin 0.5 per cent eye ointment QID for 3 weeks. However, 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
 GRANULOMATOUS CONJUNCTIVAL INFLAMMATION

characterized by:

• Proliferative lesions
• Localized to one eye
• Regional lymphadenitis.

➢ Common granulomatous conjunctival inflammations are:

• Tuberculosis of conjunctiva
• Sarcoidosis of conjunctiva
• Syphilitic conjunctivitis
• Leprotic conjunctivitis
• Conjunctivitis in tularaemia
• Ophthalmia nodosa

PARINAUD’S OCULOGLANDULAR SYNDROME:

characterized by:
• Unilateral granulomatous conjunctivitis
• Pre-auricular lymphadenopathy
• Fever.

Common causes
• Tularaemia
• Cat-scratch disease
• Tuberculosis
 • Syphilis
• Lymphogranuloma venereum.

OPHTHALMIA NODOSA
(CATERPILLAR HAIR CONJUNCTIVITIS)

➢ formation of a nodule on the bulbar conjunctiva in response to irritation caused by

the retained hair of caterpillar.
➢ The disease is common in summers.
➢ The condition may be often mistaken for a tubercular nodule.

Histopathological examination
Reveals hair surrounded by giant cells and lymphocyte.

Treatment
Excision biopsy of the nodule.
 ALLERGIC CONJUNCTIVITIS

It is the inflammation of conjunctiva due to allergic or hypersensitivity reactions which

maybe immediate (humoral) or delayed (cellular).

SIMPLE ALLERGIC CONJUNCTIVITIS

• It is a mild, nonspecific allergic conjunctivitis.

• Characterized by itching, hyperaemia and mild papillary response.
• It is an acute or subacute urticarial reaction.

Etiology
• Type-I immediate hypersensitivity reaction mediated by IgE
• Family history of atopy might be present.

➢ Simple allergic conjunctivitis occurs in two forms:

Seasonal (hay fever conjunctivitis) Perennial
Cause allergens such as tree and grass perennial allergens
pollens. such as house dust,
animal dander and
mite.
Common More common Less common
Manifestation Acute allergic conjunctivitis Subacute or chronic

Pathology
➢ Vascular response:
vasodilation and increased permeability of vessels leading to exudation.
➢ Cellular response:
conjunctival infiltration and exudation in the discharge of eosinophils, plasma cells
and mast cells producing histamine and histamine-like substances.
➢ Conjunctival response:
Swelling of conjunctiva followed by increased connective tissue formation and
mild papillary hyperplasia.
Clinical features
Symptoms Signs
• Intense itching and burning • Hyperaemia and chemosis which give a
sensation in the eyes swollen juicy appearance to the conjunctiva.
• Watery mucus, stringy discharge, • Mild papillary reaction may be seen on
and Mild photophobia palpebral conjunctiva. Oedema of lids.

Diagnosis
Diagnosis is made from:
• Typical symptoms and signs,
• Normal conjunctival flora, and
• Presence of abundant eosinophils in the discharge.

Treatment
1) Elimination of allergens if possible.
2) Topical vasoconstrictors:
i) naphazoline,
ii) antizoline and
iii) tetrahydrozoline - immediate decongestion.
3) cold compresses
4) Artificial tears:
i) cellulose -provide soothing effect.
5) stabilizers:
i) sodium cromoglycate
ii) nedocromil sodium -prevent recurrences in atopic cases.
6) Dual action antihistamines and mast cell stabilizers:
i) Azilastine
ii) olopatidine
iii) ketotifen -effective for exacerbations.
7) NSAIDs
8) Systemic antihistaminic drugs
9) Desensitization
 VERNAL KERATOCONJUNCTIVITIS (VKC)
SPRING CATARRH

➢ VKC is a recurrent, bilateral, interstitial, self-limiting, allergic inflammation of the

conjunctiva having a periodic seasonal incidence.

Etiopathogenesis
• characterized by Th2 lymphocyte alteration.
• exaggerated IgE response to common allergens is a secondary event.

Predisposing factors
▪ Age and sex. 4–20 years; more common in boys
▪ Season. More common in summer.
▪ also known as ‘Warm weather conjunctivitis
▪ Climate. More prevalent in tropics less in temperate zones non-existent in cold climate.

Pathology
• Conjunctival epithelium – hyperplasia and downward projections into the
subepithelial tissue.
• Adenoid layer -cellular infiltration by eosinophils, plasma cells, lymphocytes
and histiocytes.
• Fibrous layer- proliferation which undergoes hyaline changes.
• Conjunctival vessels - proliferation, increased permeability and
vasodilation.

Clinical features

Symptoms
• Marked burning and itching sensation
• mild photophobia, lacrimation, stringy (ropy) discharge and heaviness of lids.
Signs
❖ Palpebral form.
▪ Usually upper tarsal conjunctiva of both eyes is involved.
▪ ‘Cobble-stone’ or ‘pavement stone’, fashion or in severe cases ‘giant papillae’.
▪ Associated with white ropy discharge.
❖ Bulbar limbal form
▪ Dusky red triangular congestion of bulbar conjunctiva in palpebral area,
▪ Gelatinous thickened accumulation of tissue around the limbus
▪ Presence of discrete whitish raised dots along the limbus (Horner-Tranta’s
spots)
❖ Mixed form.
▪ It shows combined features of both
▪ palpebral and bulbar forms.

Vernal keratopathy is more frequent with palpebral form and includes following five types
of lesions:
→ Punctate epithelial keratitis
→ Ulcerative vernal keratitis (shield ulceration)
→ Vernal corneal plaques
→ Subepithelial scarring occurs in the form of a ring scar.
→ Pseudogerontoxon can develop in recurrent limbal disease with cupid-based outline

Clinical course
• Self - limited
• Burns out spontaneously after 5–10 years.

Differential diagnosis
Palpebral form of VKC needs to be differentiated from trachoma with predominant
papillary hypertrophy

Treatment

➢ Topical anti-inflammatory therapy

 o Topical anti-inflammatory therapy with combined steroids, mast cell stabilizers,
antihistamines, and NSAIDs forms the mainstay of treatment of VKC., give added
benefits.

➢ Topical lubricating and mucolytics

➢ Systemic therapy
o Oral antihistamines
o Oral steroids for a short duration -recommended for advanced, very severe, non-
responsive cases.

➢ Treatment of large papillae

Very large (giant) papillae can be tackled either by:
o Supratarsal injection of long acting steroid, or
o Cryo application
o Surgical excision is recommended for extra ordinarily large papillae.

➢ General measures include:

o Dark goggles to prevent photophobia.
o Cold compresses and ice packs have soothing effects.
o Change of place from hot to cold area is recommended for recalcitrant cases.

➢ Desensitization

➢ Treatment of vernal keratopathy

o Punctate epithelial keratitis requires increased instillation of steroids
o A large vernal plaque - surgical excision by superficial keratectomy.
o Severe shield ulcer resistant to medical treatment- surgical treatment like
• debridement
• superficial keratectomy
• excimer laser therapeutic keratectomy
• membrane transplantation to enhance re-epithelialization.
 ATOPIC KERATOCONJUNCTIVITIS

Affected age group: young atopic adults, mostly males

Pathogenesis
[Link] 1 and type 4 hypersensitivity reactions
Type 1: IgE mediated response
Type iv: cell mediated response
[Link] to inflammatory change

Clinical features
Symptoms:
▪ Itching
▪ Dry sensation
▪ Soreness
▪ Mucoid discharge
▪ Blurred vision

Signs:

Eyelid signs Conjunctival signs Corneal signs Associations

Inflamed and Milky appearance of Punctate epithelial Keratoconus
rounded posterior tarsal conjunctiva erosions
borders Atopic cataract
Chemosed and Persistent epithelial
Dennie – morgan congested bulbar defects Retinal
fold (extra lid folds) conjunctiva detachment
Filamentary keratitis
Hertoghe’s sign – Gelatinous deposits
lass of lateral and tranta’s dots Plaque formation
eyebrows present in limbal
conjunctiva Peripheral
Blepharitis, tarsal vascularisation and
margin Subepithelial fibrosis scarring
keratinisation
Clinical course:

▪ it has a protracted course with exacerbations and remissions

Treatment:

▪ Topical anti-inflammatory therapy

o topical steroids
o mast cell stabilizers,
o dual action antihistamines
o NSAID eye drops
o topical cyclosporine
o Tacrolimus

▪ Topical lubricating and mucolytics

o Acetylcysteine

▪ Systemic therapy
o oral antihistamines and oral steroids

▪ Others
o surgical resection
 PHLYCTENULAR KERATOCONJUNCTIVITIS

Introduction

• Nodular affection occurring as an allergic response of conjunctiva to an endogenous

allergen (sensitised allergen)

Etiology: type iv –delayed hypersensitivity reaction

Causative allergens: tuberculous proteins, staphylococcus proteins &others
Predisposing factors:

• 3-15 years age group

• females more affected
• under nourishment
• unhygienic living condition

Pathology: 4 stages
• Stage of nodule formation
• Stage of ulceration
• Stage of granulation
• Stage of healing

Clinical features
Symptoms: mild discomfort, irritation and reflex watering
Signs:

• simple phlyctenular conjunctivitis

• necrotising phlyctenular conjunctivitis
• miliary phlyctenular conjunctivitis
In phlyctenular keratitis -2 forms
▪ Ulcerative Phlyctenular keratitis - scrofulous ulcer, fascicular ulcer, Miliary
ulcer
▪ diffuse infiltrate keratitis
Treatment

Local therapy Specific therapy General measures

Topical steroids – dexamethasone Antitubercular therapy if TB is High protein diet
the cause
Antibiotic drops and ointment Vitamin A, C and D
Rule out tonsillitis, dental
Atropine 1% eye ointment caries

Parasitic infestation – stool

examination

GIANT PAPILLARY CONJUNCTIVITIS

Inflammation of conjunctiva with large sized papillae

Etiology:
o mechanically induced papillary conjunctivitis
o localised allergic response to a physically rough deposited surface
o sensitivity reaction

Clinical features:
• itching
• Stringy discharge
• Reduced wearing time of contact lens
• Papillary hypertrophy – in upper tarsal conjunctivitis

Treatment:
• Removal of offending cause- such a contact lens
• Use of mast cell stabilizers
• Combined use of antihistamines and mast cell stabilizers
• steroids
 CONTACT DERMATOCONJUNCTIVITIS

Allergic disorder involving conjunctiva and skin of lids

Etiology – type IV hypersensitivity

Clinical features
▪ Cutaneous involvement
▪ Conjunctival response
▪ Cornea

Diagnosis
▪ Conjunctival cytology
▪ Skin test

Treatment
▪ Discontinuation of causative medication
▪ Topical steroid eye drops
▪ Application of steroid ointment
 CICATRICIAL CONJUNCTIVITS

OCULAR MUCOUS MEMBRANE PEMPHIGOID (OOMP)

• Type II Hypersensitivity reaction involving basement membrane of epithelial cells of

conjunctiva, other mucosal surfaces and even skin.
• After 60 years of age but can occur in adolescence
• Slightly common in females

• Pathology: Chronic inflammatory subepithelial blistering disease with subsequent

cicatrisation of the involved mucosa.

• Ocular features:
Symptoms:
Insidious onset of bilateral redness, foreign body sensation, watering and
photophobia

Signs:
➢ Inflammatory signs – hyperaemia, chronic papillae and subconjunctival vesicles
which later ulcerate
➢ Cicatrization signs – loss of plica semilunaris and fornices, formation of
symblepharon leading to dry eye syndrome
➢ Corneal involvement – superficial punctuate keratitis, secondary microbial
keratitis, corneal neovascularization and perforation
➢ Lid sequelae – trichiasis and entropion formation

• Systemic features:
➢ Mucosa of oral cavity, anus, vagina and urethra may be involved
➢ Desquamative gingivitis
➢ Cutaneous vesicles, bullae and scar formation
➢ Involvement of trachea and esophagus may be life-threatening

• Differential Diagnosis: Stevens-Johnson syndrome and other cicatrizing disorders

• Treatment:

o Topical treatment – tear substitutes, antibiotics, steroids

 o systemic immunosuppression – mild: dapsone, moderate: methotrexate,
severe – methylprednisolone i.v.
o surgical intervention – punctal occlusion, correction of trichiasis and entropion,
ocular surface reconstruction, Keratoprosthesis

STEVENS-JOHNSON SYNDROME AND TOXIC EPIDERMAL NECROSIS

• Acute mucocutaneous blistering diseases usually associated with severe ocular

complications

• Type II Hypersensitivity response to certain drugs such as sulfonamides,

anticonvulsants, allopurinol and infectious agents such as mycoplasma, pneumonia,
herpes simplex virus and adenovirus

Clinical features:

a) Symptoms: Acute onset of fever, skin rash, red eyes, malaise, arthralgia and
respiratory tract symptoms

b) Systemic signs: Classic target skin lesions, haemorrhagic inflammation of mucous

membranes, ulcerative stomatitis and sloughing of epidermal surface (Nikolsky sign)
c) Ocular signs:
➢ Acute disease: Papillary or mucopurulent or pseudomembranous
conjunctivitis, episcleritis and iritis
➢ Late disease: Conjunctival scarring and symblepharon formation, trichiasis and
lid deformities, dry eye, and corneal neovascularization, ulceration, perforation
and scarring

• Treatment: Systemic and ocular treatment in acute phase and late stage intervention

SECONDARY CICATRICIAL CONJUNCTIVITIS

• Cicatricial conjunctivitis may occur secondary to injuries to conjunctiva such as

thermal, radiational or chemical burns and infective conjunctivitis such as trachoma
and viral pseudomembranous conjunctivitis
 TOXIC CONJUNCTIVITIS

Toxic conjunctivitis secondary to molluscum contagiosum:

➢ Chronic follicular conjunctivitis as a response to toxic cellular debris

desquamated into the conjunctival sac from the molluscum contagiosum
nodules present on the lid margin

Chemical toxic conjunctivitis/toxic keratoconjunctivitis:

➢ Irritative follicular conjunctival response to prolonged administration of topical

medication

➢ Common topical preparations like idoxuridine, serine, pilocarpine, contact lens

solutions, topical anaesthetise and others like cosmetics, skin & hair care
products, tear gas weapons & lacrimating agents

➢ Treatment:

o cessation of use of offending agent

o lubricating agents & ointments
o bandage contact lens
o tarsorrhaphy
o amniotic membrane transplants.
 DEGENERATIVE CONDITIONS

PINGUECULA

• Formation of a yellowish white patch on the bulbar conjunctiva near the limbus
• Extremely common

• Etiology
o Not exactly known
o Age-related change
o More common in those exposed to strong sunlight, dust and wind

• Pathology
Elastotic degeneration of collagen fibres of substantia propria of conjunctiva,
coupled with deposition of amorphous hyaline material in the substance of
conjunctiva

• Clinical features

• Bilateral, stationary condition.

• Yellowish white triangular patch near the limbus which first affects the nasal
side and the apex is away from the cornea

• Complications

• Inflammation
• intraepithelial abscess formation
• calcification

• Treatment is not required but it can be excised for cosmetic purposes. if inflamed it
can be treated with topical steroid
 PTERYGIUM

• A wing-shaped fold of conjunctiva encroaching upon the cornea from either side
within the interpalpebral fissure
• Usually seen in old age and more common in men doing outdoor work

• Etiology

▪ Not definitely known.

▪ More common in those living in hot climates and work outdoors.
▪ Exposure to sunlight (UV rays), dry heat, high wind and abundance of dust

• Pathology

▪ Degenerative and hyperplastic condition of conjunctiva.

▪ Subconjunctival tissue undergoes elastotic degeneration and proliferates as
vascularised granulation tissue under the epithelium which encroaches the
cornea
▪ Corneal epithelium, Bowman’s layer and superficial stroma are destroyed

• Clinical features: Unilateral or bilateral. Usually on the nasal side

Symptoms:
➢ Cosmetic intolerance in the early stages
➢ Foreign body sensation and irritation
➢ Defective vision
➢ Diplopia
Signs:
➢ Triangular fold of conjunctiva encroaching on the cornea in the area
of palpebral aperture usually on the nasal side
➢ Stocker line – deposition of iron in the corneal epithelium

• Parts:

➢ Head – apical part

➢ Neck – constricted part in the limbal area
➢ Body – scleral part
➢ Cap – semilunar whitish infiltrate in front of head
• Types:

1. Based on extent:
➢ Type 1 pterygium – extends less than 2 mm onto the cornea
➢ Type 2 – involves upto 4 mm of the cornea
➢ Type 3 – encroaches more than 4 mm of the cornea and involves the visual
axis

2. Based on progression:
➢ Progressive pterygium: Thick, fleshy and vascular with Fuch’s spots or islets
of Vogt
➢ Regressive pterygium: Thin, atrophic, and attenuated with very little
vascularity. Stocker’s line may be seen

• Complications

o Cystic degeneration and infection

o Neoplastic change to epithelioma
o fibrosarcoma
o malignant melanoma

• Differential Diagnosis: Pseudo pterygium

• Treatment

Medical treatment.
o tear substitutes, topical steroids

Surgical excision
o with free conjunctival limbal autograft
o with amniotic membrane graft and mitomycin – C
o with lamellar keratectomy and lamellar keratoplasty

• Recurrence after surgical excision is common (30-50%). It can be reduced by certain

measures
 Surgical technique

• After topical anaesthesia, eye is cleansed, draped and exposed using universal eye
speculum.

• Head of the pterygium is lifted and dissected off the cornea very meticulously

• The main mass of pterygium is then separated from the sclera underneath and the
conjunctiva superficially.

• Pterygium tissue is then excised taking care not to damage the underlying medial
rectus muscle

• Haemostasis is achieved and the episcleral tissue exposed is cauterised thoroughly.

• Limbal conjunctival autograft transplantation (LLAT) to cover the defect after

• pterygium excision is the latest and most effective technique in the management of
pterygium.

CONCRETIONS

• Formed due to accumulation of inspissated mucus and dead epithelial cell debris into
the conjunctival depressions called loops of Henle

• Common in elderly and in patients with scarring stage of trachoma

• Clinical features: Common on the upper palpebral conjunctiva than the lower and in
lower fornix
• Yellowish white, hard looking, raised areas, varying in size from pin point to pin head
• Hard – may produce foreign body sensations and lacrimation by rubbing the corneal
surface
• Occasionally, may cause corneal abrasions

• Treatment – removal with the help of hypodermic needle under topical anaesthesia
 AMYLOID DEGENERATION OF CONJUNCTIVA

a) Primary conjunctival amyloid – associated with deposition of light-chain

immunoglobulin by the monoclonal B cells and plasma cells
b) Secondary conjunctival amyloid – may occur secondary to systemic diseases or
secondary to chronic conjunctival inflammations

• Clinical features:
➢ Deposition of yellowish, well-demarcated, irregular amyloid material in the
➢ conjunctiva with superior conjunctiva and tarsal conjunctiva commonly
involved
➢ Subconjunctival hemorrhage – amyloid deposition in blood vessels

• Treatment – Lubricating drops, excision biopsy

 SYMPTOMATIC CONDITIONS OF CONJUNCTIVA

Common conditions include:

• Hyperaemia
• Chemosis
• Ecchymosis
• Xerosis
• Discolouration of conjunctiva

SIMPLE HYPERAEMIA OF CONJUNCTIVA

Acute exposure to minor irritants leads to congestion of conjunctival vessels.

ETIOLOGY
acute and transient:
• Acute irritants like foreign body, misdirected cilia, concretions, dust,
smoke, chemical fumes, stormy wind, bright light, extreme cold and
heat, simple rubbing of eyes with hands.
• Reflex hyperaemia due to eye strain, from inflammation of nasal
cavity, lacrimal passages and lids
• Hyperaemia associated with systemic febrile conditions.
• Nonspecific inflammation of conjunctiva

recurrent or chronic hyperaemia:

• occurs due to chronic exposure to irritants as in chronic smokers and
alcoholics, people residing in dusty, ill ventilated rooms, workers
exposed to prolonged heat, in patients suffering from rosacea and
insomnia or less sleep.

CLINICAL FEATURES
• Feeling of discomfort, heaviness, grittiness, tiredness, tightness in eyes
are common complaints.
• Mild lacrimation and minimal mucoid discharge may occur.
• On cursory examination, conjunctiva looks normal.
TREATMENT
• Removal of cause of hyperaemia e.g.: in acute transient hyperaemia, removal of
irritants gives prompt relief.
• Symptomatic relief can be achieved by use of topical decongestants or naphazoline
drops.

CHEMOSIS OF CONJUNCTIVA

• chemosis or oedema is due to laxity of conjunctiva.

CAUSES

• Local inflammatory conditions:

It includes conjunctivitis, corneal ulcers, iridocyclitis,
endophthalmitis, panophthalmitis, styes, acute meibomitis, orbital
cellulitis, acute dacryoadenitis, acute dacryocystitis, tendonitis.

• Local obstruction to flow of blood and/or lymph:

it may occur in patients with orbital tumours, cysts, endocrine
exophthalmos, orbital pseudo tumours, cavernous sinus
thrombosis, carotico-cavernous fistula, blockage of orbital
lymphatics following orbital surgery, acute congestive glaucoma.

• Systemic causes:
It includes severe anaemia and hypoproteinaemia, congestive
heart failure, nephritic syndrome, urticaria.

Clinical features and management depend upon the causating factor.

 ECCHYMOSIS OF CONJUNCTIVA

• Ecchymosis or subconjunctival haemorrhage may vary in extent from small petechial

haemorrhage to the whole of bulbar conjunctiva making white sclera of eye invisible.

ETIOLOGY
▪ Trauma
▪ Inflammation of conjunctiva:
o Associated with acute haemorrhagic conjunctivitis caused by
picornavirus, pneumococcal conjunctivitis and leptospirosis.
▪ Sudden venous congestion of head:
o Occurs owing to rupture of conjunctival capillaries due to sudden rise
in pressure.
▪ Spontaneous rupture of fragile capillaries:
o Seen in arteriosclerosis, hypertension, diabetes mellitus.
▪ Local vascular anomalies:
o Seen in telangiectasia, varicosities, aneurysm.
▪ Blood dyscrasias
▪ Bleeding disorders
▪ Acute febrile systemic infections
▪ Vicarious bleeding.

CLINICAL FEATURES
Symptoms

• generally symptomless, except for red discolouration noted by patients as a

serious symptom.

Signs

• on examination, subconjunctival haemorrhage looks as a flat sheet of

homogenous bright red colour with well-defined limits.

TREATMENT
• Treat the cause when discovered.
• Cold compress to check bleeding in initial stage and hot compress may
help in absorption of blood in late stages.
• Placebo therapy with astringent and lubricant eyedrops.
• Psychotherapy and assurance to the patient is most important.
 XEROSIS OF CONJUNCTIVA

• symptomatic condition in which conjunctiva becomes dry and lustreless.

ETIOLOGY
Parenchymatous xerosis Epithelial xerosis
Cause cicatricial disorganisation of conjunctiva due to hypovitaminosis-a.
local causes

CLINICAL FEATURES

• epithelial xerosis occurring in children is characterised by varying degree of

conjunctival dryness, thickening, wrinkling, pigmentation.
• characterised by marked dryness, thickening, scarring, keratinisation.
TREATMENT
• Treatment of the cause and their complications.
• Symptomatic local treatment with artificial tear preparations, which should be
instilled frequently.

DISCOLOURATION OF CONJUNCTIVA
CAUSES
• Red—subconjunctival haemorrhage
• Yellow—bile pigments in jaundice, blood pigments in malaria and yellow fever
• Grey—application of kajal or mascara in females.
• Brownish grey—argyrosis, following prolonged application of silver nitrate for treatment
of chronic conjunctival inflammations.
• Blue—ink tattoo from pens or effects of manganese dust.

Non Endogenous In patients with Addison’s disease and ochronosis.

melanocytic pigmentation
pigmentation Exogenous Follows long term use of adrenaline for glaucoma,
pigmentation argyrosis.
melanocytic conjunctival The pigmented spot freely moves with the movement
pigmentation epithelial melanosis of conjunctiva.
Subepithelial isolated anomaly of conjunctiva
melanosis
Pigmented tumours can be benign naevi, precancerous melanosis or
malignant melanoma
 CYSTS AND TUMOURS

CYSTS OF CONJUNCTIVA

Congenital cystic Include congenital corneoscleral cyst and cystic form of

lesions epibulbar dermoid.
Lymphatic cysts of Occur due to dilation of lymph spaces in bulbar conjunctiva.
conjunctiva Lymphangiectasis is characterised by row of small cysts. Rarely,
it occurs as a single multilocular cyst.
Retention cyst Occur due to blockade of ducts of accessory lacrimal glands of
Krause in chronic inflammatory conditions, trachoma,
pemphigus.
Epithelial implantation Develops following implantation of conjunctival epithelium in
cyst deeper layers, due to surgical injuries of conjunctiva.

Epithelial cyst due to Seen in chronic inflammatory or degenerative conditions.

downgrowth of
epithelium
Aqueous cyst Due to healing by cystoids cicatrix formation.
Pigmented epithelial Formed following prolonged topical use of cocaine or
cyst epinephrine.
Parasitic cysts Such as subconjunctival, hydatid cyst or filarial cyst are not
infrequent in developing countries.

Treatment:

• needs a careful surgical excision.

• Excised cyst is subjected to histopathological examination.
 TUMOURS OF CONJUNCTIVA

CLASSIFICATION

Non Congenital Dermoid, lipodermoid

pigmented Benign Simple granuloma, papilloma, adenoma, fibroma,
tumours angioma
Premalignant Intraepithelial epithelioma
Malignant Squamous cell carcinoma, basal cell carcinoma
Pigmented Benign Naevi or congenital moles
tumours Precancerous melanosis Superficial spreading melanoma
Malignant Primary melanoma

Non-pigmented tumours:

Congenital tumours:
Dermoid:

• It occurs at the limbus.

• They appear as solid white masses, firmly fixed to cornea.
• Dermoid consists of collagenous connective tissues, sebaceous glands and hair, lined
by epidermoid epithelium.

Lipodermoid:

• It is a congenital tumour, usually found in the limbus or outer canthus.

• It appears as soft, yellowish white, movable subconjunctival mass.
• It consists of fatty tissue.
• It may be associated with accessory auricles and other congenital defects.

Benign tumours:
Simple granuloma:

• It consists of polyploidy, cauliflower like growth of granulation tissue.

• Treatment: complete surgical removal.
Papilloma:

• Benign polyploidy tumour usually at inner canthus, fornices or limbus.

• It has tendency to undergo malignant change and hence needs complete excision.

Fibroma

• It is a rare soft or hard polyploidy growth usually in lower fornix.

Premalignant tumours:
Bowen’s intraepithelial epithelioma:

• It is a precancerous condition, now included in ocular surface squamous neoplasia.

Malignant tumours:
Squamous cell carcinoma:

• It occurs at transitional zones, at limbus and lid margin.

• The tumour invades the stroma deeply and maybe fixed to the underlying tissue.

Ocular Surface Squamous Neoplasia:

▪ It is the term used to denote a wide range of dysplastic changes involving epithelium
of conjunctiva, cornea and limbus.
▪ It includes squamous dysplasia, carcinoma in-situ i.e. Corneal or conjunctival
intraepithelial neoplasia [CIN], SCC. Very few CIN may progress to SCC.

▪ Risk factors:

▪ Exposure to intense UV radiation

▪ Advanced age
▪ Cigarette smoking
▪ AIDS and HPV infection
▪ Xeroderma pigmentosa
▪ Light complexion
 • Pathogenesis:
Since OSSN usually arise at limbus, it is postulated that various predisposing factors
act on stem cells causing their abnormal maturation and proliferation resulting in
OSSN.

Clinical features:
The morphological features are:
o Leukoplakic form appears as focal thickening of epithelium with overlying
hyperkeratotic plaque
o Papillomatous form appears a well-defined soft vascularised mass
o Gelatinous form appears as ill-defined translucent thickening.

Treatment:
▪ Surgical excision
▪ Cryotherapy to surrounding tissue
▪ Topical chemotherapy with mitomycin

Basal cell carcinoma:

▪ It may invade the conjunctiva from the lids or may arise pari-passu from plica
semilunaris or caruncle.
▪ Treated by surgical excision.

Pigmented tumours:

Naevi or congenital moles:

▪ Grey gelatinous, brown or black, flat or slightly raised nodules on bulbar conjunctiva,
mostly near limbus.
▪ Histologically, it resembles their cutaneous brethren.
▪ Malignant change is very rare and when occurs is indicated by sudden increase in size
or increase in pigmentation or appearance of signs of inflammation.
▪ Thus, excision is indicated only for cosmetic reasons and rarely for medical reasons.
 Precancerous melanosis
▪ It occurs in adults as superficial spreading melanoma.
▪ Clinically, small pigmented tumour develops at any site of bulbar or palpebral
conjunctiva, which spreads as diffuse, flat, asymptomatic pigmented patch.
▪ Treatment: in early stages, local excision with postoperative radiotherapy maybe
sufficient. But in case of recurrence, it should be treated as malignant melanoma.

Malignant melanoma
▪ It usually arises de-novo, usually near [Link] usually occurs in elderly patients.
▪ Clinically, it presents as pigmented or non-pigmented mass near limbus or on any
other part of conjunctiva.
▪ It penetrates over the surface of the globe and rarely penetrates it.
▪ histologically, neoplasm maybe alveolar, round-celled or spindle-celled
▪ treatment: enucleation or exenteration is the treatment of choice depending upon
the extent of growth.
 CORNEA

[Link]:

Cornea is a transparent, avascular, watch-glass like structure forming 1/6th of anterior eyeball or outer fibrous
coat of eyeball. It is the window to inner eye.

[Link] of Cornea:

• Refractory index = 1.37

• Refractory power = 43-44 D (Anterior surface =
+48 D Posterior surface = -5.80 D)

[Link]:
Basically, Cornea has 6 layers: (anterior to posterior)
1. Corneal epithelium
2. Stroma (Substantia propria)
3. Bowman’s membrane (condensed superficial part of stroma)
4. Pre-Descemet’s membrane (Dua’s layer)
5. Descemet’s membrane (basement membrane of corneal endothelium)
6. Corneal endothelium

FEATURES OF 6 LAYERS: (anterior to posterior)

 1) CORNEAL EPITHELIUM:
• Non-keratinized Stratified Squamous Epithelium
• 5-6 layers
2) BOWMAN’S MEMBRANE:
• Acellular Condensed Collagen Fibril
• Cannot regenerate
• Causes corneal scar/opacity on damage
3) STROMA:
• Thickest layer (90% 0f cornea)
• Lamellae arranged in many layers (parallel to each other and to corneal plane)
• Lamellae made of Collagen fibrils (type 1 and 5 fibrillae interwined with filaments of type 4 collagen)
embedded in hydrated matrix of proteoglycans
4) DUA’S LAYER:
• Discovered in 2013 by Dr. Harminder Dua. (So the newest layer to be found)
• Thick acellular membrane anterior to Descemet’s membrane
5) DESCEMET’S MEMBRANE:
• Strong and Elastic membrane usually resistant to trauma and chemical agents
• On severe trauma, membrane is torn and curls up in anterior chamber
• Its prominent peripheral end forms Schwalbe’s Line (ring)
6) CORNEAL ENDOTHELIUM:
• Single layer of flat polygonal epithelial cell (Endothelium is a misnomer)
• Most important metabolic layer for corneal transparency
• Non-proliferative and Irreparable on damage
• Endothelial count using Specular Microscope (500x)
❖ Average count = 3000 cells/mm3
❖ Every year, 0.5% is lost
❖ Corneal decompensation occurs when 75% cells are lost
❖ For corneal donation, >2000 cells should be present

[Link] supply:
• Normal cornea is avascular but some loops from anterior ciliary artery tends to supply via sub conjunctival
tissues.
• Nourishment is by diffusion from Aqueous humour and capillaries at limbus
• Oxygen Supply:
❖ O2 is acquired from air.
❖ However respiration involves both aerobic and [Link] can survive only up to 6-7 hrs
Anaerobically

• Glucose Supply:
❖ Source of glucose: mainly aqueous humour and little from limbal capillaries

[Link] Supply:
• Long ciliary nerve – a branch of Naso-ciliary nerve from Ophthalmic branch of Trigeminal nerve
• Cornea is extremely sensitive (touch, pain, temperature)

[Link]:
Develops from following germ layers:
❖ Surface Ectoderm derivatives: Corneal epithelium
 ❖ Mesoderm derivatives: Corneal stroma
❖ Neural crest cell derivatives: Corneal endothelium, Descemet’s membrane, Stromal Keratocytes

[Link]:
Functions of Cornea:
✓ Transparency, refractive surface, protection of intra ocular contents, maintains structural integrity of globe

Reasons for Corneal Transparency:

➢ Typical lamellar arrangement of cells
➢ Avascular in nature
➢ Relative dehydration (by endothelium)
➢ Normal Intra ocular pressure
➢ Hypocellularity (Low number of cells)
➢ Others like crystalline particles, etc.

Healing/Regeneration Capacity:

• Involving only Epithelium: complete regeneration (stem cells at limbus)

• Bowman’s membrane and stroma: replaced by fibrous tissue
• Descemet’s membrane: Generally resistant to trauma. On injury, can be replaced to very small extent by
endothelium. Due to tension, membrane usually curls up when trauma.
• Endothelium: Cannot regenerate. Adjacent cells may fill up the space.

[Link] ANOMALIES:

Anomalies of corneal shape and size:

a) Megalocornea:
➢ Horizontal diameter of cornea is of adult size at birth (or) ≥13mm after age of 2years.
➢ Normal vision
➢ May be associated with systemic conditions like Marfan’s, Ehlers Danlos, Down syndrome
➢ D/D: Buphthalmos, Keratoglobus
b) Microcornea:
➢ Horizontal diameter of cornea is <10mm at birth
➢ Usually hypermetropic vision
➢ Rarely an isolated anomaly. Commonly associated with Nanophthalmos and Microphthalmos
c) Cornea plana:
➢ Cornea is completely flat (bilaterally) since birth
➢ Astigmatic vision
➢ Rare anomaly, mostly associated with microcornea

Anomalies of corneal transparency:

Neonatal Cloudy Cornea:

D/D:

• Sclerocornea
• Tears in descemet’s membrane
• Ulcer
• Metabolic conditions
• Posterior corneal defect
 • Endothelial dystrophy
• Dermoid

[Link] OF CORNEA (KERATITIS) – CLASSIFICATION:

1. Infective keratitis
• Bacterial keratitis
• Viral keratitis
• Fungal keratitis
• Chlamydial keratitis
• Protozoal keratitis
• Spirochaetal keratitis
2. Allergic keratitis
• Phlyctenular keratitis
• Vernal keratitis
• Atopic keratitis
3. Trophic keratitis
• Exposure keratitis
• Neurotrophic keratopathy
• Keratomalacia
• Atheromatous ulcer
4. Keratitis associated with diseases of skin and
mucous membrane.
5. Keratitis associated with systemic collagen vascular
disorders.
6. Traumatic keratitis which may be due to
mechanical trauma, chemical trauma, thermal
burns, radiations.
7. Idiopathic keratitis e.g.,
• Mooren’s corneal ulcer
• Superior limbic keratoconjunctivitis
• Superficial punctate keratitis of Thygeson.

INFLAMATION OF CORNEA

BACTERIAL CORNEAL ULCER

DEFINITION:
The Cornea is the mostly exposed part of the eye and hence it is prone to get infection soon,

ETIOLOGY:

There are 2 causes for this infections,

 ➢ I. First involving erosion of epithelium and then invasion of bacteria (Eg. Staphylococci, Pseudomonas,
Streptococcus, Enterobacteriaceae and Neisseria, etc)
➢ II. In the other case the bacteria can directly invade the corneal layers.(Eg. [Link], [Link], ,
[Link], Haemophilus, Listeria sps.)

PATHOGENESIS:

PROGRESSIVE INFILTERATION

Charecterized by the progressive infilteration of polymorphonuclear/lymphocytes into

epithelium. Subsequently necrosis of the involved tissues.

ACTIVE ULCERATION

This is the active ulceration by necrosis of epithelium, bowman’s membrane and

stroma. This stage shows greyish infilteration and sloughing in the sides and floors of
the [Link] this causes increased hyperemia which can also affect the uveal tract,
etc, hence this futher causes Acute Anterior [Link] other exudates from the
anterior chamber leads to the formation of HYPOPYON

REGRESSION STAGE

It involves the natural host immune mechanism, Leucocytes forms a line of

demarcation, which helps in phagocytic activity on the organism and the cellular
debris. The ulcer begins to heal and epithelium starts to grow.

CICATRIZATION STAGE

Healing continues by epithelization forming a permanent covering. The stroma

thickens and fills under the epithelium pushing it forward. Degree of scarring depends
on the severity. Where superficial ulcers heals without scar while deeper involvement
like bowman’s membrane heals with a scar called “nebula”

CLINICAL FEATURES:

➢ Purulent corneal ulcer without hypopyon

➢ Hypopyon corneal ulcer

SYMPTOMS:

➢ Pain
➢ Watering eye
➢ Redness
➢ Blurred vision
➢ Photophobia
SIGNS:

➢ Swelling of lid
➢ Blepharospasm
➢ Hyperaemia and congestion in conjunctiva
➢ Corneal ulcer – greyish white in nature
➢ Hypopyon in anterior chamber
➢ Raised intraocular pressure
➢ Muddy color iris

NOW WHAT IS HYPOPYON?

It is the presence of puss in anterior chamber.

CAUSES:

There are 2 types where

HYPOPYON CORNEAL ULCER which is caused by Pseudomonas.

CORNEAL ULCER WITH HYPOPYON which is caused by the other bacterial organisms like Staphylococci, Streptococci,
Gonococci, Moraxella, etc.

FACTORS:

• Chromic dacrocystitis
• Purulent keratitis

MECHANISM:

The mechanism starts with the formation of corneal ulcer which then leads to perforation and invading the iris causing
the inflammation of iris (IRITIS). This leads to outpouring of the leucocytes or the exudates into the anterior chamber.
Therefore the’is tends to accumulate in the lower region of the anterior chamber due to gravity and have a demarcated
line. This settling down of exudates is known as Hypopyon. When the ulceration is iver the hypopyon is reabsorbed.

FEATURES:

• Ulcus serpans is the other name of Hypopyon corneal ulcer. It is a greyish white disc shaped ulcer.
• It is usually associated with violent iridocyclitis.

COMPLICATIONS:

The most important complication of the corneal ulcer is that perforation. Where the patient when sneeze or cough or
any straining causes perforation.

Perforation is usually of two types Small and Large.

SMALL PERFORATIONS:

Where the perforoati0on is very small, this tends the iris to seal the perforation. So the iris can even prolapse out which
is known as the iris prolapse.

LARGE PERFORATION: (in anterior staphyloma)

In this there is an involvement of large part of cornea. Where it cuases inflammatory cells to accumulate and form a false
layer instead of cornea.
This is known as pseudo cornea, which is formed by the exudates or the fibrotic layer. This causes increase in pressure
that leads to bulging out of the layer. Which sows “a bunch of grape like appearance”

MANAGEMENT:

CLINICAL EXAMINATION checking

• Corneal sensation
• Regurgitation to check lacrimal sac
• Biomicroscopic examination

LAB INVESTIGATIONS including TLC, DLC, ESR, Hb, urine and stool examination.

OTHER METHODS including, Gram and Giemsa staining, 10% KOH wet preparation, Calcoflour white stain, Culture on
blood agar, Culture on Sabouraud’s dextrose agar.

TREATMENT:

➢ Antibiotics can be used, Eg, Cefazolin 5% with tobramycin(1.3%) /vancomycin(5%) as eye drops and eye
ointments
➢ Cycloplegics for pain relief. Eg. Atropine can be used, which also helps in increasing vascularization in the
anterior part of uvea. Alongside others like homatropine can also be used.
➢ Vitamin (A,B and C) helps in early healing of ulcer
➢ Treat the complications
➢ In case of impending perforation, use pressure bandage, soft bandage, try to decrease strain such as sneeze
cough etc, and try to decrease the intraocular pressure.
➢ Further perforation can be treated with the help of conjunctival flaps and tissue adhesive glues
➢ Therapeutic keratoplasty and urgent tectonic keratoplasty can also be done.

VIRAL CORNEAL ULCER

Viral
corneal
ulcer

Herpes simplex Herpes zoster

keratitis ophthalmicus

primary recurrent
herpes herpes

❖ HERPES SIMPLEX KERATITIS

• Etiology:
o Herpes simplex virus (DNA virus)
 o Epitheliotropic and neurotropic
o 2 types - HSV I and HSV II
o Mode of infection:
HSV I – lips(kissing), nose, cornea,
HSV II – genitalia of mother to eyes of neonates

• Ocular lesions

Ocular lesions

primary herpes recurrent herpes

active epithelial trophic keratitis herpetic

skin lesions conjunctiva cornea stromal keratitis
keratitis (meta-herpetic) iridocyclitis

punctate
fine epithelial disciform
epithelial
punctate keratitis keratitis
keratitis

coarse epithelial diffuse stromal

dendritic ulcer
punctate keratitis necrotic keratitis

geographical
dendritic ulcer
ulcer

• PRIMARY OCULAR HERPES

Attack non-immune person (children: 6m – 5ys)
Infection by direct contact
Clinical features:
- Systemic: mild fever, malaise, non-suppurative lymphadenopathy, encephalitis
- Skin lesions: vesicular lesions (@ face, lip, lid margin, periorbital area)
- Ocular lesions: acute follicular conjunctivitis & keratitis

Treatment:
Primary infection: self limiting
-
To limit corneal involvement: Trifluridine, vidarabine, oral acyclovir
-
For ciliary spasm: atropine
-
• RECURRENT OCULAR HERPES (unilateral)
Virus is dormant in the trigeminal ganglion

Reactivation due to cold, trauma, stress, pneumonia,

relapse of malaria, UV exposure, steroids

Travels down along trigeminal nerve

Recurrent infection

1. Epithelial keratitis

A & B - Punctate epithelial keratits

C &D - Dendritic ulcer
E & F - Geographical ulcer
G & H - Disciform keratits

Clinical features
Symptoms:
- Redness, pain
- Photophobia
- Tearing
- Decreased vision
Signs:
- Punctate epithelial keratitis
 Attack deeper layers of corneal epithelium
Corneal vesicles coalesce and erupt → ulcers
No opacity

- Dendritic ulcer

increase in
length and surface
superficially,
send out over
infiltrates resembles dendritic
lateral infiltrates
develop and as grey figure is
branches - break to
spread in all striae formed
knobbed from
directions
at the ulcers
ends

Stain: floor –fluorescein & margin – rose Bengal

- Geographic ulcer

branches of dendritic ulcer

large epithelial ulcer
enlarge and coalesce

Treatment:
Definitive treatment:
- Antiviral drugs:
✓ Acycloguanosine
✓ Ganiciclovir
✓ Trifluorothymidine
✓ Adenine arabinoside
- Mechanical debridement:
Remove virus laden cells with sterile cotton applicator
- Systemic antiviral drugs: 10-21 days
✓ Acyclovir
✓ Famcyclovir
✓ Valacyclovir
Non specific supportive therapy (similar to bacterial ulcer)

2. Stromal keratitis

➢ Disciform keratitis
 disciform
corneal
imbibition of stromal oedma
aqueous
humour
endothelial
damage

Pathogenesis:
Delayed hypersensitivity reaction

Clinical features
Symptoms
- Photophobia
- Ocular discomfort
- Reduction in visual acuity
Signs
- Focal disc shaped patch of stromal oedema
- Folds in Descemet’s membrane
- Keratic precipitates
- Ring of stromal infiltrate (Wessley immune ring)
- Corneal sensations diminished
- Raise in intraocular pressure

Treatment:
- Topical steroid eye drops
- Antiviral drug – aciclovir
- If infected epithelial ulcer present → antiviral drugs started 5-7 days before steroids
- Non specific and supportive treatment

➢ Stromal necrotic keratitis

Interstitial keratitis caused by active viral invasion and tissue destruction
 Clinical features
Symptoms
- Pain
- Photophobia
- Redness
Signs
- Corneal lesion
Appearance- blotchy cheesy white infiltrate
Site- under epithelial ulcer/under intact epithelium
- Mild iritis and keratic precipitates
- Stromal vascularisation
Treatment:
- Systemic antiviral drugs
- Keratoplasty (disadvantage - recurrence)

3. Metaherpetic keratitis

Not active viral disease

Mechanical healing problem due to persistent defect in basement membrane of corneal epithelium
Site : previous herpetic ulcer

Clinical features
- Linear /ovoid epithelial defect
- Margin of ulcer -thick and grey
Treatment:
- Lubricants
- Bandage soft contact lens
- Tarsorrhaphy

❖ HERPES ZOSTER OPHTHALMICUS

• Etiology:
o Varicella-zoster virus (DNA virus)
o Produces acidophilic intranuclear inclusion bodies
o Neurotropic
A & B - Punctate epithelial keratitis
C &D - Microdendritic epithelial ulcer
E & F - Nummular keratitis
G & H - Disciform keratits
 Pathogenesis:

infection in child (manifests as chickenpox)

child develops immunity

virus remain dormant in sensory ganglion of CN V

when cellular immunity is depressed (elderly or

immunocompromised)

virus reactivates replicates and travels down along one or

more branches of ophthalmic division of CN V to produce
cutaneous and ocular lesions

Clinical features
- Involvement of frontal nerve > lacrimal and nasociliary nerves
- Ocular complications in 50% of individuals
- Lesions limited to one side of midline of head
- Hutchinson’s rule: ocular involvement is frequent if the side or tip of nose presents
vesicles

clinical phases

relapsing phase
acute phase chronic phase
(reappear even
(few weeks) (for years)
after 10 yrs)

o Acute phase lesions

General features:
- Fever
- Malaise
- Severe neuralgic pain along course of affected nerve
Cutaneous lesions:
Appear 3-4 days of onset of disease
 crusts are
red and shed and
vesicle crusting
oedematous pustules permanent
formation ulcers
skin pitted scars
are left

With subsidence of eruptive phase → neuralgic pain diminished and ocular complications appear

Ocular lesions:
1. Conjunctivitis
- Mucopurulent conjunctivitis
- Acute follicular conjunctivitis
2. Zoster keratitis
- Epithelial keratitis :
Start with coarse punctate keratitis followed by microdendritic epithelial ulcers
(pseudodendritic keratitis → peripheral and stellate shaped ; tapering ends which lack
bulb)
- Nummular keratitis
Anterior stromal infiltrates
Multiple tiny granular deposits
surrounded by stromal haze
after healing, scars left behind
- Disciform keratitis
Always preceded by nummular keratitis
- Keratouveitis with endothelitis
Acute endothelial cell loss

3. Episcleritis and scleritis

Appear at the onset of rash, concealed by overlying conjunctivitis
4. Iridocyclitis
May be associated with hypopyon and hyphaema
5. Acute retinal necrosis
6. Secondary glaucoma
Early stages – due to trabeculitis
Late stages – due to synechial angle closure
7. Anterior segment necrosis and phthisis bulbi
Due to zoster vasculitis and ischaemia

Neurological complications:
1. Motor nerve palsy (3,4,6,7 cranial nerve)
2. Optic neuritis
3. Encephalitis
o Chronic phase lesions
1. Post herpetic neuralgia
- Persistence of mild to moderate pain after subsidence of eruptive phase
- Worsens at night
- Aggravated by touch and heat
- Anaesthesia dolorosa – anaesthesia of the affected skin which when associated with
continued postherpetic neuralgia
2. Lid lesions
- Ptosis
- Trichiasis
- Entropion
- Notching
3. Conjunctival lesions
- Chronic mucous secreting conjunctivitis
4. Corneal lesions
- Neuroparalytic ulceration
- Exposure keratitis
- Mucous plaque keratitis
5. Scleritis and uveitis

o Relapsing phase lesions

Reappear even after 10 yrs of acute phase include
- Nummular keratitis
- Mucous plaque keratitis
- Episcleritis
- Scleritis
- Secondary glaucoma
Treatment:
Systemic therapy
- Oral antiviral drugs(immediate after onset of rash)
Acyclovir
Valaciclovir
- Analgesics (for pain)
Mephenamic acid &
Paracetamol/Pentazocin / pethidine
- Systemic steroids (for neurological complications)
- Cimetidine (for pain and pruritis)
- Amitriptyline (for accompanying depression)

Local therapy for skin lesions

- Antibiotic-corticosteroid skin ointment/lotions
- No calamine lotion (as it promote crust formation)

Local therapy for ocular lesions

 - for zoster keratitis, iridocyclitis and scleritis
Topical steroid eye drops
Cycloplegics – cyclopentolate or atropine eye ointment
Topical acyclovir eye ointment
- to prevent secondary infections
Topical antibiotics
- for secondary glaucoma
Timolol or betaxolol eye drops
Acetazolamide
- for mucous plaques
Topical mucolytics – acetyl cysteine
- for persistent epithelial defects
Lubricating artificial tear drops
Bandage soft contact lens

Surgical treatment (for neuroparalytic corneal ulcer)

- Lateral tarsorrhaphy
- Amniotic membrane transplantation
- Tissue adhesive with bandage contact lens
- Keratoplasty

FUNGAL CORNEAL ULCER

DEFINITION

❖ Fungal corneal ulcers are local necrosis of corneal tissue due to invasion by fungi.
❖ Other names
➢ Mycotic keratitis
➢ Fungal keratitis
➢ Keratomycosis

CAUSATIVE AGENTS

❖ Filamentous fungi – Aspergillus Fusarium

❖ Yeast – Candida albicans

PREDISPOSING FACTORS

• Immuno compromised state

• Tropical countries

• Indiscriminate use of topical steroids

• Underlying corneal diseases

• Trauma to corneal epithelium

MODE OF INFECTION
Mycotic keratitis is typically preceded by occular trauma mainly by agriculture and vegetable matters such as thorn or
wooden stick

SYMPTOMS

• Pain, redness and lacrimation

• Photophobia

• Decreased visual acuity (central area – profound blindness)

SIGNS

• Dry-looking yellowish white lesion

• Indistinct margins

• Delicate feathery, finger-like projections into adjacent stroma

• Surrounded by yellowish line of demarcation which deepens into a gutter

• Overlying epithelium is elevated and may be intact

• Immune ring ( Wesseley ) due to deposition of immune complexes and inflammatory cells around the ulcer

• Satellite lesions

• Marked ciliary and conjunctival congestion

• HYPOPYON :

➢ Leucocytes gravitate to the bottom of anterior chamber

➢ May not be sterile

➢ Thick and immobile

DIAGNOSIS

• History, Examination – signs are more

• Fluorescein dye defines the extent and confirms the diagnosis of ulcer

• Corneal scraping –

 gram stain
 Giemsa stain
 10٪ KOH
 culture – SDA sensitivity
• Local septic foci.

HEALING

Healing of the ulcer occurs by the formation of fibrous tissue

COMPLICATIONS

• Ectatic cicatrix

• Descematocele
 • Perforation and its effects

TREATMENT

➢ MEDICAL
➢ SURGICAL

• Scrapping and debridememt

• Topical cycloplegic agent

➢ atropine 1 % bid to qid

➢ cyclopentolate or homatropine - mild

• Topical antifungal agent q1h x 24-72 hrs then taper slowly as improvement noted.

➢ Natamycin 50 mg/mL

➢ Amphotericin B 1.0 - 2.5 mg/mL

➢ Miconazole 10 mg/mL

➢ Nystatin- For candida sps.

• For severe infection add systemic antifungal agent

➢ Ketoconazole 200-400 mg po qd or

➢ Amphotericin B 1 mg/Kg IV over 6 hours

• Topical steroids are contraindicated in fungal keratitis

• Endophthalmitis – vitreous tap & intravitreal antibiotics and antifungals

• Iodine cauterization.

PROTOZOAL KERATITIS
ACANTHAMOEBA KERATITIS
Increasing incidence - due to increase in usage of contact lens

Etiology:

Contact lens which are contaminated with water

● Swimming in contaminated water

● Hot tub use
● Contaminated matter such as vegetable matter
Clinical features:

Symptoms :

● Pain (mild -severe)

● Watering
● Photophobia
 ● Blepharospasm
● Blurred vision

Signs:

Worsens gradually with period of temporary remission

1. Epithelial lesions:
● Epithelial roughening and irregularities
● Epithelial ridges
● Radial keratoneuritis - 50% of cases
● Pseudodendrites formation - mistakes for herpes simplex keratitis
● Epithelial and subepithelial curvilinear opacity
2. Limbal lesions: limbitis in early stages
3. Stromal lesions:
● Patchy and satellite
● Ring infiltrates
● Ring abscess
4. Scleritis:
● Usually anterior ( diffuse/nodular)
● Contagious with keratitis
DIFFERENTIAL DIAGNOSIS:
1. Viral keratitis:
In early stages , both epithelial lesions and infiltrates ( Pseudodendrites )

2. Fungal keratitis :
Ring infiltrates with hypopyon

3. Suppurative keratitis
DIAGNOSIS:

Diagnosis is mostly made by exclusion with nonresponsive patients being treated for herpes , bacterial or fungal
keratitis

Investigation :

1. Confocal microscopy - direct visualisation of cyst

2. Stains:
● Grams stain- stains organism
● Geimsa stain- stains organism and cyst
● Calcofluor white stain- stains cyst and visualise under UV light
● KOH mount - stains cyst
3. Culture:
Culture on non nutrient agar enriched with [Link]

4. Corneal biopsy: for non-conclusive cases

TREATMENT :

1. Stop using contact lens

2. Topical antiamoebic agents:
○ Diamidines : propamidine isethionate (0.1%) and hexamidine (0.1%)
 ○ Biguanides: polyhexamethylene Biguanide (0.02%)and chlorhexidine (0.02%)
○ Aminoglycosides: neomycin and paromycin
○ Imidazole: clotrimazole and miconazole
Multiple drug therapy :

3-4 months for early epithelial lesions

6-12 months for stromal lesions

Propamidine or hexamidine + PHMB ( drug of choice)

Or

Chlorhexidine + neomycin

Or

Paromycin + clotrimazole or miconazole or itraconazole

3. Oral ketoconazole 200 mg BID or itraconazole 100 mg BD

4. Long term prophylactic therapy with PHMB twice a day for a yr

5. Keratoplasty

PERIPHERAL ULCERATIVE KERATOPATHIES

CHARACTERISTICS :

● Peripheral corneal thinning

● Infiltrate
● Ulceration
Some of the PUK is

● PUK associated with connective tissue disease

● Mooren's ulcer
● Rosacea keratitis
● Marginal keratitis
● Terrien marginal degeneration
● Pellucid marginal degeneration
● Phlyctenular keratitis
● Dellen

PUK associated with connective tissue disease:

Synonym : marginal keratolysis

ETIOLOGY :

.Organ-specific autoimmune PUK (idiopathic).

• GPA (formerly Wegener’s granulomatosis).

• RA.

• SLE.

• Sjogren’s syndrome.

• Relapsing polychondritis.

• Polyarteritis nodosa (PAN).

• Sarcoid.

• Mycobacteria spp..

• Microscopic polyangiitis.

• Churg–Strauss syndrome.

• Type 1 diabetes.

Clinical features:

● Peripheral acute corneal ulceration - one sector ass. With inflammation at limbus in one or both eyes
● Peripheral corneal guttering
● Peripheral corneal melting
● Corneal ulceration
Treatment :

1. Topical medication:
● Antibiotics
● Cycloplegics
● Lubricating drops
● Topical steroids
2. Systemic medication:
● Immunosuppressants (corticosteroids or methotrexate )
● Doxycycline
● Oral vitamin C
3. Surgical measures:
● Excision
● Bandage contact lens or conjunctival flap
● Application of cyanoacrylate tissue adhesive / Peripheral tectonic keratoplasty for active perforation

MOOREN'S ULCER:

Synonym : rodent ulcer or chronic serpiginous ulcer

ETIOLOGY :

Exact etiology not know

Most probable etiology AUTOIMMUNE DISEASE

CLINICAL FEATURES:

Two varieties :
 1. Benign or limited form - unilateral , affects elderly caucasians
2. Virulent type (progressive form) - bilateral , affects young african
SYMPTOMS:

● Severe pain
● Photophobia
● Lacrimation
● Defective vision
SIGNS:

● Superficial ulcer , starts at corneal margin as patches of grey infiltrates

● Peripheral ulcer is associated with undermining of epithelium
● Base of ulcer soon becomes vascularized
● At end stage cornea is thin
Treatment:

● Topical corticosteroids - every 2-3 hrs

● Immunosuppressive therapy with cyclosporin
● Soft contact lens used with some relief in pain
● Lamellar or full thickness corneal grafts
ROSACEA KERATITIS :

Disease of subcutaneous glands of the skin

Clinical features:

● Facial eruptions - butterfly configuration; elderly women

● Ocular lesions include blepharoconjunctivitis and keratitis
● Rosacea keratitis occurs as yellowish white marginal infiltrate
TREATMENT :

1. Local treatment :responds to topical steroids but recurrences are common

2. Systemic treatment : systemic tetracycline (250 mg QID×3wks,TDS×3 wks,BID×3wks and once a day for 3 months
)

NON-ULCERATIVE KERATITIS
 Non-
Ulcerative
keratitis

Superficial Deep (inflammation

(inflammation of stroma +/-
of epithelium) posterior layer)

Diffuse Superfical Non Suppurative

superficial punctate suppurative
deep keratitis
keratitis keratitis deep keratitis

Acute Diffuse Chronic

Diffuse
superficial superficial
keratitis keratitis

1. Non-ulcerative Superficial keratitis

• Diffuse superficial keratitis
✓ Acute diffuse superficial keratitis
- Etiology: Staphylococcal and gonococcal infection
- c/f: faint diffuse epithelial oedema grey
farinaceous appearance interspersed with
clear area
Epithelial
erosion

ulcerative if
keratitis uncontrolled
- Treatment: Tobramycin or gentamycin eye drops (2-4hourly)

✓ Chronic diffuse superficial keratitis

- Seen in rosacea, phlyctenulosis
- Associated with pannus formation

• Superficial punctate keratitis

 Etiology: (mnemonic – VIP DICTATeS)
✓ Viral infection (HSV, HZV, Adenovirus)
✓ Irritative lesions (drugs)
✓ Photo – ophthalmia
✓ Dry eye syndrome (keratoconjunctivitis sicca)
✓ Idiopathic – Thygeson’s superficial punctate keratitis Theodore’s superior limbic
keratoconjuctivitis
✓ Chlamydial infection (Trachoma and inclusion conjunctivitis)
✓ Toxic lesions (Staphylococcal toxin 
blepharoconjunctivitis)
✓ Allergic lesions (vernal keratoconjunctivitis)
✓ Trophic lesions (exposure keratitis, neuroparalytic keratitis)
✓ Skin and mucous membrane disorders (pemphigoid, acne rosacea)

Morphological types
▪ Punctate epithelial erosions (multiple superficial erosions

▪ Punctate epithelial keratitis (fig A,B) – stain: fluorescein, rose

bengal, vital dyes
▪ Punctuate sub epithelial keratitis (fig C,D)
▪ Punctuate combined epithelial and sub epithelial keratitis (fig
E,F)Filamentary keratitis (fig G,H)

Clinical features
- Pain
- Photophobia
- Lacrimation
- Conjunctivitis
Treatment:
- Topical steroids
- Artificial tears
- Specific treatment (antiviral drugs for HSV)
Major causes:

• Photo-ophthalmia
Etiology:
- Bright light exposure (short circuit)
- Naked arc light exposure (welding, cinema operators)
- UV lamp exposure
- Snow blindness ( sun UV ray exposure)

Clinical features
- Burning pain
 - Lacrimation
- Photophobia
- Blepharospasm
- Swelling of palpebral conjunctiva and retrotarsal folds
- H/o exposure to UV rays
- Fluorescein staining multiple spots seen

Prophylaxis:
- Crooker’s glass (for welding worker, cinema operatior)
Treatment:
- Cold compress
- Patching with antibiotic ointment – 24hrs
- Oral analgesics
- Reassurance
- Tranquilizer (1 dose)

• Superior limbic keratitis of Theodore

Etiology: Higher incidence in

- Females
- Hyperthyroidism patients

Clinical features
- Chronic
Symptoms
- Mild photophobia
- Redness in superior bulbar conjunctiva
 - Bilateral ocular irritation
Signs

- Congestion of superior limbic, bulbar, tarsal conjunctiva

- Punctate keratitis – superior cornea
- Corneal filaments
Treatment:
- Artificial tears
- Topical steroids
- Faint diathermy of superior bulbar conjunctiva
- Recession / resection of 3-4 mm wide perilimbal strip of conjunctiva
from superior limbus
- Soft contact lens
- Temporal punctal occlusion with collagen punctal plugs (if required)
- Acetyl cysteine 10% drops (for excessive corneal filaments and mucus
strands)

• Thygeson’s superficial punctate keratitis

Etiology:
- Viral origin
- Allergic or dyskeratotic nature
Clinical features
- Bilateral, chronic
- All ages
- No sex predilection
Symptoms
- Photophobia
- Lacrimation
- Foreign body sensation
Signs
- Conjunctiva – not involved
- Corneal lesion- coarse punctate epithelial lesions
- shape: circular, oval, stellate slightly elevated
- area: @ centre
Treatment:
- Self limiting (5-6 yrs)
- Topical steroids
- Soft contact lens
• Filamentary keratitis
 Corneal
Aberrant filaments
(longs tag of
epithelial elongated
Focal healing epithelium)
epithelial
Pathogenesis:
Etiology: erosions
- Superior limbic keratoconjunctivitis
- Following epithelial erosions in Herpes simplex keratitis, Thygeson’s
superficial punctate keratitis, trachoma
- Keratoconjunctivitis sicca
- Radiation keratitis
- Prolonged patching of eye
- Diabetes, psoriasis
- Idiopathic

Clinical features
Symptoms
- Mild pain and irritation
- Lacrimation
- Foreign body sensation
Signs
- Cornea: filaments , superficial punctate keratitis
Treatment:
- Mechanical debridement & patching (24 hrs) followed by
lubricating drops (for filaments)
- Soft contact lens
- Treat underlying cause
2. Non-ulcerative Deep keratitis

Non suppurative Suppurative

deep keratitis deep keratitis

Interstitial Central
corneal
keratitis
abscess

Disciform Posterior
corneal
keratitis abscess

Keratitis
profunda

Sclerosing
keratitis

• Interstitial keratitis

Pathogenesis:

inflammation

immunologic
infection
reaction

Ag-Ab complex complement type IV

viral bacterial
deposition mediated hypersensitivity
Etiology :
- Viral: HSV, HZV, EBV, mumps, measles,
- Bacterial: TB, Syphilis, LGV, Leprosy
- Others: Cogan’s syndrome, Sarcoidosis, onchocerciasis,
Rheumatoid arthritis

➢ Syphilitic(luetic) interstitial keratitis

Congenital (bilateral,5-15yrs) > Acquired (unilateral, 30yrs)

small scale fresh

invasion or toxins
excite the
cornea is
inflammation
sensitised
treponema
pallidum ivades
Pathogenesis: cornea (fetal
stage)

(Trigger: surgery or injury to eye)

Clinical features
- Late manifestation of congenital syphilis
- A part of Hutchinson’s triad
o Interstitial keratitis
o Hutchinson’s teeth
o Vestibular deafness
o
Salmon patch appearance Ground glass appearance

initial progressive florid stage stage of regression

stage (2w) (2m) (1-2 yrs)
• oedema of • deep • clearing of
endothelium, vascularisation cornea from
deeper stroma covered by hazy periphery to
• keratitic cornea - dull centre
precipitates reddish pink - • vessels -
(evidence of Salmon patch obliterated -
anterior uveitis) appearance ghost vessels
• diffuse corneal • superficial • some opacity
haze - ground vascularisation seen
glass appearance and conjunctiva
• pain heap at limbus-
epulit
• lacrimation
• photophobia
• blepharospasm
Diagnosis:
- clinical profile
- VDRL
- Treponema pallidum immobilization test
Treatment:
Local treatment
- Topical corticosteroid drops (dexamethasone)
- Atropine eye ointment
- Dark goggles
- Keratoplasty (for dense corneal opacities) Systemic treatment
(antisyphiliticremedies less effectiveas cornea is avascular and the reaction is
allergic)
- Penicillin (high dose)
- Systemic steroids

Tuberculous interstitial keratitis

Unilateral and involve lower sector of cornea
(other features: Similar to syphilitic interstitial keratitis)

➢ Cogan’s syndrome (Bilateral)

Comprises of:
Interstitial keratitis of unknown etiology Acute tinnitus
Vertigo Deafness

Treatment:
- Topical and systemic corticosteroids
• Disciform keratitis (unilateral) Etiology: Viral infection
(vaccinia, Herpes) Pathogenesis:

Tissue response
Direct infection
(also necrosis)
• virus from • reaction between
epithelium Ag(virus) and
infects corneal Ab(from stroma
stroma or blood stream)

Clinical features
- Central grey disc @middle layers of stroma
impaired vision
- Slit lamp – thick cornea, folds of descemet’s membrane,
immune ring of the Wessely type
- Cornea- anaesthetic
- Moderate irritation
- Permanent opacity

Treatment:
- Topical and systemic antiviral drugs (acyclovir)
- Corticosteroid
Corneal degenerations

• Corneal degenerations refers to the condition in which the normal cells undergo some
degenerative changes under the influence of age or some pathological condition.
•The differs from dystrophies as being non-hereditary and usually unilateral.

Classification

[Link] upon location:

[Link] corneal degenerations
• Fatty degeneration
• Hyaline degeneration
• Amyloidosis
• Calcific degeneration (Band keratopathy)
• Salzmann’s modular degeneration
[Link] degenerations
• Arcus senilis
• Vogt’s white limbal girdle
• Hassall-Henle bodies
• Terrien’s marginal degeneration
• Mooren’s ulcer
• Pellucid marginal degeneration
• Furrow degeneration (senile marginal degeneration)
[Link] upon etiology:
[Link] related degenerations:
• Arcus senilis ,Vogt’s white limbal girdle,Hassall-Henle bodies,Moasaic degenerations
[Link] degenerations:
• Fatty degeneration
• Amyloidosis
• Calcific degeneration
• Salzmann’s modular degeneration
• Furrow degeneration
• Pellucid marginal degeneration
• Terrien’s marginal degeneration
• Mooren’s ulcer
• Spheroidal degeneration
AGE RELATED CORNEAL DEGENERATIONS

Arcus senilis:

• It refers to an annular lipid infiltration of corneal periphery

• Age:Bilaterally in 60% of person between 40 and 60 years and all individuals over the age of
80.
Clinical features:

• It starts in the superior and inferior quadrants and progress to form a ring which is about
1mm wide
• Peripheral border of this ring opacity is sharp while central is diffuse
• This ring sometimes separated from limbus by a clear zone (the lucid interval of vogt).
• Sometimes there may be double ring of arcus
Vogt’s White Limbal Girdle:

• It is seen in elderly people

• It appears as bilateral chalky white opacities in the Inter palpebral area both nasal and
temporally
• There may or may not be a clear area
• The opacity is at the level of Bowman’s membrane
Hassall-Henle Bodies:

• They are drop like excrescences of hyaline material projecting into anterior chamber around
corneal periphery
• It arises from Descemet’s membrane
• They form the commonest senile change seen in cornea
• In pathological conditions, they become larger and invade the central area and this is called
Cornea guttata

PATHOLOGICAL CORNEAL DEGENERATIONS

Fatty Degeneration (Lipoid Keratopathy)

• It is characterised by whitish or yellowish deposits

• Fat deposit contains cholesterol and fatty acids
• Initially the deposits are intracellular but some become extracellular with necrosis of stromal
cells
• It may be primary and secondary
• Primary:It is a rare condition that occurs in a cornea free of vascularization
Serum lipids levels are normal
• Secondary:It occurs in vascularised cornea secondary to diseases such as corneal infection
,interstitial keratitis, ocular trauma, glaucoma and chronic iridocyclitis
• Treatment: Unsatisfactory
In some cases slow resorption of lipid infiltrate can be induced by Argon laser
photocoagulation of new blood vessels
Hyaline Degeneration

• Deposition of hyaline spherules in the superficial stroma and it can be primary and
secondary
• Primary:It is bilateral and associated with granular dystrophy
• Secondary:It is unilateral and associated with old keratitis, long standing glaucoma and
trachomatous pannus
• Treatment:Keratoplasty
Amyloid Degeneration

• It is characterised by deposition of amyloid material underneath it’s epithelium

• It is rare and it may be primary and secondary
• Primary is seen in a healthy cornea and secondary in a diseased cornea
Calcific Degeneration (Band shape Keratopathy)

• Band shape Keratopathy (BSK) is a degenerative change associated with deposition of

calcium salts in Bowman’s membrane and most superficial part of stroma and deeper layers
of epithelium
Etiology:

• Age related BSK is common and affects otherwise healthy cornea

• Primary BSK is familial
• Ocular diseases complicated by BSK includes chronic uveitis in children ,children with Still’s
disease, phthisis bulbi ,chronic glaucoma, chronic keratitis ,and ocular trauma
• Metabolic conditions rarely associated with BSK include hypercalcaemia,
hyperphosphatemia ,hyperuricaemia and chronic renal failure
Clinical features:

• . It typically presents as a band- shaped opacity in the interpalpebral zone with a clear
interval between the ends of the band and the limbus
• The condition begins at the periphery and gradually progresses towards the centre.
• The opacity is beneath the epithelium which usually remains intact.
• Surface of this opaque band is stippled due to holes in the calcium plaques in the area of
nerve canals of Bowman's membrane.
• In later stages, transparent clefts due to cracks or tears in the calcium plaques may also be
seen.
Treatment:

• Chelation, i.e., chemical removal of deposited calcium salts is an effective treatment.

First of all corneal epithelium is scraped under local anaesthesia. Then 0.01 molar
solution of EDTA (chelating agent) is applied to the denuded cornea with the help of
a cotton swab for about 10 minutes. This removes most of the deposited calcium.
Pad and bandage is then applied for 2- 3 days to allow the epithelium to regenerate.
• Phototherapeutic keratectomy (PTK) with excimer laser is effective in clearing the
cornea
• Keratoplasty
• Treatment of underlying causative disease
Salzmann’s Nodular Degeneration

Etiology

• This condition occurs in eyes with recurrent attacks of phlyctenular keratitis, rosacea
keratitis and trachoma.
• The condition occurs more commonly in [Link] is unilateral.
Pathogenesis

• In Salzmann's nodular degeneration, raised hyaline plaques are deposited between

epithelium and Bowman's membrane.
• There is associated destruction of Bowman's membrane and the adjacent stroma.
Clinical features

• One to ten bluish white nodules ,arranged in circular fashion within the cornea
• Patient experience discomfort due to loss of epithelium from from the surface of nodules
• Visual loss occurs when nodules impinge on central zone
Treatment:Keratoplasty

Furrow Degeneration (Senile Marginal Degeneration)

• Thinning occurs at the periphery of cornea leading to formation of a furrow.

• Thinning occurs due to fibrillar degeneration of the stroma
Treatment:Not necessary

Spheroid Degeneration

• It is also known as Climatic droplet keratopathy/Labrador keratopathy/Bietti’s

dystrophy/Corneal elastosis
Etiology

• Occurs in men who work in outdoors especially in hostile climates

• Its occurrence has been due to exposure to UV Rays and ageing and corneal disease
Clinical features

• Amber coloured spheroidal granules accumulate at the level of Bowman’s membrane

and anterior stroma in the interpalpebral zone
• In marked degeneration vision is affected
Treatment : In advanced cases is by corneal transplantation

Pellucid Marginal Degeneration

• Corneal thinning involving the periphery of lower cornea

• It induces marked astigmatism which is corrected by sclera type contact lenses
Terrien’s Marginal Degeneration

• It is non-ulcerative thinning of the marginal cornea.

Clinical features

• Males are affected usually after 40 years of age

 • Superior palpebral cornea is involved
• Initial lesion is asymptomatic corneal opacification separates from limbus by a clear zone
• The lesion progresses very slowly over many years with thinning and superficial
vascularization. Dense yellowish white deposits may be seen at the sharp leading edge.
Patient experiences irritation and defective vision (due to astigmatism).

Terrien’s Marginal Degeneration L

Complications: Perforation and pesudopterygia May develop

Treatment :

• It is non specific
• In severe thinning , a patch of corneal graft may be required

Corneal dystrophies
• They are inherited disorders
• In this the cells haven’t some inborn defects due to which the pathological changes may
occur with the passage of time leading to development of corneal haze
• They are non inflammatory characterised by bilateral and non vascularized corneal opacities

Classification
• The International Committee for Classification of Corneal Dystrophies has devised a
current and accurate nomenclature supplementing the anatomic classification with clinical,
pathologic and genetic informations.
Epithelial and Subepithelial dystrophies

• Epithelial basement membrane dystrophy (EBMD)

• Epithelial recurrent erosion dystrophy (ERED)
• Subepithelial mucinous corneal dystrophy (SMCD)
• Mutation in keratin genes: Meesmann corneal dystrophy(MECD)
• Lisch epithelial corneal dystrophy (LECD)
• Gelatinous drop like corneal dystrophy (GDLD)
EPITHELIAL AND SUBEPITHELIAL DYSTROPHIES
• Epithelial Basement Membrane Dystrophy
• It is also known as map- dot- fingerprint dystrophy or Cogan microcystic epithelial
dystrophy or Anterior basement membrane dystrophy.
• Inheritance : No inheritance documented
• Genetic locus and gene : 5q31 and TGF beta 1
• Onset, Course and Symptoms
Present in adult life
Asymptomatic or recurrent erosions with pain ,lacrimation and blurred vision
are observed
Location and degree of pathology can fluctuate with time
• Sign : They include
• MAPS. Irregular islands of thickened, gray, hazy epithelium with scalloped,
circumscribed borders, particularly affecting the central or paracentral
cornea. Isolated or combined with other signs.
• Dots (Cogan). Irregular round, oval or comma- shaped, non-staining, putty-gray
opacities. Clustered like an archipelago in the central cornea. Typically combined
with other signs, especially with maps.

• Fingerprint lines. Parallel, curvilinear lines, usually

paracentral, best seen in retroillumination. They may be isolated or combined with
other signs, especially maps.
• Bleb pattern (Bron). A subepithelial pattern like pebbled glass, best seen by
retroillumination. Isolated or combined with other signs.
2. EPITHELIAL RECURRENT EROSION DYSTROPHY
• Onset and course : It is also known as Corneal erosions or Recurring hereditary
dystrophy ,usually occurs in first decade of life
• Inheritance : Autosomal dominant
• Genetic locus and gene : Unknown
• Onset and course : Erosions occurs at 4-6 years of age but occasionally as early as 8
months of age
Attacks decline in frequency in intensity and cease by the age of
50 years
• Sign : Corneal erosions are seen
 Erosions occurs at 4-6 years of age but occasionally as early as 8
months of age

Latrice corneal dystrophy

Attacks decline in frequency in intensity and cease by the age of 50 years
Subepithelial haze or blebs may be seen between the attacks
Central Subepithelial Corneal opacities , appear early as 7 years of age .
They vary from sub epithelial fibrosis to protruding keloids like nodules
• Symptoms : Minimal trauma or spontaneous in occurrence
Redness ,photophobia, epiphora and ocular pain
• Treatment : 25% of patients need corneal grafts at age of 45
3. SUBEPITHELIAL MUCINOUS CORNEAL DYSTROPHY
• Inheritance : Autosomal dominant
• Gene locus and gene : Unknown
• Onset and course : First decade of life and progressive loss of vision in adolescence
• Signs : Bilateral Subepithelial opacities and haze
Most dense centrally and involve entire cornea
• Symptoms : Painful episodes of recurrent Corneal erosions which decrease during
adolescence
4. MUTATION IN KERATIN GENES :MEESMANN CORNEAL DYSTROPHY
• Onset and course : It is also known as Juvenile hereditary epithelial dystrophy
Occurs in early childhood and slowly progressive
Variant : Stocker Holt dystrophy

Inheritance: autosomal dominant.

• Genetic loci are 12q13 (KRT3) and 17q12 (KRT 12) for Stocker-Holt variant .
• Genes : KRT3 and KRT12 for Stocker – Holt variant
• Signs : Multiple, tiny epithelial vesicles which extend to the
limbus and are most numerous in the interpalpebral
area with clear surrounding epithelium.
Whorled and wedge-shaped epithelial patterns have also been reported.
Corneal thinning and reduction in corneal sensation may be noted.
In Stocker-Holt variant, the entire cornea demonstrates fine, grayish
punctate epithelial opacities that stain with fluorescein and fine linear opacities that
may appear in a whorl pattern.
• Symptoms : Patient are asymptomatic or some have mild visual retardation
Some complain of glare and light sensitivity.
 Recurrent painful punctiform epithelial erosion may occur

5. LISCH EPITHELIAL CORNEAL DYSTROPHY :

• Onset and course:It is also known as band-shaped and whorled microcystic
dystrophy of the corneal epithelium.
• It occurs in childhood
• There occurs slow progression of opacities with possible deterioration in vision.
• Inheritance : X-chromosomal dominant.
• Signs : .
Direct illumination shows localized gray
opacities in different patterns: whorl-like, radial, band-shaped, flame/feathery
shaped, and club shaped.
Indirect illumination demonstrates multiple, densely crowded clear cysts with clear
surrounding epithelium.
• Symptoms:. Asymptomatic
Blurring of vision occurs if the pupillary zone is involved.
6. Gelatinous Drop-Like Corneal Dystrophy (GDLD)
• Onset and course: It is also known as subepithelial amyloidosis or primary familial
amyloidosis (Grayson)
It occurs in the first decade of life
The condition is progressive.
• Genetic locus is 1p32 and gene involved is
• Inheritance is autosomal recessive.
• Signs:
Subepithelial lesions which appear initially may be similar to band-shaped
keratopathy or there may be groups of small multiple nodules, that is, mulberry
configuration.
Superficial vascularization is frequently seen.
Stromal opacification or larger nodular lesions that is, kumquat-like lesions
may appear in later life.
• Symptoms: significant decrease in vision,
photophobia,
irritation
redness
tearing.

CORNEAL DYSTROPHIES
DEFINITION:
• Corneal dystrophies are non-inflammatory, hereditary corneal disorders
which are characterized by bilateral, nonvascularized corneal opacities.
✓ They mainly affect a particular layer of the cornea.
✓ There is no associated systemic disease.
✓ Dystrophies occur bilaterally, manifesting
occasionally at birth, but more usually during first
or second decade and sometimes even later in life

CLASSIFICATION:

1]Epithelial and Subepithelial Dystrophies- a]Cogan epithelial basement membrane

dystrophy, b]MEESMANN EPITHELIAL DYSTROPHY, LISCH c]EPITHELIAL DYSTROPHY,
d] gelatinous drop like dystrophy
2]Bowman Layer Dystrophies-
THIEL BEHNK DYSTROPHY
Reis bucker corneal dystrophy

3]Stromal Corneal Dystrophies-lattice corneal dystrophies,granular corneal dystrophies,schnyder

corneal dystrophy,congenital stromal dystrophy etc

4]Endothelial Corneal Dystrophies- POSTERIOR POLYMORPHOUS DYSTROPHY,

CONGENETAL HEREDITARY ENDOTHELIAL DYSTROPHY

CORNEAL DYSTROPHIES VS DEGENERATIONS

1. Corneal dystrophies are usually inherited

2. They affect right and left eyes equally
3. Most progress gradually
4. Usually begin in one of the corneal layers then spread to all nearby layers
5. Most can occur in a healthy individual
6. Most donot affect other parts of the body nor they are related with the disease affecting
other parts of the body or eye

EPITHELIAL DYSTROPHIES

Cogan epithelial basement membrane dystrophy

• Inheritance- sporadic & rarely AD with incomplete Penetrance

• Histology-
• + thickening of basement membrane with
deposition of fibrillary protein b/w basement
membrane & bowman’s layer.
• +Absence of hemidesmosomes of basal epithelial cells which is responsible
for recurrent corneal erosions.
• THERE IS DEPOSITION OF FIBILARY MATERIAL BETWEEN THE BASEMENT MEMBRANE&
BOWMANS LAYER
 • Onset 2nd decade. 10% of pts develop recurrent corneal erosions in 3rd
decade & others remain asymptomatic throughout life.

• Signs-
• 1]Dot like opacities
• 2]Epithelial microcysts
• 3]Subepithelial map-like patterns surrounded by a faint haze
• Whorled fingerprint - like lines

MEESMANN EPITHELIAL DYSTROPHY

• Very rare, non-progressive abnormality of corneal epithelial metabolism,

underlying which mutations in the gene encoding corneal epithelial keratins
have been SEEN.

• Inheritance is AD
• Histology- irregular thickening of the epithelial basement membrane &
intraepithelial cysts

Symptoms are variable. Pts may be

asymptomatic or ocular irritation may begin
in the first few mnths of life.
Signs
Myraid tiny intraepithelial cysts of uniform size but variable density are maximal
centrally & extend towards but do not reach
the limbus
Cornea may be slightly thinned & sensation reduced.
• Treatment- lubricants
LISCH EPITHELIAL DYSTROPHY

• Previously thought to be a variant of meesmann, now believed to be

genetically distinct.

• Inheritance is AD or X- linked dominant

SIGNS:
Grey bands with a whorled configuration
Retroillumination shows Densely packed Microcysts
GELATINOUS DROP LIKE DYSTROPHY-EPITHELIAL&SUBEPITHELIAL DYSTROPHY
Rare disorder Inheritance is AR Histology shows subepithelial & anterior stromal
accumulation of amyloid
Onset is within 1st & 2nd decades with severe photophobia, watering & visual
impairement
Signs
Grey subepithelial nodules
Gradual confluence, stromal involvement &
increase in size giving rise to a mulberry like appearance

BOWMAN LAYER/ANTERIOR STROMAL DYSTROPHIES

1. Reis- Bucklers dystrophy categorized as form of granular stromal dystrophy

2. Inheritance is AD with (gene TGFB1)

3. Histology shows replacement of Bowman layer & epithelial basement

membrane with fibrous Tissue

4. Onset is in 1st or 2nd decade with severe recurrent corneal erosions.

Signs
5. Grey-white, fine, round & polygonal subepithelial opacities similar to
those of
granular dystrophy type 1, most dense centrally.

6. Changes increase in density with age

resulting in a reticular pattern due to the
laying down of irregular bands of collagen replacing Bowman layer.

7. Onset is in 1st or 2nd decade with severe recurrent corneal erosions.

8. Corneal sensation is reduced & visual impairment may occur due to

scarring at level
of Bowman layer.
9. Treatment is directed at recurrent erosion

THIEL BEHNK DYSTROPHY

Inheritance is AD

Histology shows curly fibres in Bowman layer

on electron microscopy
Onset is at end of 1st decade with recurrent
erosions
Signs
1]subepithelial opacities in a honeycomb morphology involving central
cornea
Treatment
1]not required as visual impairment is
less than Reiss- Bucklers dystrophy

SCHNDYER CENTRAL CRYSTALLINE DYSTROPHY

1] Disorder of corneal lipid metabolism
2]Central, oval, subepithelial crystalline opacity is seen

STROMAL DYSTROPHIES

Lattice corneal dystrophy

Inheritance is AD
Histology shows amyloid, staining with congo
red & exhibiting characteristic green
birefringence when viewed with a polarizing
filter
Signs
Anterior stromal, glassy, refractile dots
Coalescence into fine lattice lines, best seen
on retroillumination
Deep & outward spread sparing the periphery
Generalized stromal haze that progressively
impairs vision & may obscure some of the
lattice lines
Corneal sensation is reduced
Treatment by penetrating or deep lamellar
keratoplasty is frequently required.
Recurrence in graft may occur.

LATTICE CORNEAL DYSTROPHY 2

Inheritance is AD

Histology shows amyloid deposits in corneal stroma & other involved sites
Signs
Randomly scattered, short, fine lattice lines
which are sparse, more delicate, more rapidly
oriented & more peripherally located than in
LCD1
Corneal sensation is impaired
Systemic features
Progressive bilateral cranial & peripheral
neuropathy
Dysarthria
Mask like facial expression due to bilateral
facial palsy
Protruding lips & pendulous ears
Dry & extremely lax itchy skin

LATTICE CORNEAL DYSTROPHY TYPE3

Thick rope like bands of deposited amyloid
Inheritance autosomal dominant[tgfr gene]
GRANULAR CORNEAL DYSTROPHY TYPE1
• Inheritance is AD
• Histology shows amorphous hyaline deposits
which stain bright red with masson trichrome
• Onset is in 1st decade but vision is usually not
affected in early stage of disease

Signs
• Small, white, sharply demarcated deposits
resembling crumbs, sugar granules, rings or
snowflakes in central anterior stroma
• Overall pattern of deposition is radial or disc
shaped or may be in the form of a christmas
tree
• Gradual increase in number & size of deposits
with deeper & outward spread but not
reaching the limbus
• Gradual confluence & diffuse haze of
intervening stroma causes visual impairement
• Corneal sensation is impaired
GRANULAR CORNEAL DYSTROPHY
Inheritance is AD

Specular reflection shows tiny dark spots caused by disruption of regular

endothelial mosaic
Progression occurs to a beaten metal appearance which may be associated with
melanin deposition
Endothelial decompensation gradually leads to central stromal oedema & blurred
vision, worse
in the morning & clearing later in the day.
Epithelial oedema develops when stromal
thickening has increased by about 30%
Persistent epithelial oedema results in the
formation of microcysts & bullae (bullous
keratopathy) which causes pain & discomfort
on rupture, thought to be due to exposure of
naked nerve endings
Treatment
Topical sodium chloride 5% drops or
ointment, reduction in IOP
Bandage contact lens
Penetrating or deep lamellar keratoplasty
Other options- conjunctival flaps & amniotic
membrane transplants
Cataract surgery may accelerate endothelial
cell loss, a triple procedure (cataract surgery,
lens implantation & keratoplasty) may be
considered in eyes with corneal epithelial
oedema .

ENDOTHELIAL DYSTROPHIES
POSTERIOR POLYMORPHOUS DYSTROPHY
Rare, innocuous & asymptomatic condition in
which corneal endothelial cells display
characteristics similar to epithelium.

Inheritance AD

Onset is at birth or soon thereafter, although it

is most frequently identified by chance in
later life
Signs
Subtle vesicular endothelial lesions that may
become confluent band-like lesions or diffuse opacities which may be asymmetrical
Ocular associations
Iris abnormalities
Glaucoma
Alport syndrome
Treatment not required

CONGENETAL HEREDITARY ENDOTHELIAL DYSTROPHY

Rare dystrophy in which there is focal or
generalized absence of corneal endothelium
2 main forms CHED1 & CHED2, later being
more severe
Onset is perinatal
Signs
Bilateral, symmetrical, diffuse corneal
oedema resulting in a blue-grey, groundglass
appearance to total opacification
Visual impairment is variable & visual acuity
may surpass than expected from corneal
appearance
Treatment
by penetrating keratoplasty has a
reasonable chance of success when
performed early but is risky & more difficult
than in adults. Undue delay carries risk of
dense amblyopia
D/D
Congenital glaucoma
Birth trauma
Rubella keratitis
Sclerocornea
mucopolysaccharidoses

ECTATIC CONDITIONS OF CORNEA: Ectasia- dilation.

KERATOCONUS:
• Keratoconus is a non-inflammatory bilateral ectatic condition of cornea in its axial part.
• It usually starts at puberty and progresses slowly.

Etiopathogenesis:
• Unclear
 • Frequently due to a congenital weakness of the cornea
• Secondarily following trauma in which case it is unilateral.
• Patients with vernal keratoconjunctivitis or Down syndrome due to repeated rubbing of the
eye.

Clinical features:
Symptoms:

Patient presents with a defective vision due to progressive myopia and irregular astigmatism,
which does not improve fully despite full correction with glasses.

Signs:

➢ Munson’s sign- conical distortion of lower lid on downward gaze

➢ Slit lamp examination-
o thinning and ectasia of central cornea, opacity at the apex
o Fleischer’s ring- Iron deposits at the base of the cone(cone shaped cornea)
o Vogt lines- corneal stromal stretch lines – possibly due to thinning of corneal
stroma.
➢ Retinoscopy-
o Scissor reflex (yawning reflex) – 2 bands are seen which move towards and away
like a scissor on moving the light source, due to irregularity in the curvature of
cornea.
o high oblique or irregular astigmatism is obtained.
➢ Placido disk examination- shows irregular circles instead of uniform concentric circles which
are seen normally.
➢ Distant direct ophthalmoscopy- Oil droplet reflex (Charleaux sign)-On retro illumination of
the cornea with pupillary dilatation, the centre and peripheries appear bright while there is a
circular ring like shadow between the centre and the periphery of the cornea.
➢ Keratometry- values are increased.
o Normal- 45D
o Mild Keratoconus- 45-48D
o Moderate Keratoconus- 48-54D
o Severe Keratoconus- >54D
➢ Window reflex is distorted; Window reflex- ask the patient to look at a window with railings.
If they fall on the cornea in a straight arrangement, it indicates a smooth cornea. The lines
are distorted in an irregular cornea.
➢ Corneal topography – demonstrates cone and typical astigmatic pattern.

Morphological classification:
• Nipple cone- small size (<5 mm) and steep curvature.
• Oval cone- larger (5–6 mm) and ellipsoid in shape.
• Globus cone- very large (>6 mm) and globe like.

Complication:
Descemet’s membrane may rupture, where stroma becomes suddenly oedomatous giving
rise to Acute hydrops.

Treatment:
℞ Corneal collagen cross-linking- Riboflavin (0.1%) eye drops-> 3 mW/cm2 of UVA radiation ->
insertion of a bandage soft contact lens to permit the epithelium to heal
 ℞ Corneal transplantation(Keratoplasty) in progressive cases- penetrating keratoplasty or
lamellar keratoplasty.
℞ Intra corneal ring segments ( INTACS) are useful in selective cases.
℞ Spectacles can be used but effective only in early cases.
℞ Hydrops (if complication develops)- topical steroids, lubrication, and cycloplegia

KERATOGLOBUS:
o Familial and hereditary bilateral congenital disorder characterised by thinning and
hemispherical protrusion of the entire cornea.
o Nonprogressive and inherited as an autosomal recessive trait
o No raise in intraocular pressure (D/D: Buphthalmos- raised intraocular pressure, angle
anomaly and/or cupping of optic disc.)
o Types-
✓ Acquired- end stage keratoconus
✓ Congenital- associatd with Ehlers Danlos type VI and brittle cornea syndrome.

KERATOCONUS POSTERIOR:
• rare non-progressive congenital abnormality of the cornea in which there is abnormal
steepening of the posterior cornea in the presence of normal anterior corneal surface
• usually an isolated unilateral finding but may be associated with ocular (e.g. anterior
lenticonus, anterior polar cataract) or systemic abnormalities.
• Treatment usually not necessary but requires Penetrating keratoplasty if there’s significant
loss in visual acuity.

PELLUCID MARGINAL DEGENERATION:

▪ painless bilateral corneal thinning affecting the inferior cornea sually from 4 to 8 o’clock.
▪ epithelium is intact and there is no anterior chamber reaction.
▪ Cornea becomes ectatic with myopic ‘against the rule’ astigmatism.

ABNORMALITIES OF CORNEAL TRANSPARANCIES

CORNEAL OEDEMA:
• Corneal oedema occurs when there is an imbalance between factors that maintain the
normal water content(78%) of the cornea.
• Factors which draw water in the cornea - intraocular pressure and swelling pressure of the
stromal matrix = 60 mm of Hg
• Factors which draw water out of cornea - the active pumping action of corneal endothelium
and the mechanical barrier action of epithelium and endothelium.

Causes:
1. Raised intraocular pressure
2. Endothelial damage
• Injuries- birth trauma (forceps delivery), surgical trauma during intraocular operation,
contusion injuries and penetrating injuries.
 • corneal dystrophies- Fuchs dystrophy, congenital hereditary endothelial dystrophy and
posterior polymorphous dystrophy.
• Inflammatory conditions such as uveitis, endophthalmitis and corneal graft infection.
3. Epithelial damage- • mechanical injuries • chemical burns • radiational injuries • thermal
injuries • inflammation and infections.

Clinical features:
➢ stromal haze with reduced vision.
➢ In long-standing cases with chronic endothelial failure (Fuch’s dystrophy) there occurs
permanent oedema with epithelial vesicles and bullae formation (bullous keratopathy). This
is associated with marked loss of vision, pain, discomfort and photophobia, due to periodic
rupture of bullae.

Treatment:
➢ Treat the cause e.g., raised IOP and ocular inflammations.
➢ Dehydration of cornea may be tried by use of:
o Hypertonic agents- 5% sodium chloride or anhydrous glycerine may provide
sufficient dehydrating effect.
o Hot forced air from hair dryer may be useful.
o Soft contact lenses used to get relief from discomfort of bullous keratopathy.
➢ Penetrating keratoplasty for longstanding cases of corneal oedema, non-responsive to
conservative therapy.

CORNEAL OPACITY:
▪ Loss of normal transparency of cornea due to scarring.

Causes:
1. Congenital opacities- developmental anomalies or following birth trauma.
2. Healed corneal wounds.
3. Healed corneal ulcers.

Clinical features:
Corneal opacity may produce loss of vision (when dense opacity covers the pupillary area) or
blurred vision (due to astigmatic effect).

Types of corneal opacity:

▪ Nebula
o superficial scars involving Bowman’s layer and superficial stroma.
o more discomfort to patient due to blurred image owing to irregular astigmatism
o details of the iris can be seen through the opacity.
▪ Macula
o semi-dense opacity - scarring involves about half the corneal stroma
o details of the iris cannot be seen but the iris and pupillary margins are visible.
▪ Leucoma
o dense white opacity - scarring of more than half of the stroma
o totally obscures the view of the iris and pupil.
▪ Adherent leucoma
o healing occurs after perforation of cornea with incarceration of iris
▪ Corneal facet
 o the corneal surface is depressed at the site of healing (due to less fibrous tissue)
such a scar is called facet.
▪ Kerectasia
o In this condition, corneal curvature is increased at the site of opacity (bulge due to
weak scar).
▪ Anterior staphyloma
o 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

Secondary changes in corneal opacity:

Long-standing cases: hyaline degeneration, calcareous degeneration, pigmentation and
atheromatous ulceration.

Treatment:
℞ Optical iridectomy with pupillary dilalation
℞ Phototherapeutic keratectomy (PTK) performed with excimer laser- useful in superficial
(nebular) corneal opacities.
℞ Keratoplasty
℞ Cosmetic coloured contact lens- where vision cannot be recovered
℞ Tattooing of scar

VASCULARISATION OF CORNEA:
Normally cornea is avascular.

In pathological states, it can be invaded by vessels as a defence mechanism against the

disease or injury. However, vascularization interferes with corneal transparency and occasionally
may be a source of irritation.

Pathogenesis:
normally prevented by the compactness of corneal tissue. during pathological states, mechanaical
and chemical factors give rise to vascularisation of cornea.

Types:
• Superficial corneal vascularization.
• Deep vascularization

Superficial corneal vascularization.

o vessels are arranged usually in an arborising pattern.
o below the epithelial layer
o Their continuity can be traced with the conjunctival vessels
o Common causes- trachoma, phlyctenular keratoconjunctivitis, superficial corneal ulcers and
rosacea keratitis.
o Pannus- When extensive superficial vascularization is associated with white cuff of cellular
infiltration, it is termed as pannus. In progressive pannus, corneal infiltration is ahead of
vessels while in regressive pannus it lags behind.
Deep vascularization:
o Vessels are generally derived from anterior ciliary arteries lie in the corneal stroma.
o These vessels are usually straight, not anastomosing
o Their continuity cannot be traced beyond the limbus.
o Deep vessels may be arranged as terminal loops, brush, parasol, umbel, network or
interstitial arcade
o Common causes- interstitial keratitis, disciform keratitis, deep corneal ulcer, chemical
burns, sclerosing keratitis and corneal grafts

Treatment:
Vascularization may be prevented by timely and adequate treatment of the causative
conditions.
℞ Corticosteroids may have vasoconstrictive and suppressive effect on permeability of capillaries.
℞ Application of irradiation is more useful in superficial than the deep vascularization.
℞ Surgical treatment in the form of peritomy may be employed for superficial vascularization.

KERATOPLASTY
KERATOPLASTY OR CORNEAL GRAFTING IS COMMONLY CALLED AS
CORNEAL TRANSPLANTATION.
• IT IS AN OPERATION IN WHICH THE PATIENT’S DISEASED CORNEA IS
REPLACED BY THE HEALTHY CLEAR CORNEA.
• TYPES OF CORNEAL GRAFTING/ KERATOPLASTY :
ALLOGRAFTS -
1. FULL THICKNESS / PENETRATING KERATOPLASTY- FULL THICKNESS
GRAFTING.
2. PARTIAL THICKNESS / LAMELLAR KERATOPLASTY - PARTIAL
THICKNESS GRAFTING. IT MAYBE OF THESE TWO TYPE:
• ALK (ANTERIOR LAMELLAR KERATOPLASTY )
It is performed when descemet’s membrane and endothelium are NORMAL.
DEPENDING UPON THE DEPTH OF DISSECTION ALK CAN BE
1. SUPERFICIAL ALK
2. DEEP ALK
• PLK (POSTERIOR LAMELLAR KERATOPLASTY)
It is performed when endothelium is defective.
It includes deep lamellar keratoplasty,
Endothelial keratoplasty,
Descement's stripping endothelial keratoplasty(mannual)
Descement's striping automated endothelial keratoplasty
Descement's membrane endothelial keratoplasty
Pre-descements' stripping automated endothelial keratoplasty
• SMALL PATCH GRAFT – FOR SMALL DEFECTS.
WHICH MAYBE FULL THICKNESS OR PARTIAL THICKNESS.
AUTOGRAFTS -
1. ROTATIONAL KERATOPLASTYPATIENT'S OWN CORNEA IS TREPHINED AND ROTATED TO TRANSFER
THE PUPILLARY AREA HAVING SMALL CORNEAL OPACITY TO THE PERIPHERY.
2. CONTRALATERAL KERATOPLASTYPATIENT’S CORNEA OF ONE EYE IS OPAQUE AND THE OTHER EYE
IS BLIND WHICH IS DUE TO POSTERIOR SEGMENT DISEASE ( i.e, OPTIC ATROPHY, RETINAL
DETACHMENT etc.)
Indications
1. Optical - to improve vision. Important indications are: corneal opacity, bullous keratopathy,
corneal dystrophies, advanced keratoconus.
2. Therapeutics - to replace inflamed cornea not responding to conventional therapy.
3. Tectonic grqft - to restore integrity of eyeball [Link] corneal perforation and in marked
corneal thinning.
[Link] -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.
Evaluation of donor cornea. Biomicroscopic examination of the whole globe, before
processing the tissue for media storage, is very important.
Methods of corneal preservation

1. Short-term storage (up to 48 hours). The whole globe is preserved at 4° C in a moist

chamber.

2. Intermediate storage (up to 2 weeks) of donor cornea can be done in McCarey-Kaufman

(MK) medium and various chondroitin sulfate enriched media such as optisol medium.

3. Long-term storage up to 35 days is done by organ culture method or by cryopreservation

at –70°C.

Surgical technique of penetrating keratoplasty

1. Excision of donor corneal button. The donor corneal button should be cut 0.25 mm larger

than the recipient, taking care not to damage the endothelium. Donor cornea is placed in a

tephlon block and the button is cut with the help of a trephine from the endothelial side.
2. Excision ofrecipient corneal button. With the help of a corneal trephine (7.5 mm to 8 mm in
size) a partial thickness incision is made in the host cornea. Then , anterior chamber is
entered with the help of a razor blade knife and excision is completed using corneoscleral
scissors.

3. Suturing of corneal graft into the host bed is done with either continuous or interrupted
10–0 nylon sutures.

Complications:

1. Early complications. These include flat anterior chamber, iris prolapse, infection,
secondary glaucoma, epithelial defects and primary graft failure.

2. Late complications. These include graft rejection, recurrence of disease and astigmatism.

Graft rejection

It refers to the immunological response of the host to the donor corneal tissue. It can occur
as early as 2 weeks and upto several years after grafting. Graft rejection is classically
believed to be a delayed type of hypersensitivity response.

Risk factors:

include younger age of recipient, previous graft failure, corneal vascularization, larger graft
size, donor epithelium and massive blood transfusion.

Clinical presentations include:

Epithelial rejection characterized by an elevated epithelial rejection line which stains with
fluorescein. Subepithelialubepithelial infiltrates known as Kayes dots.

Stromalrejectionis characterized by sudden onset of full thickness stromal haze in a

previously clear graft.

Endothelial rejection may present as:

• Khodadaust line demarcating healthy and damaged endothelium.

Diffuse endothelial rejection with lot of Keratic precipitates.

REFRACTIVE CORNEAL SURGERY:

Refractive corneal surgery includes:

• Radial Keratotomy (RK),
• Astigmatic Keratotomy (AK),
• Photorefractive Keratotomy (PRK),
• Laser assisted in situ Keratomileusis (LASIK) and its varieties,
• Thermal Laser Keratoplasty (TLK),
• Conductive Keratoplasty (CK),
• Orthokeratoplasty, and
• Intracorneal Ring (ICR) implants
 PHOTOTHERAPEUTIC KERATECTOMY
Phototherapeutic Keratectomy (PTK) refers to the ablation of superficial corneal lesion with
the help of excimer laser (198 nm).
Indications include:-
• Superficial corneal scars,
• Corneal degenerations, e.g. band-shaped Keratopathy, Salzman nodular
degeneration and oil droplet keratopathy,
• Epithelial dystrophies (e.g. Reis-Buckler dystrophy), and
• Recurrent corneal erosions.
Procedure:
The modern excimer laser machines have two modes for PTK:
• Spot mode, where a small spot (<1 mm) can be ablated, and
• Shapping mode, which allows uniform removal of corneal tissue from a large zone.
Contraindications include:
• Excessive thin corneas,
• Moderate to severe dry eye, and
• Deep corneal lesions.
Complications.
Faint corneal haze is a usual end result of the PTK. Other complications include:
• Secondary infections,
• Induced hypermetropia, and
• Secondary keractesia.
KERATOPROSTHESIS

Keratoprosthesis refers to an artificial corneal device used in patients unsuitable for

keratoplasty.

Types:

Keratoprosthesis basically consists of a central optical cylindrical part made of poly

methylmethaacrylate (PMMA). Based on the surrounding fixation device, the commonly used
keratoprosthesis of various designs are as below:

• Boston keratoprosthesis consists two plates and one cylinder. It is fixed using the
donor cornea.

• Alfa cor keratoprosthesis consists of an outer porous skirt made up of high water
content PHEMA and a transparent central optic made from low water content PHEMA. An
interpenetrating polymer network (IPN), which is a junction zone between the skirt and
central optic and serve as a permanent bond. It has a refractive power close to
that of human cornea.

• Osteo-odonto-keratoprosthesis is fixed with the help of patients own tooth root and
alveolar bone.
• Chondro-keratoprosthesis is fixed with patients own cartilage.
•Onycho-keratoprosthesis is fixed with patient’s nails.
• Stanford keratoprosthesis is a recently introduced device which incorporates the grafting of
bioactive factors with a change in the bulk material design.
•Singh and Worst collar-stud keratoprosthesis is fixed with stainless steel sutures.
Indications. Prerequisites for keratoprosthesis include bilateral blindness due to corneal
diseases (not suitable for keratoplasty) with accurate perception of light, normal
electrophysiological tests and absence of gross posterior segment disorders on
ultrasonography, e.g:
• Stevens-Johnson syndrome,
• Chemical burns,
• Ocular cicatricial pemphigoid,
• Severe trachoma
• Multiple previous failed corneal grafts.
Complications include:
• Extrusion of prosthesis,
• Intractable glaucoma,
• Retroprosthetic membrane formation,
• Uveitis,
• Retinal detachment.
 SCLERA

What we will learn here?

• Anatomy of sclera
• Blue sclera
• Staphyloma
Anterior Staphyloma
Intercallary Staphyloma
Cilliary Staphyloma
Equitorial Staphyloma
Posterior Staphyloma
• Scleritis
Immune mediated
Infectious

ANATOMY
SCLERA:
The sclera is a tough,white,outer layer of the eye ball . That almost covers 80% of the
surface area of the eyeball. Where it extends from the limbus of cornea all way towards the
optic nerve on the posterior side of eyeball. The anterior part of the sclera is only visible to
us.

LAYERS:
The sclera is made upof three layers :
 • Episclera:
This is the outer most layer of Sclera. It covers the sclera proper and contains
fibroblasta,macrophages and lymphocytes.
• Sclera proper:
It is the intermediate layer of sclera , which is made upof crossed collagen fibres.
These belongs to Type 1 collagen.
• Lamina Fusca:
It is the innermost layer of sclera. They contain melanocytes which gives them color.
This is responsible for the Blue sclera.
BLOOD SUPPLY: The episcleral is the highy vascularized layer, which gains its arterial supply
from anterior and posterior ciliary arteries arising from ophthalmic artery.
NERVE SUPPLY: It is supplied by the branches of long ciliary nerves which pierces near the
limbus to form a plexus.

BLUE SCLERA

This condition can be defined as the bluish discolouration of the white eye. Where the
conjunctiva becomes bluish in color, this is due to the thinning and transparancy of the
collagen fibres of the sclera. Where this allows the veins under the tissue to show through.
Mostly this occurs in all the connective tissue disorders,For eg:
Osteogenesis imperfecta, paget’s disease, Ehler-danles syndrome, pseudo xanthoma
elasticum, congenital glaucoma, Mrfans syndrome, Scleritis, Nevus of ota.

STAPHYLOMA
Staphyloma can be defined as the bulging of the outer layer of the eyeball. Where this
bulging is lined by the uveal tissues from inside. This is also known as the
“Ectasia of the outer coat of eyeball”
(Ectasia- a bulge)
 TYPES OF STAPHYLOMAS:

[Link] STAPHYLOMA:
It is the bulging or ectasia of the anterior part of the eyeball, the cornea. Which is
underlined by iris through inside. This may be due to thinning of the cornea or any sloughing
corneal ulcers.
[Link] STAPHYLOMA:
It Is the buliging of cornea over the limbal part where the ectasia is underlined by the root of
iris. This is also mostly caused by a sloughing corneal ulcer or by any thinning of corneal
layer.
[Link] STAPHYLOMA:
It is the bulge presenting above the ciliary bodies present inside the eyeball, and hence it is
underlined by the ciliary bodies. This is mostly caused because of Scleritis, Glaucoma, Injury
that causes thining of the scleral layer.
[Link] STAPHYLOMA:
It is the bulge present over the equatorial region of the eyeball. This is underlined by the
choroid layer , which runs along with the sclera all over the eyeball. The most common
cause of equatorial staphyloma is a pathological myopia.
[Link] STAPHYLOMA:
It is as same as the equatorial staphyloma, where the underlining tissue is the chorid layer,
this occurs over the posterior side of eyeball which can be visualized by a B-Scan. It is also
caused by pathological myopia.
DIAGNOSIS: B-Scan,CT scan, etc
 TYPE ECTATIC UVEAL CAUSES TREATMENT
LAYER TISSUE
Anterior Cornea Iris Peripheral trauma / Staphylectomy
sloughing corneal
ulcer
Intercalary Limbus Root of iris Peripheral trauma / Staphylectomy
sloughing corneal
ulcer
Ciliary Sclera Ciliary bodies Scleritis/glaucoma/any Staphylectomy
kind of trauma
Equatorial Sclera Choroid Pathological myopia Staphylectomy
Posterior Sclera Choroid Pathological myopia Usually
untreatable

COMMON MANAGEMENT:

• Treating the underlying cause of every staphyloma will help.

• After staphylectomy keratoplasty is done to replace the removed tissues.

SCLERA AND EPISCLERA

EPISCLERITIS
Episcleritis is defined as the inflammation of episcleral without involving the scleral layer.
This involves the tenon’s capsule. Which leads to infilteration of local lymphocytes into the
episcleral tissues.
CAUSES:

• Usually idiopathic
• Hypersensitivity reactions
• Infections like : herpes zoster,lyme disease,tuberculosis,syphilis,etc
• Diseases like: gout, psoriasis and connective tissue disorders.
SIGNS AND SYMPTOMS:

• Redness
• Burning sensation
• Discomfort
• Lacrimation
• Photophobia (rarely)
TYPES:

• SIMPLE EPISCLERITIS:
In this the vessels involved are large and runs radially below the conjunctiva and
hence they are often diagnosed as conjunctivitis.
 • NODULAR EPISCLERITIS:
There will be a presence of nodular thick appearance near the limbus. Which can be
freely moved.
DIFFERENTIAL DIAGNOSIS:

• Simple episleritis as mentioned before may be wrongly diagnosed to be

conjunctivitis .
• Nodular episcleritis may be diagnosed as pinguecula, etc.
TREATMENT :

• Usually yreated with NSAID’s like: ketorolac (0.3%) , flurbiprofen (300mg OD),
indomethacin (25mg).
• Corticosteroids
• Artificial tearing agents
• Cold compress

SCLERITIS
Scleritis is basically defined as the inflammation of the sclera.
Scleritis is divided into 2 types known as :
➢ Immune mediated
➢ Infectious
IMMUNE MEDIATED SCLERITIS
Of which majority comes under immune mediated and it is further divided into two classes
with respect to equator,

• Anterior
• Posterior
ANTERIOR SCLERITIS:
It is defined as the inflammation occurring anterior to the equator.
Causes: mostly caused due to Rheumatoid arthritis and also by anyother connective tissue
disorders.
This anterior scleritis is further divided into;

• Non-Necrotizing
• Necrotizing
NON-NECROTIZING :
Symptoms:
 • Redness
• Thickening
Non necrotizing anterior scleritis is further divided into two types namely,
DIFFUSE: It is the commonest variety. Where it gives a wide spread inflammation .
NODULAR: It is presented with thick nodules inbetween the conjunctiva. Immovable in
nature.
TREATMENT: topical steroid and systemic indomethacin 75mg.
NECROTIZING:
Necrotizing anterior scleritis is of two types again :

• With inflammation
• Without inflammation
WITH INFLAMMATION : This is due to the increased inflammation of the vascular bodies
(vasculitis).
This causes an infarction.
This area is further thinned out and leads to exposing and inflammation of uveal structures.
WITHOUT INFLAMMATION: This is also known as scleromalacia perforans.
It presents with avascular necrosis and hence has no pain.
Characterized by yellowish patch of melting sclera.
Soft appearance with no inflammation and perforation is rare.
Complications: Staphyloma
TREATMENT:
Treatment of the underlying cause with the help of Systemic NSAID’s, Systemic steroids and
immune suppressants(methotrexate,etc).
Vision is mostly normal in anterior scleritis.

POSTERIOR SCLERITIS:
It constitutes to 20% of the total scleritis .
Symptoms : pain, redness and some times reduction in vision.
Mostly idiopathic and may be due to the retinal detachment which causes an accumulation
of tenon’s fluid inside the scleral layers.
Diagnosis: any scan including B-scan,MRI,Ct scans. Which shows a T-sign , a specific indicator
of posterior scleritis.
Treatment: systemic steroids.
INFECTIOUS SCLERITIS:
With any sort of infectious etiologies.
Signs and symptoms: formation of fistulae, painful nodules, purulent discharges, ulcers in
conjunctiva and sclera.
Complications : sclerosing keratitis, complicated cataract, secondary glaucoma.
INVESTIGATIONS: TLC,DLC,ESR,VDRL,Serum level,urine analysis, Mantoux test, x-rays of
chest, etc.
TREATMENT: anti microbial therapy and surgical procedures.
 UVEAL TRACT

What we will learn here?

• Anatomy of uveal tract

• Uveitis
• Types of Uveitis
• Anatomical Uveitis
• Pathological Uveitis
• Etiological Uveitis
• Uveitis in systemic diseases
• Degeneration of Uveal Tract

ANATOMY

UVEAL TRACT:

The uveal tract is a combination of Iris, Ciliary body, Choroid. They constitute th middle vascular
coat of the eyeball. Detailed anatomy of each is given below.

IRIS

The iris is the anterior limiting membrane of the uveal tract. The centre part of iris is known as
the pupil ,which is of diameter 4mm. Iris divides the cornea and lens.

ARRANGMENT: Collarette pattern of arrangement (wheel spokes like). The layer is divided into
pupillary zone and ciliary zone. Pupillary zone is a pigmented layer where it gives color to the iris.
Ciliary zone has crypts and underlying blood vessels in it.

LAYERS OF IRIS: It is of 4 layers namely,

• Anterior limiting layer

• Iris stroma
• Anterior pigmented epithelial layer
• Posterior pigmented epithelial layer

CILIARY BODY
 Ciliary body is divided into two posrtions :

• The anterior fingerlike portion named as Pars plicata (2mm)

• The posterior smooth portion named as Pars plana (4mm)

LAYERS: It is made upof 5 layers namely:

• Supraciliary lamina
• Stromal layer
• Pigmented epithelium layer
• Non pigmented epithelium layer
• Internal limiting epithelium

This ciliary body helps in formation of aqueous humour and the body helps in accommodation.
The ciliary body layer is pigmented and epithelial which is prone for infection to occur.

CHOROID

It is the posterior part of uveal tract. It is also the most

Major arterial circle
vascularized part of the uveal tract. It is a smooth brown layer
holding contact with sclera.

LAYERS: it is made up of 3 layers,

• Suprachoroidal lamina
• Stromal layer
• Basal lamina (bruch’s membrane): it is a pigmented layer which lies in contact with the outer
layer of retina (Retinal pigmented layer)

BLOOD SUPPLY

Minor arterial circle

Blood supply to the uveal tract is by two circulations :

• Major arterial circle:

It is also known as Circus Arteriosus Major. It is formed by the anterior and posterior ciliary
arteries. They supply blood at the root of iris.
• Minor arterial circle:
It is also known as Circus arteriosus minor. It is formed or originated as the branches from
the major arterial circle. They supply at the pupillary margin.

[diagram]

The posterior part of the uveal tract is supplied by the Long and short posterior ciliary
arteries. They pierce the scleral layer and there by supplies the uveal tract.

VENOUS DRAINAGE
Venous drainage of the uveal tract is carried out by Vortex veins. The vortex veins are 4 in number
divided into : supratemporal , supra nasal , infra temporal , infra nasal.

Where the supra temporal and supranasal drains into the superior ophthalmic vein and the infra
nasal and infra temporal drains into the inferior ophthalmic vein.

These two ophthalmic veins directly drains into the Cavernous sinus.

UVEITIS

Uveitis can be defined as the inflammation of the uveal tissues or any part of the uveal tract . The
parts of uveal tract are too closely arranged so that when one part is affected it usually affects the
whole uvea.

CLASSIFICATION

There are 4 types of classification :

• Anatomical classification
• Clinical classification
• Pathological classification
• Etiological classification

ANATOMICAL CLASSIFICATION :

This is the most common and standardly used type of classification

This type is divided into :

ANTERIOR UVEITIS:

This involves the anterior part of the uveal tract,the iris and pars plicata of the uveal tract and hence
it is also known as IRIDOCYCLITIS.

INTERMIDIATE UVEITIS :

This involves the middle part of the uveal tract , the pars plana. And hence it is also known as PARS
PLANITIS.

POSTERIOR UVEITIS:

This involves the posterior part of the uveal tract, the choroid layer and the retina. Hence they are
also known as CHORIORETINITIS.
When there is an inflammation of the entire uveal tract(as a whole) then it is known as PANUVEITIS.

CLINICAL CLASSIFICATION :

ACUTE UVEITIS :

In this type of uveitis the disease onset is very short with shown symptoms and lasts only for 3
months (max.)

CHRONIC UVEITIS:

In this type, there will be a long asymptomatic period where the defect lasts more than 3 months
and sometimes leading to defective vision.

RECURRENT UVEITIS :

In this type, there will be repeated episodes of the disease with a gap period of 3 months in
between.

PATHOLOGICAL CLASSIFICATION:

SUPPURATIVE UVEITIS :

This is a type of inflammation formed by pyogenic organisms, which leads to puss formation. This is
also known as purulent uveitis.

NON-SUPPARATIVE UVEITIS:

This type is comprised of 1)granulomatous and 2)non-granulamatous uveitis

ETIOLOGICAL UVEITIS :

ETIOLOGICAL UVEITIS

INFECTIOUS NON INFECTIOUS MASQUERADE SYNDROMES

• IMMUNE RELATED
UVEITIS • NON-NEOPLASMIC
• BACTERIAL UVEITIS
• TRAUMATIC UVEITIS MASQUERADE
• VIRAL UVEITIS
• TOXIC UVEITIS SYNDROME
• FUNGAL UVEITIS
• IDIOPATHIC UVEITIS • NEOPLASTIC
• PARASITIC UVEITIS
• ASSOCIATED WITH MASQUERADE
• RICKETISIAL UVEITIS
NON INFECTIOUS SYNDROME
SYSTEMIC DISEASES

ANATOMICAL UVEITIS
 ANTERIOR UVEITIS

Anterior uveitis is defined as the inflammation of anterior part of uveal tract. (iris and pars plicata) it
is also known as Iridocyclitis.

ETIOLOGY:

• Viral infection (CMV,HSV,VZV)

• Post traumatic
• Post surgical
• Malignancy, etc.

CLINICAL FEATURES:

• Iridocyclitis
• Iritis
• Cyclitis

SYMPTOMS:

• Sudden pain , especially near scalp and forehead.

• Diminishing of vision, due to induced myopia
• Photophobia : fear of light
• Redness, due to hyperaemia and circum corneal congestion.
• Watering/lacrimation
• Lid spasm

SIGNS:

• Lid edema
• Circumcorneal congestion, which is also known as deep ciliary ingestion. This is often
differentially diagnosed to be Acute conjunctive glaucoma. And severe in congestive
glaucoma.
• CORNEAL APPEARANCE:
✓ Corneal Oedema
✓ KP’s | Keratic Precipitates : This is the most common sign seen. They are
inflammatory cells or proteinaceous cellular deposits which are found in the
posterior surface of the cornea in the base line. They’ll be in the form of
triangular fashion. They are also known as Artl’s triangular. The types of KP’s
are: (a)MUTTON FAT (bulky yellow fat like and granulomatous, seen in
Syphillis, Sarcoidosis, Brucellosis, etc), (b)FINE PIGMENTED (Small granule
and non granulomatous), (c)small and medium KP’s (d) Old KP’s.
• ANTERIOR CHAMBER APPEARANCE:
✓ Aqueous flare
✓ Haziness
✓ Turbidity(earliest sign due to protein deposits)
✓ Hypophyon (puss in anterior chamber due to increase in exudates)
• Deep, irregular, funnel shaped anterior chamer due to synechiae formation.
• Change in the angle of anterior chamber due to synechiae.
• IRIS APPEARANCE:
✓ Dark brown coloured
 ✓ Iris nodule formation (Koeppe’s nodules at the base of iris and koeppe’s
nodule at the papillary border)
✓ Iris neovascularisation
✓ Posterior synechiae: they are the adhesions between the posterior surface
of iris and anterior capsule of lens. They are of 3 types :

SEGMENTAL RING TOTAL

✓ Adhesion of
pupillary
margin of
iris to lens
✓ Aqueous ✓ total
collection adhesion
✓ Increased of iris in
✓ Present in
iris pressure lens
some ✓ Iris bombe’ ✓ degenarati
areas of ✓ Irido on of
iris corneal ciliary
✓ Irregular cataract
body
pupil ✓ Acute angle
✓ no
closure
glaucoma aqueous
✓ Peripheral
synechae
✓ Chronic
congestive
glaucoma

• PUPILLARY CHANGES:
Small, irregular, constricted, narrow, occluso pupil known as “Cork Screw Pupil”,
when dilated and atrophied testroned pupil.
• LENS CHANGES: Complicated cataract, with exudates filled and pigment dispersed.

COMPLICATIONS:

• Complicated cataract: most common complication.

• Secondary glaucoma : which may present of two types (early glaucoma and late
glaucoma)
• Choroiditis
• Papillitis
• Band shaped keratopathy: due to long standing chronic uveitis
• Phthisis bulbi: It is the end result of the chronic uveitis, showing soft, shrinken and
atrophic eye.

DIFFERENTIAL DIAGNOSIS:

• ACUTE RED EYE: In this case, acute iridocyclitis is differentiated to be congestive glaucoma or
acute conjunctivitis.
INVESTIGATIONS:

• Since there is presence of inflammation, can go for TLC,DLC,ESR,BLOOD URIC ACID,C-

REACTIVE PROTIENS,ETC)
• Urine examination for WBC,RBC and puss cells
• Stool examination for cyst and ova
• Skin test: tests like tuberculin test, kveim’s test, lepromin test, toxoplasmin test for behcet’s
disease.

TREATMENT:

(I)TREATMENT OF CHOICE will be Mydriatics and Cycloplegics like:

• Atropine
• Homatropine
• Cyclopentolate
• Tropicamide

Mechanism of action:

✓ Prevents posterior synechiae

✓ Dilates pupil – so rests the ciliary spasm
✓ Relief to ciliary spasm

Atropine is usually preferred in children.

(II)TOPICAL STEROIDS:

✓ Beta methasone
✓ Dexa methasone
✓ Prednisolone
✓ Flurometholone
But usually not used since it can cause GTCS.

(III) NSAIDs: used when steroids are contraindicated. Phenylbutazone, oxyphenbutazone are potent
anti inflammatory drugs.

(IV) Heat fomentation : a. Dry heat (ironing) b. Wet heat (lukewarm water with salt pinch) reduces
venous stasis, therby reducing pain.

(V) Dark goggle for photophobia, lacrimation and blepharospasm.

(VI)Other symptomatic treatments.

CONTRADICTION:

Antibiotics are not used and not mandatory and usually not [Link] can be provided with steroids.

INTERMEDIATE UVEITIS

Intermediate uveitis is defined as the inflammation of pars plana of ciliary body. It is also known as
Pars planitis.

ETIOLOGY:
 ✓ Idiopathic is the major cause linked with HLA-DR2 gene.
✓ Known infectious causes like tuberculosis, syphilis, sarcoidosis, lyme disease and multiple
sclerosis.

SYMPTOMS:

• Mostly asymptomatic
• Floaters
• Blurring and decreased of vision
• Pain, photophobia, redness of eye

SIGNS:

ANTERIOR SEGMENT:

KP’s due to anterior uveitis, low graded flare cells, lens shows complicated cataract signs.

POSTERIOR SEGMENT:

• Snowball opacities: grey whitish fibrovascular plaques over the pars plana. When these
opacities settle down, then it is known as Snow banking.
• Vitreous cells
• Anterior vitreous condensation
• Severe vitreous opacification

PROGNOSIS:

Has a good prognosis.

COMPLICATIONS:

• Complicated cataract
• Cystoid macular oedema
• Band keratopathy
• Secondary glaucoma , etc.

TREATMENT:

TROPICAL STEROIDS (triamcinolone) administered as subcutaneous injection , if not working go for

systemic steroids, immune suppressive therapy(cyclosporine,azathioprine), cryotherapy or laser
therapy (in snow banking) and finally pars plana vitrectomy.

POSTERIOR UVEITIS

Posterior uveitis is defined as the inflammation of choroid and retina. Hence it is also known as
chorioretinitis.

ETIOLOGY:

INFECTIOUS: Due to virus (CMV,HSV, Herpes zoster, rubella), Bacteria (TB, Lyme’s disease,
Brucellosis), Fungi (candida, histoplasma, aspergillus, cryptococcus), Parasite (toxoplasma, toxocara,
cysticercus, onchocerca)
NON-INFECTIOUS: Auto-immune (Behcet’s disease, SLE, Wegener’s syndrome, sympathetic
ophthalmia), malignancy (lymphoma,leukemia), unknown etiology including other infectious
diseases.

CLINICAL FEATURES:

• Defective vision: vitreous haze

• Retinitis- Photopsia (flashes of light)
• Floaters – due to vitritis and clump formation
• Metamorphopsia: showing distorted images
• Micropsia: objects appears smaller
• Macropsia: objects appearing larger
• Positive scotoma
• Choroiditis : positive scotoma (blind spots: apart from physiological single spot , presence of
many blind spots are known as positive scotoma)

SIGNS:

✓ Anterior segment: KPs may be seen

✓ Vitreous opacities (fine, coarse, stringy or snowball opacities)

CLINICAL TYPES:

• CHOROIDITIS: It is further classified into

FOCAL CHOROIDITIS: the lesions are of single patch or few smaller patches localized to a
particular area.
MULTIFOCAL CHOROIDITIS: characterisied by multiple focals of lesions in a smaller area ,
may be due to syphilis or tuberculosis.
DIFFUSE CHOROIDITIS: large spreading lesion involving huge part of choroid.

COMPLICATION:

• Complicated cataract
• Anterior uvea inflammation
• Vitreous degeneration
• Retinal detachment

TREATMENT:

• SYSTEMIC CORTICOSTEROIDS: posterior subtenon injections with cortico steroids are usually
effective.
• IMMUNO SUPPRESSIVES
• SPECIFIC TREATMENT with respect to diseases like toxoplasmosis, tuberculosis, syphilis, etc.

PATHOLOGICAL UVEITIS

SUPPARATIVE / PURULENT UVEITIS

Purulent uveitis is the direct inflammation of uvea due to any pyogenic organism invasion. It may
start as anterior or posterior uveitis and then progress to retina, vitreous to form endophthalmitis
and then panophthalmitis.
 ENDOPHTHALMITIS

It is defined as the inflammation of inner structures of eyeball. Where the retina and uveal tissues
could pour the exudates into the anterior chamber, posterior chamber, vitreous, etc.

ETIOLOGY:

Caused by two types : (A)Infectious (B)Non-infectious

INFECTIOUS CAUSES

MODES ORGANISMS

EXOGENOUS ENDOGENOUS SECONDARY BACTERIAL FUNGAL

INFECTION

Usually followed Rarely through Gram +ve cocci: Caused by:

by perforating blood stream, Followed by ~[Link]
~Aspergillus
injuries, from affected orbital cellulitis, ~[Link]
perforation of focus in the thrombophlebiti ~Pseudomonas ~Fusarium
infected corneal body such as s & infected ~Pneumococci
teeth carries, ~Streptococci ~Candida
ulcers or post corneal ulcer.
septicaemia & ~Corynebacteriu
operative. ~etc.
puerperal sepsis. m

NON-INFECTIOUS CAUSES

POST-OPERATIVE POST-TRAUMATIC PHACOANAPHYLACTIC I.O TUMOR NECROSIS

~Chemical adherent to
I.O lens
Retained intraocular Masquerade syndrome
Induced by lens proteins
~Chemicals adherent to foreign body after any
with morgagnian (a sterile type of
instruments trauma (eg. Pure
cataract. endophthalmitis)
copper)
~Toxic anterior segment
syndrome

CLINICAL FEATURES:
SYMPTOMS:

• Severe ocular pain

• Redness
• Lacrimation
• Photophobia
• Loss of vision

SIGNS:

• Red and swollen lids

• Cicumcorneal congestion
• Oedematous, Cloudy, ring infilterated cornea
• Yellow necrotic wounds
• Presence of hypopyon
• Vitreous exudation
• Increased intraocular pressure

TREATMENT:

ANTIBIOTIC: Intra vitreal injection as soon as possible can help. (eg vancomycin – 1mg, amikacin –
0.4mg)

TOPICAL ANTIBIOTICS: Administered in a combination of two drugs.

(eg. Vancomycin or cefazoline / Amikacin or tobramycin)

SYSTEMIC ANTIBIOTICS:

Have less role (eg. Ciprofloxacin, vancomycin, cefazoline)

STEROID THERAPY:

Limits the damage caused by inflammation. (eg. Lansoprazole)

SUPPORTIVE THERAPY:

(antiglaucoma drugs, cycloplegics)

VITRECTOMY:

When all the above treatments fails , we’ll go for vitrectomy. It helps in removal of toxins,
organisms,etc)

PANOPHTHALMITIS:

It is defined as the inflammation of the entire eyeball. As similar to endophthalmitis, it starts with
posterior or anterior uveitis and spreads through out the eyeball.

ETIOLOGY:

• It is mainly due to bacterial infection

• Other causes are as similar as endophthalmitis

CLINICAL FEATURES:
SYMPTOMS:

• Severe ocular pain

• Loss of vision
• Lacrimation
• Purulent discharge
• Redness, swelling, etc.

SIGNS:

• Edema and hyperemia of lids

• Chemosis and conjunctival congestion in conjunctiva
• Cloudy cornea
• Increased intraocular pressure
• Puss filled
• Lost vision

COMPLICATIONS:

• Orbital cellulitis
• Cavernous sinus thrombosis
• Meningitis

TREATMENT:

• Anti inflammatory drugs

• Antibiotics
• Evisceration operation

ETIOLOGICAL CAUSES

INFECTIOUS UVEITIS NON-INFECTIOUS UVEITIS MASQUERADE SYNDROME

Associated with:
[Link] infectious
Associated with: systemic diseases:
[Link] systemic
~Uveitis in sarcoidosis
bacterial infections:
~Behchet’s disease
~Tubecular
[Link]:
~Leprotic
[Link] infections: ~Ankylosing spondylitis
~Syphilitic ~Reiter’s syndrome
[Link] infections: ~Still’s disease
~HSV [Link]-induced: [Link]-neoplastic
~Herpes Zoster ~Phacotoxic uveitis
[Link]
~Cytomegalo virus ~Phacoanaphylictic
[Link]: endophthamitis
~Toxoplasmosis [Link] uveitis
~Onchocercasis [Link] specific:
~Amoebiasis ~Fuch’s uveitis
[Link]
syndrome
~Histoplasmosis
~intermediate
syndrome
~Candidiasis ~Vogt-Koyanagi-
Harada’s syndrome
 BACTERIAL UVEITIS
• Tubercular uveitis
• Tuberculosis - chronic granulomatous infection
• caused by Mycobacterium tuberculosis
• It may cause both anterior and posterior uveitis
in developing countries it still continues to be a common cause of uveitis.
Clinical presentations
1. Tubercular anterior uveitis.
may occur as
• non granulomatous iridocyclitis – Allergic or immune inflammatory in nature
• granulomatous anterior uveitis which in turn may be in the form of
➢ miliary tubercular iritis
▪ small yellowish white nodule surrounded by numerous satellites.
▪ Situated near pupillary or ciliary margin
▪ Develops in patient with severely impaired immunological response or
in case of widespread dissemination of bacteria

➢ conglomerate granuloma (solitary tuberculoma)

▪ Larger yellowish white tumor
▪ Smaller satellites present
▪ Nodules contain giant cells
2. Tubercular posterior uveitis. It may occur as:
i. Multiple miliary tubercles
➢ in the choroid which appear as round yellow white nodules one-sixth to two and half
disc diameter in size ,
➢ appear as single large subretinal choroidal mass
➢ associated with tubercular meningitis.
➢ Diagnostic evidence of tuberculosis in – meningitis and general disease
ii. Douse or multifocal choroiditis may occur in chronic tuberculosis.
[Link] granuloma may occur rarely as a focal lesion.
3. Vasculitis.(Eales’ disease)
Diagnosis (There is no specific clinical finding in tubercular uveitis.)
 • from positive skin test (does not prove)
• associated findings of systemic tuberculosis,
• intractable uveitis unresponsive to steroid therapy,
• a positive response to isoniazid test (a dramatic response of iritis to isoniazid 300 mg
OD for 3 weeks)
Differential diagnosis :
• Sarcoidosis
• Bechet syndrome
• Leprosy
• Syphilis
• Cat -scratch disease
• Leptospirosis
• Brucellosis
Treatment - In addition to usual treatment of uveitis, chemotherapy with rifampicin and
isoniazid should be given for 12 months. Systemic corticosteroids should be deferred.

Leprotic Uveitis Leprosy (Hansen’s disease)

• caused by Mycobacterium leprae
• The disease occurs in two principal forms: lepromatous and tuberculoid.
• Leprosy involves predominantly anterior uvea; more commonly in lepromatous than
in the tuberculoid form of disease.
• Ocular involvement is Indirect, caused by complications resulting from
neuroparalytic and neurotrophic keratopathy.
• The eyes can also be involved in Lepra reaction.
Clinical types Lepromatous uveitis may occur as
1. Acute iritis.
• Non -granulomatous
• caused by antigen-antibody deposition
• characterised by severe exudative reaction.
2. Chronic granulomatous iritis.
• granulomatous
• occurs due to direct organismal invasion
• characterised by presence of small glistening ‘iris pearls’ near the pupillary margin in
a necklace form; small pearls enlarge and coalesce to form large pearls.
• a nodular lepromata may be seen.
Treatment Besides usual local therapy of iridocyclitis, antileprotic treatment with Dapsone
50–100 mg daily or other drugs should also be instituted.

Brucellosis
• Uveitis of chronic non – granulomatous type is the most common presentation.
• Prone to relapse
Diagnosis : it can only be suggested following exclusion of other forms of chronic
iridocyclitis by agglutination test, cutaneous test or opsonocytophagic test.
Treatment :Sulphonamide or Chlortetracycline.

Whipple`s Disease
• Ocular inflammation manifest as –
o corneal infiltrate,
o anterior uveitis
o vitritis with characteristic whitish opacities in the shaped mulberries,
o vasculitis
o retinitis
o disc edema.
• Supportive evidence – elevated WBCs and thickened jejunal mucosa on radiological
examination
• Definitive diagnosis – Jejunal biopsy

SPIROCHETAL UVEITIS
• Acquired Syphilitic Uveitis Acquired syphilis is a chronic venereal infection caused
by Treponema pallidum (spirochaete). It affects both the anterior and posterior
uvea.
1. Syphilitic anterior uveitis

Syphilitic anterior
uveitis

acute plastic iritis granulomatous iritis

tertiary stage of syphilis

It is characterised by
Herxheimer reaction formation of yellowish
secondary stage of 24–48 hours after red highly vascularised
syphilis therapeutic dose of the multiple nodules
penicillin arranged near the
pupillary border or
ciliary border of iris
.
2. Syphilitic posterior uveitis It may occur as disseminated, peripheral or diffuse choroiditis.
Diagnosis - confirmed by FTA-ABS (fluorescent treponemal antibody absorption) blood test
Treatment- In addition to local therapy of the uveitis, patient should be treated by systemic
penicillin or other anti-syphilitic drugs.

Leptospirosis
➢ Uveitis occurs in 10% of the patient.
➢ Associated with hypopyon
Diagnosis : Anti- Leptospira antibody tests in blood and culture of line organism
Treatment : Topical steroids + cycloplegics + intravenous penicillin (in severe) or oral
doxycycline (in milder) cases.

PARASITIC UVEITIS
Toxoplasmosis
• protozoan infestation caused by Toxoplasma gondii
• cats -definitive host, Humans -intermediate hosts.
• primarily affects central nervous system (brain and retina)
 • Systemic lesions are more marked in immunocompromised patients (e.g., HIV+
patients) as
• most common cause of posterior uveitis
• accounts for approximately 90% of focal necrotizing retinitis.
Clinical presentation Systemic toxoplasmosis occurs in humans in three forms:
1. Congenital toxoplasmosis
• more common than the acquired form
• acquired by -transplacental route from the mother c
• 49% infants are born with the disease which may be active or inactive at birth.
• Most of the infants are born with inactive disease - characterised by bilateral healed
punched out heavily pigmented chorioretinal scars in the macular area
2. Acquired toxoplasmosis
• acquired by eating the under-cooked meat of intermediate host containing cyst form
of the parasite.
• Most of the patients are subclinical (asymptomatic)
• lesions include -punctate outer retinal toxoplasmosis (PORT).
-chorior retinal scars
• More common in HIV+ patients
3. Recurrent toxoplasmic retinochoroiditisPathogenesis
In addition to this lesion, an inflammation in the
mother infected
iris, choroid and retinal vessels is excited due to
antigen-antibody reaction

parasites reaching the foetus

through placenta

involve its brain and retina-

stimulate antibody formation

the parasites remain

encysted in inactive form

After 20-40 years

retinal cysts rupture and
release hundreds of parasites

focal necrotizing
retinochoroidits

Characteristic features
 • whitish-yellow, slightly raised area of infiltration located near the margin of old
punched out scarred lesion in the macular region associated with severe vitritis.
• associated nongranulomatous type of mild anterior uveitis.
Diagnosis : lesion is confirmed by ‘
• Indirect fluorescein antibody test
• haemagglutination test or ELISA test.
Treatment. The active lesion of toxoplasmosis is treated by topical and systemic steroids
along with a course of a antitoxoplasmic drug either spiramycin, clindamycin, sulfadiazine or
pyrimethamine.

Toxocariasis
caused by an intestinal roundworm - dogs (Toxocara canis) and cats (Toxocara catis).

produce
young
the
children infested by ova develop Ocular
condition Larva
who play ova of into larva in toxocariasis
visceral migrate to
with dogs these the human (always)
larva the eye
and cats or worms gut unilateral
migrans
eat dirt
(VLM)

Clinically presentation it can present as follows:

■Toxocara chronic endophthalmitis.
• usually presents with leucocoria due to marked vitreous clouding.
• seen in children between the age of 2–10 years and mimics retinoblastoma.
■Posterior pole granuloma.
• It presents as a yellow-white, round, solitary, raised nodule, about 1–2 disc diameter
in size, located either at the macula or in the centrocaecal area.
• usually seen in children between 5 and 15 years of age, presenting with unilateral
loss of vision.
■Peripheral granuloma
• situated anterior to the equator and may be associated with vitreous band
formation.
• usually seen from 6 to 40 years of age.
Diagnosisis – made on the basis of clinical feature and ELISA blood test.

Treatment. It consists of periocular (posterior sub-Tenon) injection of steroid and systemic

steroids. Pars plana vitrectomy may be required in unresponsive patients with
endophthalmitis and in patients with vitreous band formation.

FUNGAL UVEITIS
Presumed Ocular Histoplasmosis Syndrome (POHS)
• Etiology -caused by the fungus Histoplasma capsulatum (though the fungus has not
been isolated from the affected eyes)
• disease is more common in areas where histoplasmosis is endemic (e.g.,
Mississippi-Ohio-Missouri river valley)
• 90% of patients with POHS show positive histoplasmin skin test
Clinical features
➢ Histospots.
▪ atrophic spots scattered in the mid-retinal periphery
▪ roundish, yellowish white lesions measuring 0.2 to 0.7 disc diameter in size.
▪ appear in early childhood
▪ represent the scars of disseminated histoplasma choroiditis.
➢ Macular lesion. Formation of macular lesion:
atrophic macular scar
hole in the Bruch’s membrane
in growth of capillaries
sub-retinal choroidal neovascularisation .

Leakage of fluid from the neovascular membrane

serous detachment, which when complicated by repeated haemorrhages

haemorrhagic detachment .

fibrous disciform scar, associated with a marked permanent visual loss.

Diagnosis
• positive histoplasmin test (supportive test )
• complement fixation tests (negative in two-thirds cases).
 • Fluorescein angiography helps in early diagnosis of subretinal neovascular
membrane.
Treatment
• Active lesions at the macula - treated with systemic corticosteroids
• Early laser photocoagulation of subretinal neovascular membrane - prevent
permanent visual loss which occurs due to fibrous disciform scars.
• For subfoveal membrane PDT should be considered.

Candidiasis
It is an opportunistic infection caused by Candida albicans.
• occurs in immunocompromised patients which include: patients suffering from
AIDS, malignancies, those receiving long-term antibiotics, steroids or cytotoxic
drugs. Patients with long-term indwelling intravenous catheter used for
haemodialysis, and drug addicts are also prone to such infection.
• Ocular candidiasis It is not a common condition . May occur as
➢ Anterior uveitis is associated with hypopyon.
➢ Multifocal chorioretinitis (more common)
▪ characterised by- multiple small, round, whitish areas, may be
associated with areas of haemorrhages with pale centre (Roth’s
spots).
➢ Candida endophthalmitis
▪ characterised by areas of severe retinal necrosis associated with
vitreoretinal abscesses.
▪ Vitreous exudates present as ‘puff ball’ or ‘cotton ball’ colonies,
which when joined by exudative strands form ‘string of pearls’.
Treatment It consists of:
• Topical cycloplegics, and antifungal drugs
. • Systemic antifungal drugs like ketoconazole, flucytosine or amphotericin-B are also
needed.
• Pars plana vitrectomy is required for Candida endophthalmitis

VIRAL UVEITIS
Herpes Zoster Ophthalmicus
It is the involvement of ophthalmic division of fifth nerve by varicella zoster
 ➢ Anterior uveitis develops in 40–50% cases with HZO within 2 weeks of onset of the
skin rashes
➢ A typical HZO keratitis may be associated with mild iritis especially in patients with a
vesicular eruption on the tip of nose.
➢ The iridocyclitis is non-granulomatous characterised by presence of small KPs, mild
aqueous flare and occasional haemorrhagic hypopyon.
➢ Complications like iris atrophy and secondary glaucoma are not uncommon.
Complicated cataract may also develop in late stages.
Treatment. Topical steroids + cycloplegics to be continued for several months.
Systemic acyclovir helps in early control of lesions of HZO.

Herpes Simplex Uveitis

It is associated with keratitis in most of the cases. It may be seen in association with
dendritic or geographical corneal ulceration or with disciform keratitis. Rarely, anterior
uveitis may occur even without keratitis
Treatment- antiviral drugs + cycloplegics.
➢ Steroids for iritis are contraindicated in the presence of active viral ulcers.
➢ Nonsteroidal anti-inflammatory drugs may be added in such cases

Cytomegalovirus (CMV) retinitis

• usually occurs in immunocompromised
• most frequent (40% prevalance) ocular opportunistic infection in patients with AIDS(
CD 4+ counts < 50 cells mm3
Clinical features
➢ Symptoms :Often asymptomatic, some patients may present with scotoma or
decreased vision and/or floaters in one or both eyes
➢ SIGNS :
✓ Anterior segment signs are usually absent. Rarely few stellate KPs may be
seen.
✓ Posterior segment signs include:
▪ Haemorrhagic retinitis - areas of necrosis (yellow white exudates)
associated with areas of vasculitis (perivascular sheathing)
▪ retinal haemorrhages and loss of fundal details (pizza pie
appearance)
▪ progressive retinal atrophy.
▪ Granular retinitis characterised by peripheral granular
Complications : retinal detachment (up to 30%), retinal atrophy and optic nerve disease

Acute Retinal Necrosis

Etiology rare clinical syndrome caused by any of the following viruses:
• Varicella-zoster virus ( commonest )
. • Herpes simplex virus 1 and 2 (HSV 1 & 2( in younger patients)
. • Cytomegalovirus (CMV) (very rarely)
Clinical features
➢ Symptoms include decreased visual acuity, floaters, ocular discomfort, pain and
photophobia.
➢ Signs are as follows:
o Anterior segment may or may not show signs of inflammation in the
anterior chamber.
o Vitritis is usually marked.
o Retinal lesions include areas of focal, well demarcated peripheral necrotising
retinitis, associated with occlusive arteritis. Posterior pole is typically spared.
Complications : retinal detachment and ischaemic optic neuropathy.
Treatment • Systemic antiviral drugs e.g., aciclovir IV 10 mg/kg body weight TID, for two
weeks then PO dose for 6–12 weeks. (Alternative drug is valaciclovir)
• Systemic steroids are needed to control inflammation.
• Aspirin to prevent arterial occlusion
. • Barrier laser photocoagulation for retinal breaks.
• Vitrectomy with silicon oil injection for associated retinal detachment.
Progressive outer retinal necrosis (PORN) –
It is a rare devastating necrotizing retinitis caused by a Varicella Zoster Virus (VZV) infection
in immunocompromised patients (usually in patients suffering with AIDS with CD4+ T-cell
counts <50/mm2.
Clinical features
• Painless rapid loss of vision in one or both eyes
• Retinal lesions include rapidly coalescing white areas of outer retinal necrosis (often
central as well as peripheral) but with minimal vasculitis, retinitis or viritis (cf ARN).
Complication : Retinal detachment ( common)
Treatment consists of intravenous injection of ganciclovir or foscarnet combined with
intravitreal ganciclovir.

NON INFECTIOUS UVEITIS

[Link] WITH SYSTEMIC DISEASES
∆ Sarcoidosis - It is a granulomatous multi-system disease
Etiology: Unknown
FEATURES:Non- caseating epithelioid cell granuloma formation. It presents with bilateral
hilar lymphadenopathy,pulmonary infiltration,skin and ocular lesions. It either resolves or
replaced by hyalinised scar tissue.

❖ Ocular lesions - 20-50% patients present with ocular lesions and it includes:
➢ Sarcoid uveitis- It maybe anterior, intermediate, posterior or panuveitis.
■ Anterior uveitis presents as granulomatous iridocyclitis characterised
by iris nodules, large mutton fat KPs, anterior chamber cells and flare
and posterior synechiae.
■ Intermediate uveitis characterised by vitreous cells,snowball opacities
and snowbanking.
■ Posterior uveitis (choroidal and retinal granulomas, cystoid macular
oedema, periphlebitis retinae with sheathing, appearing as candle
wax droppings.) Peripheral multifocal chorioretinitis characterised by
small,punched out atrophic spots,are highly suggestive of sarcoidosis.
■ Uveoparotid fever (Heerfordt's syndrome)- characterised by bilateral
granulomatous panuveitis, painful enlargement of parotid glands,
cranial nerve palsies,skin rashes, fever and malaise.
Complications- complicated cataract, inflammatory glaucoma and cystoid
macular oedema.

➢ Conjunctival lesions- sarcoid nodules and keratoconjunctivitis sicca.

➢ Lacrimal glands may be enlarged.
Diagnosis:

• Kveim test – Positive

• Abnormal X-ray chest
• Gallium scan of head and neck and mediastinum for increased uptake
• Raised serum ACE
• Estimation of [Link].
• Confirmatory test- histological proof
Treatment: Depending on severity, topical, periocular and systemic steroids are used.

∆ Behcet's disease- It is an idiopathic multi-system disease characterised by

recurrent,non- granulomatous uveitis, aphthous ulceration, genital ulceration and erythema
multi- forme.
● Etiology- obliterative vasculitis by circulating immune complexes. It affects young
men positive for HLA- B51.
● Clinical features- bilateral, acute recurrent iridocyclitis associated with hypopyon,
and also posterior uveitis,vitritis, periphlebitis retinae and retinitis
 ● Treatment- Corticosteroid (helpful initially) and immunosuppressive drugs (resistant
cases and for acute flare).

[Link] WITH ARTHRITIS

∆ Ankylosing Spondylitis- It is an idiopathic, pauciarticular, chronic inflammatory
arthritis, usually involves sacroiliac and posterior intervertebral joints. Young males (20-
40years) positive for HLA-B27 are affected. 30-35% patients develop uveitis.
● Clinical features: Acute, recurrent, non- granulomatous type of iridocyclitis. One eye
at a time is usually affected.
● Treatment: Usual treatment of anterior uveitis. Long- term aspirin or indomethacin
decrease the recurrence.

∆ Reiter's Syndrome- characterised by triad of urethritis, arthritis and conjunctivitis with

or without iridocyclitis.
● Etiology. Unknown; young males positive for HLA-B27 are affected. It is
pauciarticular involving large joints. 3 forms: post- veneral,post- dysenteric and
articular form.
● Ocular features.
○ Acute mucopurulent conjunctivitis
○ Acute non- granulomatous type of iridocyclitis
● Treatment. A course of systemic tetracycline 250mg QID for 10 days may be useful in
post- veneral form caused by Chlamydia infection.

∆Juvenile Idiopathic Arthritis- It is a chronic inflammatory arthritis involving multiple

joints in children <16 years.
It occurs in 4 forms: Pauciarticular form (+ for ANA,- for RF) ; Rheumatoid form (+ for RF);
Spondyloarthropathy form; Still's disease- Polyarthritis with hepatosplenomegaly and other
systemic features.
● Ocular lesions. Anterior uveitis which is bilateral, chronic granulomatous disease
developing before 6 years. Females more commonly affected (4:1). They maybe
positive for HLA-DW5 and ANA. The onset is asymptomatic and hence slit- lamp
examination is mandatory.
● Complications: Posterior synechiae, complicated cataract, band shaped keratopathy,
pars planitis, glaucoma.
● Treatment is on usual lines.

[Link] -INDUCED
∆Phacoanaphylactic uveitis- It is an immunologic response to lens proteins in
sensitized eyes presenting as severe granulomatous anterior uveitis.
● Etiology. May occur following extracapsular cataract extraction, trauma to lens or
leak of proteins in hypermature cataract.
● Clinical features. Severe pain, loss of vision,marked congestion and signs of
granulomatous iridocyclitis with lens matter in anterior chamber.
● Treatment. Removal of causative lens matter, topical steroids and cycloplegics.
Visual prognosis is poor
Phacotoxic Uveitis- A mild iridocyclitis associated with presence of lens matter in anterior
chamber. Treatment is removal of lens matter, topical steroids and cycloplegics.

[Link] UVEITIS
1. Traumatic miosis- due to irritation of ciliary nerves; maybe associated with spasm of
accommodation.
2. Traumatic mydriasis- permanent and associated with traumatic cycloplegia.
3. Rupture of pupillary margin
4. Radiation tears in iris stroma
5. Iridodialysis
6. Antiflexion of iris
7. Retroflexion of iris
8. Traumatic iridemia
9. Angle recession
10. Inflammatory changes
Treatment: atropine, antibiotics and steroids. Atropine is contraindicated in rupture of
pupillary margin and subluxation of lens.

[Link] SPECIFIC UVEITIS SYNDROMES

∆Fuchs' Uveitis Syndrome(FUS)
● It is a unilateral, chronic, non- granulomatous anterior uveitis associated with early
cataract formation occurring in middle aged person.
● It is characterised by heterochromia of iris, diffuse stromal iris atrophy (moth eaten
appearance), fine stellate KPs,faint aqueous flare.
● Treatment with topical corticosteroid. Associated glaucoma is treated as for POAG.
Cycloplegics are not required.
∆Glaucomatocyclitic Crisis
Posner Sclossman syndrome affecting young adults (most are positive for HLA-BW54) is
characterised by
 ● Recurrent unilateral attacks of acute rise of IOP(40-50mmHg) without shallowing of
anterior chamber associated with
○ Fine KPs without posterior synechiae
○ Epithelial edema of cornea
○ Dilated pupil
○ White eye
● Treatment is with antiglaucoma drugs and topical steroids
∆Sympathetic Ophthalmitis
● A rare bilateral, granulomatous panuveitis following a penetrating ocular trauma
with incarceration of uveal tissue.
● Injured eye is the 'exciting' eye and the fellow eye which also develop uveitis is
'sympathising' eye.
∆Vogt- Koyanagi- Harada (VKH) Syndrome
● An idiopathic, multi-system disorder which includes cutaneous, neurological and
ocular lesions.
● More common in Japanese and those positive for HLA-DR4 and DW15
● It maybe of autoimmune to melanocytes
● Clinical features
○ Cutaneous lesions- alopecia,poliosis, vitiligo
○ Neurological lesions- meningism, encephalopathy
○ Auditory features- tinnitus, vertigo, deafness
○ Ocular features- bilateral chronic granulomatous anterior uveitis
characterised by iris nodules and posterior synechiae; posterior uveitis
● Complications. Cataract, glaucoma and CNV membrane
● Treatment. Corticosteroid is the mainstay. Immunosuppressive drugs are for
resistant and recurrent cases.
∆Acute Posterior Multifocal Placoid Pigment Epitheliopathy(APMPPE)
● It is a rare, idiopathic, self-limiting disorder affecting both eyes,either sex within 20-
30 years.
● Obstructive vasculitis involving choriocapillaris —> ischemic injury —> swelling of
retinal pigment epithelial cells —> bilateral,deep,cream coloured placoid lesions
involving posterior pole and post-equatorial part of the fundus.
● Visual loss, due to macular lesions, which usually recovers within 2 weeks.
● Complications. Mild anterior uveitis, vascular sheathing and exudative retinal
detachment
● Differential diagnosis. Multifocal choroiditis, primary retinal pigment epithelium
detachment
● Treatment. No treatment is effective
∆Serpiginous Geographical Choroidopathy
 ● A rare idiopathic, recurrent, bilaterally asymmetrical inflammation involving
choriocapillaris and pigment epithelium of retina
● It affects patients between 40-60 years
● Ophthalmoscopic view: small,grey,disc- like confluent lesions and choroidal scars
with slight pigment dispersion, resulting in depigmentation in serpiginous
configuration.
● No treatment is effective
∆Bird-shot Retinochoroidopathy
● A rare, idiopathic, bilaterally symmetrical chronic multifocal chorioretinitis
● Characterised by numerous flat creamy- yellow spots resembling the pattern of 'bird-
shot scatter from a shotgun'.
● More common in middle aged, females and who are positive for HLA-A29
● Treatment with corticosteroid is not effective

Degenerative changes of Uveal tract

• Uveal tract = Iris + choroid + ciliary body

Degenerative changes of Iris

1. Essential/ Progressive Atrophy of Iris

• Usually unilateral
• Part of iridocorneal endothelial syndrome
• Lacunae are formed
• Onset of glaucoma => vision loss
• Synechia adhesion of iris to cornea or lens
• Corectopia displacement of pupil
• Ectropion uveae pigmented epithelium faces anteriorly
• Dyscoria abnormal pupil shape
• Polycoria multiple pupils

2. Iridoschisis

• Senility or trauma
• Dehiscences on anterior mesodermal layer (i.e) in stroma and anterior limiting
membrane.
• High incidence of glaucoma
 3. Pigment Dispersion Syndrome

• Associated with pigment dispersion in anterior surface of iris

• Mechanical rubbing of posterior surface of iris against lens zonules
• Mid peripheral iris is concave anteriorly
• Krukenberg Spindle melanin phagocytosis
• Sampaolesi Line deposition of melanin
• Glaucoma

Degenerative Changes Of Choroid

More common in the posterior chamber than in the anterior
Secondary changes

• Loss of nourishment or inflammation

• Pigments migrates from posterior to superficial layers
• Deposition of pigment in perivascular space causes mapping of retinal veins
• Jet black branched pigmented spots
• Pseudoretinitis pigmentosa
Primary changes

1. Senile central choroidal atrophy

• Progressive with age
• Yellowish drusens are seen in fundus and particularly in the macular area

2. Central areolar choroidal atrophy

• Macular origin
• Bilateral, punched out lesions
• Base of lesion is sclera crossed over by choroidal network of vessels

3. Essential Gyrate Atrophy

• Ornithine metabolism error
• Progressive nature from first decade
• Night blindness
• Complete atrophy of fundus by 40-50 years of age
• Macula is spared
4. Choroideremia
• Hereditary dystrophy
• Seen in males from first decade
• Whitish atrophy patches in RPE and choroid
• Night blindness
• Complete atrophy and blindness by 40 years of age

5. Myopic choroidoretinal degeneration

• Choroidoretinal atrophic patches with pigmentation around them
• Foster-Fuch's spot due to choroidal hemorrhage
• Snail track degeneration
• Retinal detachment
• Total retinal dystrophy
• Liquefaction of vitreous or opacity formation
• Strabismus fixus convergence

THANK YOU!!!
 ANATOMY OF LENS & CATARACT

LENS

The lens is a crystalline, transparent, biconvex structure in the eye that, along with the
cornea, helps to refract light to focus on the retina.

It does not posses nerves , blood vessels, or connective tissue.

Diameter - 9 to 10 mm

Thickness varies with age from 3.5 mm to 5 mm

Weight varies from 135 mg to 255 mg

Surfaces : Anterior surface is convex (Radius of curvature 10 mm) than the posterior (Radius of
curvature 6 mm)

Equator is a place where anterior and posterior surfaces of lens meet.

POSITION OF LENS :

Located between iris and the vitreous

- at the pupillary area

- in the saucer shaped depression patellar fossa

REFRACTIVE INDEX AND POWER :

Refractive index : 1.39 (Mean) , 1.41 ( Nuclear ) , 1.38 ( Cortex)

Total dioptric power : 15 - 16

Accommodation power of lens : 14 - 16 D (at birth) , 7 - 8 D (at 25yrs) , and 1 - 2 D (at

50yrs).

STRUCTURE OF LENS :

Lens consist of

1. Lens capsule :

Capsule is a thin , transparent , hyaline membrane surrounding the lens which is

thicker over the anterior than the posterior . The lens capsule is thick at pre equator regions and
thinner at posterior pole.

2. Lens epithelium :

Anterior epithelium is a single layer of cuboidal cells which lies deep to the anterior
capsule .

In equatorial region , these cells become columnar and are actively dividing and
elongating to form new lens fibre throughout the life

There is no posterior epithelium.

 3. Lens substance comprises lens fibres :

(I) Nucleus :

It is the cental part containing the oldest fibres .

Depending upon the development the different zones of lens they are categorized as
Embryonic nucleus, Foetal nucleus, Infantile nucleus, Adult nucleus.

(II) cortex ::

It is the peripheral part which comprises the youngest lens fibres.

SUSPENSORY LIGAMENT OF LENS :

It is also called as cilliary zonules consist a series of fibres passing from cilliary body to lens

This holds the lens in position and enables the cilliary muscles to act on it
ARRANGEMENT OF ZONULAR FIBRES :

The ZONULAR fibres run a more or less complex but continuous course from ora serrata to the
edge of lens .

It can be divided into following parts :

1. Para orbicularis : Zonular fibres which lines pars plana part of cilliary body

2. Zonular plexus : Intervening network of zonular fibres which are attached between cilliary
processes in the region of pars plicata part of cilliary body.

3. Zonular fork : consolidated bundles of zonular fibres which bends at right angle from anterior
margin of pars plicata toward the lens after dividing into three zonular limbs.

• Anterior limb : These fibres are denser and insert on the anterior lens capsule .

• Equatorial zonular limb : These fibres are sparse and can out in brush like manner to get
inserted into the lens capsule.

• Posterior zonular limb : Inserted on the posterior lens capsule.

PHYSIOLOGICAL AND BIOCHEMICAL ASPECTS OF LENS :

The lens is an transparent structure playing main role in the focussing mechanism for vision

Their physiological aspects includes

 * Lens transparency : The significant role in maintaining outstanding clarity and
transparency of crystalline lens are due to
• Avascularity of lens
• Epithelium is single layer
• Lens capsule semipermeable in nature
• Characteristics of lens fibres
• Role of lens proteins ( aquaporin MIP26 or aquaporin 0 )
• Pump mechanism of lens
• Auto-Oxidation and high concentration of reduced glutathione.

Metabolic activities of lens

➢ lens requires a continuous supply of energy (ATP) for active transport of ions and amino
acids, maintanence of lens dehydration , and for a continuous protein and GSH synthesis.
➢ source of nutrient supply is through metabolism on chemical exchanges with the aqueous
humour , since lens is an avascular structure.
➢ Glucose metabolism is very essential for normal working of lens. The glucose from the
aqueous humour diffuses into the lens and is rapidy metabolised through Glycolytic , HMP,
Citric acid cycle and Sorbitol pathway.
➢ Respiratory quotient of lens is 1
➢ Anti-oxidant mechanism of lens has protective mechanism against oxidative damage caused
by various oxidants generated such as hydrogen peroxide, superoxide and lipid peroxide .

Accomodation : Changes in contraction of the ciliary muscles alter the focal distance of the eye,
causing nearer or future images to come into focus on the retina; this process is known as
accommodation.

CATARACT :

The word 'cataract' means waterfall, which means an abnormal aqueous flow happening in the
anterior part of the eyes.
As of today , the term cataract refers to development of any opacity in the lens or its capsule .
They may occur due to formation of opaque lens fibres or degenerative process leads to
opacification.
CLASSIFICATION :
A. Etiological classification
(I) Congenital and developmental cataract

(II) Acquired cataract

1. Senile cataract

2. Traumatic cataract

3. Complicated cataract

4. Metabolic cataract

5. Electric cataract
 6. Radiational cataract

7. Toxic cataract e.g.

* Corticosteroid induced cataract

* Copper & iron induced cataract

8. Dermatological cataract

9. Cataract associated with osseous diseases.

10. Cataract with miscellaneous syndrome

* Dystrophica myotonica

* Downs syndrome

* Lowe's syndrome

* Treacher-Collin's syndrome

B. Morphological classification

1. Capsular cataract : Involves the capsule

* Anterior capsular cataract

* Posterior capsular cataract

2. Subcapsular cataract : It involves superficial most part of cortex

* Anterior subcapsular cataract

* Posterior subscapular cataract

3. Cortical cataract : It involves major part of the cortex

4. Supranuclear cataract : It involves deeper part of cortex

5. Nuclear cataract : Involves nucleus of crystalline lens

6. Polar cataract : It involves the capsule and superficial part of the cortex in the polar
region

* Anterior polar cataract

* Posterior polar cataract.

OPACIFICATION OF LENS OR ITS CAPSULE

• CORTEX
• NUCLEUS
CLASSIFICATION OF CATARACT
ETIOLOGICAL CLASSIFICATION
➢ Congenital cataract/ developmental cataract
➢ Acquired cataract
• AGE RELATED
• TOXIC
• SYSTEMIC DISEASE
• OCULAR DISEASE
• TRAUMATIC
• RADIATIONAL
CONGENITAL CATARACT

CAUSES OF CONGENITAL CATARACT

✓ INHERITED/HEREDITARY – 1/3rd
✓ METABOLIC/INFECTIOUS – 1/3rd
✓ IDIOPATHIC – 1/3rd
• Hereditary congenital cataract – autosomal dominant inheritance
• Gene mutation associated with congenital cataract
• Most common cry G gene on chromosome 29-40%
• Connexin gene Cx46 gene on chromosome 139-25%
• AQPO GENE on chromosome 10q

METABOLIC / INFECTIOUS CAUSES

1. HYPOCALCEMIA – MATERNAL / NEONATAL
2. HYPOGLYCEMIA
3. GALACTOSEMIA
4. LOWE’S SYNDROME
5. TORCH INFECTION
CONGENITAL RUBELLA
▪ INFECTION IN 1st TRIMESTER
▪ INVOLVE FETAL NUCLEUS
▪ PEARLY IN APPEARANCE
▪ LIVE VIRUSES PRESENT IN THE NUCLEUS
BLUE DOT CATARACT

✓ MOST COMMON TYPE OF CONGENITAL / DEVELOPMENTAL CATARACT

✓ IT IS ALSO KNOWN AS PUNCTATE CATARACT / CATARACT PUNCTATA CERULEA
✓ IT IS STATIONARY / NON PROGESSIVE
✓ VISUALLY INSIGNIFICANT

ZONULAR / LAMELLAR CATARACT

▪ MOST COMMON VISUALLY SIGNIFICANT CONGENITAL CATARACT

▪ IT INVOLVES FOETAL NUCLEUS
▪ RIDERS – RADIAL SPOKES OF OPACITY COMING FROM THE MAIN OPACITY ; CART WHEEL
APPEARANCE
▪ ZONULAR CATARACT IS SEEN IN HYPOPARATHYROIDISM
CATARACT PULVERULENTA

▪ POWDWERY DEPOSITS AT FETAL NUCLEUS

▪ CATARACT PULVERULENTA INVOLVING EMBRYONIC NUCLEUS

ANTERIOR POLAR CATARACT

o OPACITY LOCALIZED TO ANTERIOR POLE

o OCCURS INCONDITIONS WHERE THERE IS DELAYED FORMATION OF ANTERIOR CHAMBER -:
CORNEAL ULCER IN UTERO WHICH IS PERFORATED -: PETER’S ANOMALY
o DELAYED SEPARATION OF LENS PLACODE FROM THE SURFACE ECTODERM POSTERIOR
POLAR CATARACT
❖ ONION RING APPERANCE
❖ IT IS DUE TO PERSISTANT ATTACHMENT OF HYALOID ARTERY AT THE POSTERIOR POLE
❖ IT IS ASSOCIATED WITH MITTENDORF’S DOTS IN VITEROUS
❖ SUTURAL CATARACT
❖ THESE ARE NON PROGRESSIVE
❖ DOESN’T AFFECT THE VISION
❖ ARROR MARK – ANTERIOR ERECT Y-SHAPED
❖ CIRCLED PART – POSTERIOR INVERT Y-SHAPED

MANAGEMENT OF CONGENITAL CATARACT

▪ IN VISUALLY SIGNIFICANT CATARACT
▪ CENTRALLY LOCATED OPACITY
▪ IF DIAMETER OF THE OPACITY IS > OR = TO 3mm
▪ DENCE OPACITY
▪ RISK OF SENSORY DEPRIVATION AMBLOPIA

TIMING OF SURGERY

▪ AS EARLY AS POSSIBLE WITHIN 4 MONTHS OF AGE

▪ BECAUSE FOVEAL MATURATION / FIXATION DEVELOPS AT 4 MONTHS OF AGE
▪ IN UNILATERAL CATARACT – should operate within 6 weeks of age , because unilateral
cataract are more amblyogenic
▪ IN BILATERAL CATARACT WITHIN 8 WEEKS OF AGE

TECHNIQUE OF SURGERY

1. LENS ASPIATION ( THROUGH LIMBAL ROUTE) +PRIMARY POSTERIOR CAPSULATORY[PPL] +

ANTERIOR VITERECTOMY[AV] + IOL IMPLANTATION
2. LENSECTOMY (THROUGHPARS PLANA) + PPC +AV + ILO IMPLANTATION

IOL POWER

▪ < 2 YRS OF AGE : 20% UNDERCORRECTION

▪ 2 – 8 YRS OF AGE : 10% UNDERCORRECTION
▪ > 8 YRS OF AGE : CALCULATED IOL POWER
 IOL MATERIAL

▪ FOLDABLE ACRYLIC PC – IOL - PREFERRED

▪ PMMA (POLY METHYLMETHACRYLATE)
▪ HEPARIN COATED IOL’S - IN INFECTIOUS CAUSE - CONGENITAL RUBELLA

CLASSIFICATION OF CATARACT

ANATOMICAL CLASSIFICATION:

❖ CAPSULAR CATARACT
❖ CORTICAL CATARACT
❖ NUCLEAR CATARACT

CAPSULAR CATARACT

✓ ANTERIOR CAPSULAR CATRACT

✓ ANTERIOR SUBCAPSULAR CATARACT
✓ ANTERIOR POLAR CATRACT
✓ POSTERIOR CAPSULSULAR CATARACT
✓ POSTERIOR SUBCAPSULAR CATARACT
✓ POSTERIOR POLAR CATARACT

MANAGEMENT OF CATARACT

✓ MAHNAGEMENT OF CATARACT IS SURGERY

✓ IN SURGERY WE REMOVE THE OPACITY , WHICH MEAN REFRACTORY POWER OF THE EYE
✓ LENS CONTRIBUTE TO 1/3rd OD 1/4th OF ENTIRE REFRACTION
✓ SO, WE HAVE TO REPLACE THE REFRACTORY POWER
✓ IN ORDER TO REPLACE THE REFRACTORY POWER OF THE LENS , WE SHOULD KNOW THE
POWER OF INTRAOCULAR LENS
✓ METHOD TO CALCULATE THE IOL POWER : BIOMETERY

BIOMETERY:

➢ SRK FORMULA ( SANDERS,RETZLAFF & KRAFT FORMULA)

IOL POWER = A-0.9-2.5L - A:CONSTANT ; K:KERATOMETRY ; L:AXIAL LENGTH

➢ AXIAL LENGTH OF THE EYEBALL IS MEAUSRED USING A-SCAN

➢ HERE WE MEASURE THE DISTANCE B/W THE CORNEAL SPIKE AND RETINAL SPIKE - GIVES
AXIAL LENGTH
➢ OCULAR/ORBITAL ULTRASOUND - PROBE FEQUENCY : 8-10 mega HZ
➢ AXIAL LENGTH CAN ALSO BE MEASURED BY IOL MASTER
➢ IOL MASTER - MOST ACCURATE - IOL POWER - PC-IOL IN THE CAPSULAR BAG, TO
ACHIEVE EMMETROPIA FOR DISTANCE
➢ I mm CHANGE IN CORNEAL CURVATURE - 6D CHANGE IN IOL POWER
➢ 1mm CHANGE IN AXIAL LENGTH - 3D CHANGE IN IOL POWER
➢ THERE ARE TWO SURGICAL TECHNIQUES
- INTRACAPSULAR ; CATARACT/ LENS REMOVED WITH THE CAPSULE INTACT
 - EXTRACAPSULAR ; HALLMARK,ANTERIOR CAPSULAR LEAVING BEHIND THE
CAPSULAR BAG

STEPS

ANAESTHESIA

1. GENERAL ANAESTHESIA - FOR CHILDREN

2. LOCAL ANAESTHESIA - RETROBULBAR NERVE BLOCK , PERIBULBAR NERVE BLOCK
3. TROPICAL ANAESTHESIA - LIGNOCAINE , PAARACAINE

SCRUBBING

FOR PERIORBITAL SKIN - 10% PROVIDED IODINE EYE DROP OR 5% PROVIDED IODINE FOR 3 MIN,
BEST WAY TO PREVENT POST OPERATIVE ENDOPHTHALMITIS

✓ ECCE ( extra capsular cataract extraction)

✓ Tenon’s capsule & conjunctiva - inverted at limbus
✓ In order to make limbal incision , peritomy is done
✓ After peritomy , limbal incision is given
✓ SICS ( small incision cataract surgery)
✓ Sclerocorneal tunnel , hallmark of of SICS , self sealing incision

Phacoemulsification

Anterior chamber entery - after incision ,instrument is with in the ac entery

Irrigating fluid - normal saline , ringer’s lactate , BSS plus

Viscoelastics - HPMC , SODIUM HYALURONATE , CHONDROITIN SULPHATE

IOL IMPLANTATION STEPS

1. CAPSULORRHEXIS
2. NUCLEAR FRAGMENTATION
3. CORNEAL INCLUSION

MOST COMMON COMPLICATION POST OPERATIVELY , ALSO KNOWN AS AFTER CATARACT.

✓ TWO TYPES OF PCO - ELSCHNIG’S PEARLS , SOMMERING’S RING

✓ MANAGEMENT OF PCO - POSTERIOR CAPSULATORY.

ACQUIRED CATARACT
Congenital and Developmental cataract → Opaque lens fibres are produced

Acquired cataract → Opacification occurs due to degeneration of the already formed normal fibres.

Types of Acquired cataract:

Senile cataract
Traumatic cataract

Complicated cataract

Metabolic cataract

Electric cataract

Radiational cataract

Toxic cataract

Dermatogenic cataract

Cataract associated with osseous diseases

Cataract with miscellaneous syndromes

Age Related Cataract:

Commonest type, >50yrs, Affects both the sexes equally.

Usually Bilateral but one eye is affected earlier than the other.

Two forms

cortical (soft cataract)

nuclear (hard cataract)

Cortical senile cataract may start as cuneiform or cupuliform - posterior subcapsular (PSC) cataract.

Frequency: cuneiform 70%, nuclear 25% and cupuliform 5%.

Risk factors:

Age

Sex

Heredity

UV irradiations

Dietary factors

Dehydrational crisis

Smoking

Pre senile cataract:

Similar to senile cataract, <50yrs

Causes: Heriditary, Diabetes mellitus, Myotonic dystrophy (Christmas tree cataract), Atopic
dermatitis.

Mechanism of loss of transparency:

1. Cortical senile cataract:

2. Nuclear senile cataract:

Intensification of the age-related nuclear sclerosis associated with dehydration and compaction of
the nucleus.

Water insoluble proteins ↑, May or may not be associated deposition of pigment urochrome and/or
melanin.

Stages of maturation:

A. Maturation of the cortical type of senile cataract

1. Stage of lamellar separation → demarcation of cortical fibres owing to their separation by fluid.

2. Stage of incipient cataract: Opacities with clear areas between.

a) Cuneiform senile cortical cataract.

Wedge-shaped, extend from equator towards centre.

First seen in the lower nasal quadrant, present both in anterior and posterior cortex, apices slowly
progress towards the pupil.

On oblique illumination these present a typical radial spoke-like pattern of

greyish white opacities.

On distant direct ophthalmoscopy, these opacities appear as dark lines against the red fundal glow.

b) Cupuliform senile cortical cataract.

Saucer-shaped opacity, just below the capsule, usually in the central part of posterior cortex, which
gradually extends outwards.

Demarcation between the cataract and the surrounding clear cortex.

Early loss of visual acuity.

3. Immature senile cataract (ISC): Opacification progresses further.

The lens appears greyish white, but clear cortex is still present and so iris shadow is visible.

Lens may become swollen due to continued hydration (intumescent cataract).

Anterior chamber becomes shallow.

4. Mature senile cataract (MSC) (Ripe cataract): Opacification becomes complete.

Lens becomes pearly white in colour.

5. Hypermature senile cataract (HMSC): When the mature cataract is left in situ, the stage of
hypermaturity sets in.

Two forms:

a. Morgagnian hypermature cataract.

Whole cortex liquefies; lens is converted into a bag of milky fluid.

Small brownish nucleus settles at the bottom, altering its position with change in the position of the
head.

Calcium deposits may also be seen on the lens capsule.

b. Sclerotic type hypermature cataract.

Cortex becomes disintegrated; lens becomes shrunken due to leakage of water.

Anterior capsule is wrinkled and thickened due to proliferation of anterior cells.

Dense white capsular cataract may be formed in the pupillary area.

Anterior chamber becomes deep and iris becomes tremulous (iridodonesis).

B. Maturation of nuclear senile cataract

Progressive nuclear sclerotic process renders the lens inelastic and hard, decreases its ability to
accommodate and obstructs the light rays.

These changes begin centrally and spread slowly peripherally almost up to the capsule.

The nucleus may become diffusely cloudy (greyish) or tinted (yellow to black) due to deposition of
pigments.

Clinical features:

Symptoms:

1. Glare

2. Uniocular polyopia (doubling or trebling of objects)

3. Coloured halos
4. Black spots in front of eyes

5. Image blur, distortion of images and misty vision

6. Deterioration of vision

As opacification progresses, vision steadily diminishes, until only perception of light and accurate
projection of light rays remains.

Signs:
Differential diagnosis:

1. Immature senile cataract (ISC) and nuclear sclerosis.

2. Mature senile cataract and leukocoria.

Complications:

❖ Phacoanaphylactic uveitis
❖ Lens induced Glaucoma
❖ Phacomorphic glaucoma
❖ Phacolytic glaucoma
❖ Phacotopic glaucoma
❖ Subluxation or dislocation of lens.
1. TRAUMATIC CATARACT
Occurs due to – (a) direct effects of the mechanical injury of
the lens
(b) imbibition of aqueous humour
Subtypes [Link] shapes:
• Discrete subepithelial opacities- most commonly seen
• Early rosette(punctate) cataract – feathery lines of opacities along the star shaped suture
lines – in posterior cortex
• Late rosette cataract – posterior cortex- 1 to 2 years after-sutural extentions shorter and
compact
• Total(diffuse) concussion cataract
• Early maturation of senile cataract – blunt trauma
• Traumatic zonular cataract- rare

2. METABOLIC CATARACT
Cause: [Link] disorders
[Link] abnormalities
• DIABETIC CATARACT:

TRUE DIABETIC CATARACT:

✓ Also called snowstorm or snowflake cataract

✓ Occurance- young adults
✓ Osmotic overhydration of lens-accumulation of sorbitol-metabolism of glucose
by aldose reductase(NADPH+)
✓ Initially large [Link] fluid vacuoles- under ant $ posterior capsule- later occupied
by characteristic opacity in the cortex

SENILE CATARACT IN DIABETICS:

✓ Early appearance
✓ Rapid progression
• GALACTOSAEMIC CATARACT:
✓ Galactosaemia- inborn error in metabolism
✓ Two types - Classical(deficieny of GPUT)
Deficiency of galactokinase
✓ Bilateral oil droplet like opacity
✓ Condition can b reversed –diagnosed early- milk n related products stopped

• HYPOCALCAEMIC (tenanic) CATARACT:

✓ parathyroid tetany due to-atrophy
-removal (thyroidectomy)
✓ two forms small discrete white flecks-in cortex
thin opacified lamella- deep in cortex-seen in infants(zonular
cataract)

• CATARACT DUE TO ERROR OF COPPER METABOLISM (WILSON’S DISEASE)

 ✓ Sunflower cataract- yellowish brown dots- deposition of Cu2O –in ant. Lens
capsule £ subcapsular cortex-in stellate pattern
✓ Kayser-Fleischer ring(KF ring)- golden ring – deposition of copper- peripheral
descemet’s membrane.

• CATARACT IN INBORN ERROR IN Aacid METABOLISM (LOWE’S SYNDROME)

✓ It is an oculo- cerebral-renal syndrome
✓ Ocular abnormalities- congenital cataract-glaucoma-blue sclera
✓ Systemic abnormalities-mental retardation-dwarfism-osteomalacia-muscular
hypotonia-frontal prominence
• DOWN’S SYNDROME: punctate subcapsular cataract

[Link] CATARACT

• Opacification of lens secondary to any other intraocular disease

• Etiology: lens (opacification)
(intraocular fluids)

Nutrition disturbed circulation/

inflammatory toxins

• Conditions giving rise to complicated cataract:

Inflammatory conditions:

▪ anterior uveitis
▪ Endophthalmitis
▪ Uveal inflammation
▪ hypopyon corneal ulcer
✓ Degenerative conditions: retinitis pigmentosa

Myopic chorioretinal

Degeneration

✓ Retinal detachment
✓ Glaucoma(primary /secondary): raised IOP-embarrassment to the intraocular
circulation- opacification

Intraocular tumors:

▪ retinoblastoma
▪ Melanoma

• Clinical features: posterior subcapsular cortical cataract – irregular – variable density

✓ Breadcrumb appearance
✓ Polychromatic lustre(rainbow cataract)
✓ Diffuse yellow haze
 ✓ Chalky white/dirty white (entire lens)
✓ Calcium deposits
• Drug induced cataract:
✓ Corticosteroid induced cataract: children are more susceptible- patient should be
regulary examined- intermittent regimen prefferd- steroids substituted by
NSAIDs.
✓ Miotics induced cataract: (anterior subcapsular granular cataract)
✓ Other drug induced cataract-amiodarone-chlorpromazine-busulphan-allopurinol

[Link] CATARACT:

• INFRARED(HEAT) CATARACT:(glass blower’s / glass worker’s cataract) glass workers-

prolonged exposure to IR radiations- discoid posterior subcapsular opacity – true
exfoliation of anterior capsule
• IRRADIATIONAL CATARACT:(X rays, gamma rays, neutrons) – latent period (6mnths) –
common in technicians, patient on treatment for malignancies, atomic energy plant
workers
• UV RADIATION CATARACT

5. MANAGEMENT IN ADULTS:

( NON SURGICAL MANAGEMENT)

• TREATMENT OF CAUSE OF CATARACT

[Link] of diabetis mellitus
[Link] of cataractogenic drugs
[Link] of irradiation
[Link] treatment of ocular diseases
• MEASURES TO DELAY PROGRESSION:
✓ Iodide salts of Ca and K(topical)-to delay progression
✓ Vitamin E
✓ Aspirin
• TO IMPROVE VISION IN THE PRESENCE OF INCIPIENT AND IMMATURE CATARACT:
✓ Use of glasses
✓ Arrangement of illumination- in peripheral opacities
✓ Use of dark goggles – central opacities
✓ Mydriatics

(SURGICAL MANAGEMENT)

• INTRACAPSULAR CATARACT EXTRACTION:

Whole cataractous lens – along with capsule is removed

• EXTRACAPSULAR CATARACT EXTRACTION:

Major portion of anterior capsule with epithelim- nucleus-cortex- removed- and
posterior capsule is left intact.
 Surgical management of cataract

It involves two processes.

• Extraction of cataractous lens

• IOL implantation

TYPES

Intracapsular Extracapsular

• Lens/cataract is removed with the • Cataract is removed leaving behind

the capsular bag
Capsule intact.
• Obsolete • Widely practised nowadays
• Only indication : dislocation of • Hallmark: anterior capsulotomy
lens
• Techniques: • Techniques:
ICCE (Intracapsular cataract ECCE (extracapsular cataract
extraction) extraction)
SICS (Small incision cataract surgery)
Phacoemulsification
FLACS (femtosecond laser assisted
cataract surgery)

Preoperative meditations & Preparation (Common for all)

• Consent
• Scrub bath, care of hair & marking of the eye
• Preoperative antibiotics & disinfectants
To prevent post op endophthalmitis
Topical antibiotics - Moxifloxacin - QID x 3 days and every 15 mins for 2 hours before
surgery.
Povidone Iodine - 10% paint the lids
Povidone Iodine - 5% Eye Drops onto the conjunctival sac for 3 minutes
• Lower the IOP (IV mannitol or acetaminophen)
• Mydriasis
Anaesthesia
• General anaesthesia - Children and non-cooperative pts
• Local anaesthesia - retrobulbar nerve block / peribulbar nerve block
Composition: Lignocaine (Short acting) + Bupivacaine (Log acting) + Hyaluronidase ±
Adrenaline
• Topical anaesthesia - paracaine lignocaine on cornea only for phaco through corneal incision
– in addition Intraoperatively supplement 1% preservative free lignocaine intracamerally
(Into AC)

STEPS FOR INTRACAPSULAR EXTRACTION

STEPS:
Steps
▪ Superior rectus (bridle) suture - To fix the in downward gaze
▪ Conjunctival flap (fornix based) - to expose the limbus.
▪ Partial thickness groove/gifter is made through about 2/3rd depth of anterior limbal area
▪ Corneoscleral section
▪ Iridectomy using this forceps and de wecker’s scissors
▪ Lens delivery methods
• Smith Indian method - Lens is deliver with tumbling technique
• Cryoextraction :

Cryoprobe on the ant surf of lens

Freezing

Creates adhesion between lens and probe

Zonules ruptured

Lens is extracted by sliding movts

• Capsule forceps method - Arruga’s capsule holding forceps into

• Irisophake method - obsolete
• Wire vectis method

▪ Formation of AC
▪ Implementation of AC IOL
▪ Closure of incision done with 5-7 interrupted suture
▪ Conjunctival flap is reposited subconjuctival injection of dexamethasone and gentamicin 0.5
ml
▪ Patching of eye - with pad + sticking plaster/ bandage

STEPS FOR EXTRACAPSULAR EXTRACTIONS

▪ Superior rectus suture
▪ Incision:
Peritomy- conjunctiva is opened for ECCE and SICS
ECCE: 8 to 9 mm medium sized limbal incision is done.

SICS: 6 to 7 mm incision
Self sealing sclerocorneal tunnel is made
Steps:
External scleral incision
↓
Sclerocorneal tunnel
↓
Internal corneal incision
 PHACOEMULSIFICATION: 3.2 to 3.5 mm small incision- peripheral clear corneal incision
(closed corneal incision) self sealing

▪ Entry into anterior chamber

AC is maintained by irrigating solution - normal saline/RL/BSS(Balanced salt solution plus
glutathione)
Or by viscoelastics - HPMC hydroxypropyl methyl cellulose, sodium hyaluronate, chondroitin
sulfate
▪ Anterior capsulotomy
Trypan blue - used to stain Anterior capsule capsulotomy is done by following techniques.
➢ Linear capsulotomy
➢ Can opener technique
➢ Continuous circular capsulorrhexis
• Removal of cataractous lens
ECCE:
Hydrodissection⁕ (separation of capsule)
↓
Bring out the nucleus as whole
SICS:
Hydrodissection⁕
↓
Hydrodelineation (separating the nucleus & cortex)
↓
Nucleus delivery
↓
Cortex aspiration
PHACOEMULSIFICATION:
Nuclear fragmentation using ultrasound energy
↓
Phaco probe with titanium needle vibrate @ 20000 Hz
↓
 Lens breaks down into pieces
↓
Aspirate the nuclear fragments
↓
Aspirate the cortex

• Implantation of posterior chamber IOL

In ECCE & SICS rigid IOL is placed
In phaco foldable IOL is used
• Removal of viscoelastic
• Reform the anterior chamber with normal saline or air bubble
• Closure of incision
ECCE- Incision is closed with sutures using 10-0 monofilament nylon (Interrupted or contin.
suture)
SICS & Phacoemulsification do not require suturing. They are self sealing incision.
• Conjunctival flap reposition
• Subconjunctival injection of dexamethasone 0.25 ml + gentanicin 0.5 ml is given.
• Patching of eye - with pad + sticking plaster/ bandage
Note:⁕ hydrodissection is done by injecting fluid below the capsule, this force will cleave the
cortex and capsule.

FLACS (FEMTOSECOND LASER ASSISTED CATARACT SURGERY)

It is based on the principle of photodisruption
Steps:
Laser assisted
Flattening of cornea
↓
Capsulorrhexis
↓
Nuclear fragmentation
↓
Corneal incision
Remaning steps are completed manually by the surgeon.

SURGICAL TECHNIQUES EMPLOYED FOR CHILDHOOD CATARACT

TWO TYPES
➢ Irrigation and aspiration of lens matter
➢ Lensectomy

Irrigation and aspiration of lens matter

Superior rectus suture

↓
 Peritomy

Sclerocorneal tunnel is made with the incision of 3-4 mm

Entry into anterior chamber

Anterior capsulorrhexis

Irrigation and aspiration of lens matter by either of the technique

➢ Manually with a two way irrigation and aspiration simcoe cannula

➢ With a phacoprobe
↓

Posterior capsulorrhexis

Anterior vitrectomy

Implantation of IOL (Foldable acrylic IOL is preferred in children)

Removal of viscoelastic material

Intracameral antibiotics (Preservative free vancomycin or moxifloxacin)

Wound closure (Eventhough well-constructed corneoscleral tunnel does not require closure in
adults, it is mandatory to close the wound in children to avoid post-op astigmatism). Absorbable
suture 10-0 vicryl is used.

Note: Steps in parenthesis are measures taken to prevent the formation of after cataract, the
incidence of which is very high in children

LENSECTOMY

Most of the lens including the anterior and posterior capsule along with anterior vitreous is removed
with the help of vitreous cutter.

Done in children less than 2yrs of age in which primary IOL implantation is not planned.
Done under GA.

Approach either pars plana or limbal approach

In pars plana approach

Lens is punctated at its equator

Stirred with the help of a Ziegler’s or any other needle-knife introduced through the sclera and ciliary
body, from a point about 3.5–4 mm behind the limbus

The cutter (ocutome) of the vitrectomy machine is introduced after enlarging the sclerotomy

Lensectomy along with anterior vitrectomy is completed using cutting, irrigation and aspiration
mechanisms.

The aim of modern lensectomy is to leave in situ a peripheral rim of capsule as an alternative to
complete lensectomy.

Secondary IOL implantation is done later.

INTRAOCULAR LENS IMPLANTATION

• First implanted by Sir Harold Ridley in 1949
Indications:

• In cataract surgery
• In refractive surgeries
Sites:
• Bag supported – best location
• Sulcus supported
• Iris supported
• Angle supported- in anterior chamber
• Types:
• Based on method of fixation in eye
1. Anterior chamber IOL
❖ angle supported
❖ higher incidence of bullous keratopathy
❖ Kelmann multiflex most commonly used type
❖ used only when PCIOL is contraindicated

2. Iris supported lens

❖ Support in iris with suture,loops or claws
❖ High incidence of postoperative problems
❖ Eg:Singh and Wrists iris claw lens
3. Posterior chamber IOL – commonly used type; supported and fixed as below
In capsular bad fixation

Ideal method

E.g.: modified C and Quadri loops

In ciliary sulcus fixation

In absence of intact capsular bag

In scleral fixation

In absence of capsular support

Types: trans scleral suture fixation

Trans scleral suture less fixation

In retro iris fixation

• Based on material of manufacturing

Rigid IOL.

Made entirely from PMMA

Foldable IOL

Through small incision of 2 to 3mm after phacoemulsification

Made of silicone,acrylic,hydrogel and collamer

Implant with help of IOL injector

Rollable IOL

Ultrathin IOL

1 mm incision in MCIS technique

Made of hydrogel

• Based on focusing ability of IOL

[Link] IOL :

➢ Most commonly used type

➢ Make patient emmetropic/hypermetropic/myopic

[Link] IOL:

➢ Separate optics for near and distant vision

➢ Known as simultaneous vision lens
➢ 2 types-refractive and diffractive types
 ➢ Pseudoaccomadative lens

[Link] IOL:

➢ Exhibit anterior movement to improve near vision

Available types- crystalens on optic shift principle

Synchrony lens on dual optic mechanism

• Aphakic versus phakic refractive lens

a. Aphakic lens after lens extraction+phakic lens to correct refractive errors
b. Also called implantable collamer lens
• Special function IOL
I. Toric IOLs - to correct astigmatism
II. Aspheric IOLs - to reduce spherical aberrations
III. Aniridian IOLs – cosmetically to cover defects of aniridia and partial iris loss during
trauma.
• Calculation of IOL power:
Most commonly used method SRK(Sanderr Retzaff Kraff)method
P=A-2.5L-0.9K
▪ P is the power of IOL,
▪ A is a constant which is specific for each lens type.
▪ L is the axial length of the eyeball in mm, which is determined by A-scan ultrasonography.
▪ K is average corneal curvature, which is determined by keratometry

• Equipment for biometry

A–scan ultrasonic biometer.

Optical biometers

Based on the principle of partial coherence interferometry(PCI). Quick and more accurate device

Commercially available optical biometers are:

❖ IOL Master Tm (Zeiss Humphrey system) and

❖ Lenstar.

• Techniques of IOL implantation:

➢ Anterior chamber IOL implantation
▪ Lens extraction
▪ Constriction of pupils by injecting miotics
▪ Fill anterior chamber with 2% methylcellulose or healon
▪ Hold IOL with forceps
 ▪ Slid into anterior chamber
▪ Inferior haptic pushed into inferior angle at 6o clk position
▪ Upper haptic pushed to engage into upper angle

➢ Posterior chamber IOL implantation

• Implantation of rigid IOL:
▪ Implantation after conventional ECCE and SICS
▪ Enlarge incision through phacoemulsification
▪ Fill anterior chamber and capsular bag with 2% methylcellulose /1% sodium hyaluonate
▪ Hold PCIOL with IOL forceps
▪ Insert the inferior haptic and optic of IOL gently at 6 o clk positon
▪ Engage upper haptic at upper capsular bag behind iris.
• Implantation of foldable IOL
▪ Using folder forceps or foldable IOL injector
• Scleral fixation of posterior chamber IOL
▪ Fixated to sclera in ciliary sulcus with help of sutures or biological glue.
POSTOPERATIVE MANAGEMENT AFTER CATARACT OPERATION:
▪ Ask to lie quietly upon the back for about 2–3 hours
▪ Ask to take nil orally.
▪ Diclofenac sodium for postoperative pain
▪ Next morning bandage/eye patch is removed
▪ Inspect for any postoperative complication.
▪ Antibiotic eye drops QID for 10-14 days.
▪ Topical steroids (Prednisolone) eye drops 3 to 4times a day for 6–8 weeks.
▪ Topical ketorolac or other NSAID eye drops 2 to 3 times/ day for 4 weeks
▪ Topical timolol (0.5%) eye drops BD for about 7–10 days.
▪ Topical cycloplegic-mydriatic, e.g., homatropine eye drops OD for 10–14 days.

1. Cataract surgery complications and management?

ANS: Performed by: Extra capsular cataract extraction

COMPLICATIONS:
 1. PREOPERATIVE
2. OPERATIVE
3. EARLY POST OP
4. LATE POST OP
5. IOL COMPLICATIONS PRE OPERATIVE COMPLICATIONS

ANXIETY ALLERGIC CONJUNCTIVITIS COMPLICATION TO LOCAL

ANAESTHETIC
• Fear Cause: preoperative
• Apprehension topical antibiotic drug. 1. Retro bulbar hemorrhage
Rx: Rx: 2. Oculocardiac reflex
Postpone the op for 2 3. Perforation of globe
ALPRAZOLAM
4. Subconjunctival hemorrhage
(Anxiolytic drug) days.
5. Spontaneous dislocation of lens
•

1. RETROBULBAR HAEMORRHAGE :

Cause: due to retro bulbar block.

Rx: Immediate pressure bandage after instilling one drop of 2% pilocarpine and
postponement of operation for a week.

2. OCULOCARDIAC REFLEX:

Clinical features: Bradycardia or cardiac arrhythmia.

Rx: Intravenous injection of atropine.

3. PERFORATION OF GLOBE :

Rx: gentle injection with blunt tipped needle and bulbar anaesthesia may be preferred.

4. SUBCONJUNCTIVAL HAEMORRHAGE:

Minor complication – no treatment

5. SPONTANEOUS DISLOCATION OF LENS :

Cause: during vigorous ocular massage after retro bulbar block.

Rx: operation should be postponed

• should be removed through limbal route – anterior chamber

• Should be removed through pars plana vitrectomy.

OPERATIVE COMPLICATIONS

1. SUPERIOR RECTUS MUSCLE LACERATION:

Cause: While applying bridle suture in Conventional ECCE and SICS

 Rx: No treatment is required

2. EXCESSIVE BLEEDING:

Cause: During scleral incision and conjunctival flap in ECCE and SICS

Rx: Bleeding vessels should be cauterized

3. INCISION RELATED COMPLICATION :

➢ CONVENTIONAL ECCE : due to irregular incision leading to coaptation of wound

➢ MANUAL SICS AND PHACOEMULSIFICATION :
• Due to self-sealing tunnel incision
• Button holing of anterior wall of tunnel
• Premature entry into the anterior chamber
• Scleral disinsertion

4. INJURY TO CORNEA, IRIS, LENS:

Cause: Due to entry of anterior chamber by sharp tipped instruments

Rx: Gentle handling reduces injuries

5. IRIS INJURY AND IRIDODIALYSIS:

Cause: during intra ocular manipulation

5. COMPLICATIONS RELATED TO ANTERIOR CAPSULORRHEXIS:

• Escaping capsulorrhexis
• Small capsulorrhexis
• Very large capsulorrhexis
• Eccentric capsulorrhexis

6. POSTERIOR CAPSULAR RUPTURE:

Cause: during forceful hydro dissection, cortex aspiration

7. ZONULAR DEHISCENCE:
Cause: During nuclear prolapse in manual SICS

8. VITREOUS PROLAPSE AND LOSE:

Most dangerous complication
Rx:
➢ To decrease vitreous volume: Preoperative use of 20% mannitol
➢ To decrease aqueous volume :Preoperatively acetazolamide 500mg
➢ To decrease orbital volume : Adequate orbital massage and orbital compression
➢ Better ocular akinesia and anaesthesia : decrease pressure from eye muscles
➢ Minimizing the external pressure on eye ball : by not using eye speculum
➢ Use of Flieringa ring : prevent collapse of sclera
➢ IOP is high: posterior sclerotomy with drainage.
 9. NUCLEUS DROP INTO THE VITREOUS CAVITY:
Cause: frequently with phacoemulsification
Rx: anterior vitrectomy and cortical clean up

10. POSTERIOR LOSS OF LENS FRAGMENTS:

Cause: during phacoemulsification which results in glaucoma.
Rx: pars plana vitrectomy and removal of nuclear fragments.

11. EXPULSIVE CHOROIDAL HAEMORRHAGE:

Cause: occurs in hypotensive and atherosclerotic patients.
Incidence: high in ICCE and conventional ECCE
Treatment: equatorial sclerotomy

EARLY POST OPERATIVE COMPLICATIONS

1. HYPHAEMA :
Occur: Collection of blood during ECCE and SICS
Treatment: No treatment is required,
If associated with increases IOP, lowered by acetazolamide.

2. IRIS PROLAPSE:
Cause: due to inadequate suturing of incision.
Treatment: abscission and suturing of wound.

3. STRIATE KERATOPATHY:
Occur: due to endothelial damage.
Rx: instillation of hypertonic saline drops

4. FLAT ANTERIOR CHAMBER:

Occur: due to wound leak, ciliochoroidal detachment and pupil block

5. POST OP ANTERIOR UVEITIS:

Cause: Induced by instrumental trauma
Mx: topical steroids NSAIDS, cycloplegics

6. TOXIC ANTERIOR SEGMENT SYNDROME

7. BACTERIAL ENDOPHTHALMITIS:
Cause: Infection and instrumentation
C/F: Ocular pain, diminished vision, corneal edema
Mx: Antibiotic therapy and steroid therapy

LATE POST OPERATIVE COMPLICATIONS

1. CYSTOID MACULAR EDEMA:

Collection of fluid in henles layer of macula
 On fundoscopy: Honey comb appearance seen
On fluorscein angiography: Flower petal pattern seen
Prevention: Immediate pre and post op prostaglandins eye drops should be given
Rx: Mostly spontaneous regression occurs, in case of CME with vitreous incarceration –
anterior vitrectomy with steroids and prostaglandins should be given

2. DELAYED CHRONIC POST OPERATIVE ENDOPHTHALMITIS:

Cause: Staphylococcus epidermidis
Rx: Pars plana vitrectomy and antifungal drugs

3. PSEUDOPHAKIC BULLOUS KERATOPATHY:

Cause: due to post op corneal edema
Rx: Penetrating keratoplasty

4. RETINAL DETACHMENT:
Cause: Due to ICCE than ECCE and IOL implantation

5. EPITHELIAL INGROWTH:
Cause: Due to defect in the incision, the epithelial cells lines the cornea back and
trabecular meshwork leading to intractable glaucoma

6. FIBROUS DOWNGROWTH:
Cause: Due to imperfect wound opposition leading to secondary glaucoma,
disorganization of anterior segment and phthisis bulbi
7. AFTER CATARACT:
Types: Residual opaque and Proliferative type

Clinical types:

• Posterior capsular opacification

• Dense membranous
• Soemmerings ring
• Elschnigh pearls

Rx: YAG –laser capsulotomy, surgical membranectomy

8. GLAUCOMA- IN- APHAKIA AND PSEUDOPHAKIA

IOL RELATED COMPLICATIONS

1. COMPLICATIONS LIKE

• Cystoid macular edema

• Uveitis due to IOL
• Secondary glaucoma implantation
• Corneal endothelial damage
• UGH syndrome
 2. MALPOSITIONS OF IOL:

• SUNSET syndrome
• SUNRISE syndrome
• lost lens syndrome
• windshield wiper syndrome

3. PUPILLARY CAPTURE OF IOL:

Cause: proliferation of lens fibers

4. TOXIC ANTERIOR SEGMEN SYNDROME:

Cause: ethylene gas

C/F: violent inflammation

Displacement of lens

• Lens is displaced from its normal position

TYPES:

Clinico-Etiological Types

1) Congenital types

• Simple ectopia lentis – autosomal dominant inheritance

• Ectopia lentis et papillae – autosomal recessive inheritance with slit shaped pupil
• Ectopia lentis with systemic abnormalities – Marfan’s syndrome, Homocystinuria,
Ehlers-Danlos, Weil-Marchesani, Homocystinuria, Sulphite oxidase deficiency,
hyperlysinemia, Stickler syndrome.

2) Traumatic displacement of eyes

• Commonly due to concussion

• Couching-iatrogenic posterior dislocation of lens

3) Consecutive or spontaneous development

• Hypermature cataract, buphthalmos, high myopia, staphyloma, intraocular tumours,

uveitis.

Topographical Types

1) Subluxation- partial displacement of lens and it remains behind the pupil.

Etiology- Partial or unequal stretching of zonules

Clinical features-

• Defective vision
• Uniocular diplopia
• Iridodonesis
• Phacodonesis
 • Anterior chamber- deep and irregular
• Edge of subluxated lens – dark crescent on direct ophalmoscopy
• Retinoscopy reveals hypermetropia in aphakic area and myopia in phakic area

Complications – Complete dislocation, Cataract, Uveitis, Secondary glaucoma.

Management: Spectacles or Contact lens, Surgery, Lensectomy.

2) Dislocation or luxation of the lens

• All the zonules are severed from the lens.

• The dislocated lens may be seen in the anterior chamber or posterior chamber,
incarcerated into the pupil, in the sub-retinal space, sub sclera space.
• Posterior dislocation : Lens in vitreous cavity
• Anterior dislocation: Looks like an oil drop in the aqueous humor.

Complications: Uveitis and secondary glaucoma

Management: Immediate removal of lens if dislocated incarcerated in the pupil.

In posterior dislocation – removal only if it causes glaucoma or uveitis.

Congenital Anomalies of Lens

• Coloboma of Lens: Hereditary disorder. Seen as a notch in the lower quadrant of the
equator.
• Congenital Ectopia Lentis
• Lenticonus : Cone shaped elevation of anterior pole or posterior pole of lens.
• Congenital Cataract
• Microspherophakia : Spherical lens and small in size. Occurs in Marfan’s or Weil-
Marchesani syndrome.

GLAUCOMA: AN INTRODUCTION

TOPIC OUTLINE: We will discuss about

• Applied anatomy
• Applied physiology
i) Constituents
ii) Formation
iii) Drainage mechanisms
iv) Factors involved in maintenance of IOP

APPLIED ANATOMY:
The principal ocular structures concerned with glaucoma are:

• Ciliary body
• Angle of anterior chamber
• Aqueous outflow system

CILIARY BODY

In cross-section, it is triangular in shape.

Outer side of the triangle lies against the sclera.

Inner side of the triangle is divided into two parts:

a) Anterior part has several finger like projections called ciliary processes
b) Posterior part is smooth and is called pars plana

Ciliary process:

• They are finger like projections

• They are lined by two layers of epithelial cells
• The core of the process has blood vessels and loose connective tissue
• The site produces aqueous humour

ANGLE OF ANTERIOR CHAMBER

• Formed by
i) Root of iris
ii) Part of ciliary body
iii) Scleral spur
iv) Trabecular meshwork
v) Schwalbe’s line(prominent end of Descemet’s membrane)
• The angle varies in every individual
• Visualised by gonioscopic examination
ANGLE OUTFLOW SYSTEM

It constitutes of:

1) Trabecular meshwork
2) Schlemm’s canal
3) Collector channels
4) Aqueous veins
5) Episcleral veins

Trabecular meshwork: Sieve like structure which is composed of

• Uveal meshwork
• Corneoscleral meshwork
• Juxtacanalicular meshwork

Schlemm’s canal: endothelial lined oval channel.

It has giant vacuoles and aqueous valves on the inner wall.

Outer wall has openings of collector channels.

Collector channels: Intrascleral aqueous vessels which leave the Sclemm’s canal and terminate in
episcleral veins by two systems.

• Direct system
• Indirect system

PHYSIOLOGY

Aqueous humour is a clear watery fluid.

Functions:

1) Maintain IOP
2) Metabolic and nutritional role
3) Maintain optical transparency
4) Clearing function-takes the place of lymph absent in the eyeball

Composition:

1) Water-99.9%
2) Solid-0.1%
 a) Colloidal protein
b) Amino acids
c) Non-colloidal solids-Glucose, urea, Na+, K+etc
3) O2

Formation: derived from plasma within the capillary network of ciliary processes. It is formed by:

1) Passive diffusion of ions

2) Ultrafiltration
3) Active secretion

Drainage of Aqueous humour: It can be drained by two methods:

1) Trabecular outflow: Trabecular meshwork is the main outlet for aqueous
from the anterior chamber. Free flow of aqueous occurs from trabecular meshwork up to inner wall
of Schlemm’s canal(SC) which appears to provide some resistance to outflow
Mechanisms:

• Passive filter: There are many theories but the vacuolation theory is the most accepted till
date.
▪ Vacuolation theory: it says that transcellular spaces exist in the endothelial cells forming
the inner walls of SC open as a system of vacuoles which transport the aqueous into the
SC.
• Active pump mechanism: It is said to be a biomechanical pump.

Outflow pump system

Cardiac diastole

IOP decreases due to decreased

blood flow in the choroidal plexus

Negative pressure is created

inside the SC

Trabecular network is retracted

inward and opens the aqueous
valves

Aqueous flows into the SC

Collector Channels

2) Uveoscleral outflow: Episcleral veins

Aqueous in posterior chamber

Uveal trabecular meshwork

Ciliary body

Suprachoroidal space

Venous circulation of ciliary body,

choroid and sclera
Maintenance of Intraocular pressure(IOP):

Normal IOP=16+2.5 mmHg

The normal level of IOP is essentially maintained by a dynamic equilibrium between the formation
and outflow of the aqueous humour.

Local factors: General factors:

1) Rate of aqueous 1) Heredity
formation 2) Age
2) Resistance to aqueous 3) Sex
outflow 4) Postural changes
3) Increased episcleral 5) Blood pressure
venous pressure 6) Osmotic pressure
4) Dilation of pupils 7) Exercise
5) Refractive errors 8) Seasonal variations
 Glaucoma
Definition
• Progressive optic neuropathy
• Characteristic optic disk changes
• Irreversible visual filed defects
• With or without increase in IOP

Aqueous humor
Production: non pigmented epithelium of ciliary process

• 70% - active secretion

• 20% - ultra filtration
• 10% - osmosis
Secretion: posterior chamber → pupil → anterior chamber → angle of anterior chamber
(iridocorneal angle) → 90% - trabecular mesh work, 10%- uveoscleral outflow.
Normal IOP – 11 to 21 mm Hg.

Priamary open angle glaucoma

• Aka chronic simple glaucoma
• Usually bilateral and symmetric

Risk factros:
• High IOP
• Family history – gene mutations like myocitin C, optineurin, WD repeat domain 36
• Age – 50 to 70
• Myopes
• Thin central corneal thickness
• Diabetes mellitus, smoking., hypertension
• Thyrotixicity, corticosteroid responsiveness

Pathogenesis
• Decreased outflow
• Failure of aqueous outflow pump mechanism → trabecular meshwork stiffness →
apposition of Schlem’s canal → low outflow of aqueous fluid.

Symptoms:
• Mainly asymptomatic
 • Headache, frequent changes in presbyopic glasses, delayed dark adaptation,
scotoma, loss of vision and blindness.

Signs:
1. IOP
a. >21mmHg
b. >5mmHg difference between both eyes
c. >8mmHg diurnal variation
2. Optic disc changes
a. Early changes
i. Loss of neuroretinal rim
ii. Vertically oval cup
iii. Large cup – cupping (c:d – 0.5 or above)
iv. Spinchter hemorrhage on disc margin
v. Retinal nerve fibre layer defect (wedge shaped)
b. Advanced
i. Marked cupping (0.7- 0.8)
ii. Thin neuroretinal rim
iii. Nasal shifting of blood vessels
iv. Bayonetting sign – double angulation of vessels
v. Lamellar dot sign
vi. Pulsation of retinal vessels
c. Glaucomatous optic atrophy (papillary)

Visual field defects

d. Isoptre contraction (earliest change)
e. Baring of blind spot
f. Paracentral scotoma
g. Seidel’s scotoma
h. Arcuate / Bjerrum scotoma
i. Double arcuate / ring scotoma
j. Step defects
k. Loss of central vision
l. Loss of temporal vision

Management
Investigation

• Tonometry (applanation)
• Central corneal thickness
• Gonioscopy
• Diurnal variation test
• Optic disc changes
 • Slit lamp
• Perimeter
• Nerve fibre layer analyser
• Provocation test
Medical treatment
1. Prostaglandin analogues: (PGF2alpha analogues)
• MOA – increase uveoscleral outflow
• Drugs – Latanoprost, travoprost – OD at 9pm
• Side effects – hyperpigmented eyes, hypertrichiasis, uveitis, cystoid macular
oedema, reactivation of herpetic keratitis
2. Beta- blockers
• MOA – decrease aqueous secretion
• Drugs
i. Timolol maleate – non selective, contraindicated in asthma patients
ii. Betaxolol – beta 1 selective, can be used in asthma
iii. Levobunalol – long action – once a day
iv. Carteolol – used in hyperlipidemia and atherosclerosis patients
• Side effects: blepharoconjunctivitis, nasolacrimal duct blockage, corneal
anesthesia
3. Adrenergic drugs (alpha agonists)
• Apraclonidine
i. MOA – increase trabecular outflow, decrease aqueous secretion
ii. Adverse effects – follicular conjunctivitis, mydriasis, eyelid retraction
• Brimonidine
i. MOA – increase uveoscleral outflow, decrease aqueous secretion
ii. Side effects – CNS depressant, contraindicated in children
• Epinerine hydrochloride, dipivefrin hydrochloride
i. MOA – increase aqueous outflow
4. Carbonic anhydrase inhibitors
• MOA – decrease aqueous secretion
• Contraindicated in sulfa allergies
• Drugs – acetazolamide (not given topically), brizolamide, dorzolamide (used
in children)
Surgical:

• Laser trabeculoplasty
o Argon laser, diode laser, selective laser trabeculoplasty
o Increase outflow of aqueous b collagen shrinkage on the inner asect of
meshwork
Primary angle closure disease
• Aka acute congestive glaucoma

Risk factors
• Hypermetropia
• Shallow anterior chamber
• Small cornea
• Plateau Iris
• Small eye a) Large Teks 3) Big cilliary body 4) Small diameter of cornea

PATHOGENESIS
1. Pupillary block mechanism
• Most common pathology
• predisposing factors
i. Physiological mydriasis
ii. Pharmacological mydriasis
iii. Pharmacological myosis
iv. valsalva manoeuver,
a) Mild dilation of pupil due to above mentioned predisposing factors
b) Relative pupillary block - pupil apposition lens
c) Iris Bombe - Umbrella shaped iris
d) Appositional angle closure – iridotrabeculaocorneal contact
e) Synechal angle closure – peripheral anterior synechiae
Central Deep, peripheral shallow Anterior chamber

2. Plateau Iris:

• ACG without pupillary block

• ciliary process positioned Anteriorly
• Pushes peripheral Iris anteriorly
• Closes TM flow

3. Phacomorphic Mechanism
Abnormal lens - pupillary block, Peripheral iris forward

CLASSIFICATION:
 1. Primary Angle Closure Suspect - Latent PACG
2. Primary Angle closure - Acute PACG, sub-Acute PACG, Chronic PACG
3. Primary Angle Closure Glaucoma – chronic PACG

PAC - suspect PAC PAC - Glaucoma

IOP Normal high High
Optic disc Normal Normal Cupping
Visual field Normal Normal defective
Iridotrabecular contact >270 degree >270 degree >270 degree
Peripheral anterior synechia no present present

Primary angle closure suspect

• Symptoms: no symptoms
• Signs: Eclipse sign, decreased anterior chamber depth
• Treatment: periodic follow-up, prophylactic laser iridotomy

Primary angle closure

Subacute acute
Symptoms Symptoms
• Blurred vision • pain, nausea, vomiting
• Coloured halos • rapid loss of vision
• Headache • redness, photophobia
• Recurrent attacks • lacrimation
• eyeache • coloured halos
Signs Signs
• eye not congested • lids – oedematous
• conjunctiva – chemosed, congested
• cornea – edematous, insensitive,
haze
• AC – very shallow
• Angle of AC – completely closed
• Pupil – mid dilated state, vertically
oval, non-reactive
• Optic disc – edematous, hyperemic
• IOP - high
 Treatment Treatment
• Peripheral laser iridotomy Medical
• Systemic hyperosmitics – mannitol
• Systemic CA inhibitors –
acetazolamide
• Topical antiglaucoma drugs
• Analgesics
• Anti – emitics
• Topical steroids
Surgical
• Laser peripheral iridotomy
• Trabeculectomy
• Clear lens extraction
Prophylaxis of the other eye

Primary angle closure glaucoma:

Clinical features

• IOP – high
• No congestion
• Painless
• Optic disc – glaucomatic cupping
• Gonioscopy – PAS >270 degree

Treatment

• Laser iridotomy
• Trabeculectomy
• Prophylactic treatment for the other eye

Absolute primary angle glaucoma

• Untreated PACG leads to Absolute PACG (final stage)
Clinical features

• Painful blind eye

• Preilimbal blue zone
• Capute medusa
• Cornea clear to hazy, bullous keratopathy (epithelial bullae), filamentary keratitis
(filaments)
• AC – very shallow
• Iris – atrophy
• Pupil – fixed and dilated
 • IOP high
• Visual field defects and disc changes present
• Eye – stony hard

Management

• Retrobulbar alcohol injection

• Destruction of secretory ciliary epithelial
• Enucleation of eyeball

Secondary Glaucoma
Lens induced glaucoma
1. Phacomorphic glaucoma
i. Acute secondary angle closure glaucoma
ii. Due to intumescent cataract, anterior subluxation, dislocation of lens
b. Lens pushes iris forward
i. Obliteration of angle
ii. Iridolenticular contact → pupillary block → iris bombe formation
c. Clinical features – cataractous and swollen lens
d. Treatment
i. Medical
1. Iv mannitol
2. Systemic acetazolamide
3. Topical beta blockers
ii. Surgical – laser iridotomy
iii. Cataract extraction and PCIOL placement (main treatment)

2. Phacolytic glaucoma
a. Lens protein glaucoma
b. Secondary open angle glaucoma
c. Trabecular meshwork clogged by
i. Lens proteins
ii. Macrophages
iii. Inflammatory debris
d. Seen in hypermature cataract (morgagnian)
e. Clinical features –
i. Hypermature cataract
ii. Pesudohypopyon in anct chamber
iii. AC angle is open
f. Treatment
i. Medical treatment to lower IOP
 ii. Surgery to extract lens
3. Lens particle glaucoma
a. Secondary open angle glaucoma
b. TM blocked by floating lens particles in aqueous
c. Clinical feature – lens particles in anterior chamber
d. Management:
i. Medical treatment to lower IOP
ii. Irrigation and aspiration of lens particles

Congenital / developmental glaucoma

Newborn glaucoma At birth
Infantile glaucoma Upto 3 years
Juvenile glaucoma 3 to 17 years

Pathogenesis
Trabecular disgenesis: maldevelopment of trabeculum including Iridotrabecular junction
Characterized by absence of angle recess – as in flat iris insertion, concave iris insertion

Clinical Features
1. Classical triad
a. Lacrimation – most common
b. Photophobia – 2nd common, most troublesome symptom
c. Blepharospasm
2. Cornea
a. Oedematous (1st sign) – initially epithelium, later stroma
b. Enlargement (>13mm)
c. Descemet’s membrane breaks – Haabs striae (peripheral and concentric)
3. Sclera – thin, blue
4. Anterior chamber – deep
5. Iridodonesis
6. Lens – anteroposteriorly flat, may subluxate backwords
7. Optic disc – cupping and atrophy
8. Raised IOP
9. Axial Myopia – anisometropic amblyopia

Examination
• Measure IOP – Perkins Applanation tonometer or tonopen
• Measure corneal diameter
• Slit lamp examination
• Ophthalmology
 • Gonioscopic examination

Treatment
Medical

• hyperosmotic agents
• CA inhibitors
• Beta blockers
Surgical

• Incision angle surgery

o Goniotomy
o Trabeculotomy
• Filteration surgery
o Trabeculectomy alone, or combined with trabeculotomy
• Glaucoma drainage device
Preface

Agam is a group of budding medicos, who are currently doing their under graduation in
various Medical Colleges across Tamil Nadu and Pondicherry. The group was initiated on 18th
November 2017, in the vision of uniting medicos for various social and professional causes.

We feel delighted to present you Agam Ophthalmology notes prepared by Agam Divide and
Rule 2020 Team to guide our fellow medicos to prepare for university examinations.

This is a reference work of 2017 batch medical students from various colleges. The team
took effort to refer many books and make them into simple notes. We are not the authors of the
following work. The images used in the documents are not copyrighted by us and is obtained from
various sources.

Dear readers, we request you to use this material as a reference note, or revision note, or
recall notes. Please do not learn the topics for the 1st time from this material, as this contain just the
required points, for revision.
Acknowledgement

On behalf of the team, Agam would like to thank all the doctors who taught us Ophthalmology.
Agam would like to whole heartedly appreciate and thank everyone who contributed towards the
making of this material. A special thanks to Barath Raj R, who took the responsibility of leading the
team. The following are the name list of the team who worked together, to bring out the material in
good form.

 Anchitha
 Kareeshmaa H C  Gowsigan
 [Link]  Abidivya
 Mruddula V  Nahveena
 Praveena  Saahini
 Indhumathi  Arun vidhyasagar
 Yogesh  Shobana
 Kavya kala  Manasa
 Ramya  Anupama Bhaskaran
 Aparna  [Link]
 Adithya  [Link]
 Yogesh  [Link] Raja
 Syed  Sneha
 Ragha Dharshini  Kamakshi
 Bhavik Shah  Maya sundar
 Pranesh  Arun
 Shane  Bhavik shah
 Juwain  Annapoorna
 Menaka
 Aravind Krishna
 Sudharshan
 Aparna
 Mrudhulagi
 Heera
 Anusha
 Shrilekha
 Harini
 Vignesh
 Sneha jenifer
 Ramprasad
 Shanmathi
 Puvashree
 Volume 2

 Diseases of Vitreous
 Diseases of Retina
 Neuro Ophthalmology
 Ocular motility and Strabismus
 Diseases of Eyelids
 Diseases of Lacrimal Apparatus
 Diseases of Orbit
 Ocular Injury
 VITREOUS

What You Will Learn Here?

• Anatomy of Vitreous
• Vitreous Haemorrhage
• Vitreous Detachment
• Vitreous Opacities
• Vitreous Surgeries

Anatomy of the Vitreous

Vitreous humour:

➢ Inert, transparent, jelly like structure that fills the posterior four fifth(80%) of the cavity of eye ball
➢ 4ml in volume and 4g in weight
➢ It is a fluid-like substance composed of more than 99% water.
➢ The remaining part is formed of collagen and hyaluronic acid (rigidity and viscosity).
➢ Bounded :
• anteriorly: by the lens, iris and ciliary body
• Posteriorly: by the retina and optic disc.
Vitreous body:
➢ Somewhat spherical posteriorly
➢ Cup shaped depression (patellar fossa) anteriorly
➢ The outer portion of the vitreous body is called the cortex (denser), and its surface is called the hyaloid
membrane.
➢ Cloquet’s canal runs antero-posteriorly in the center of the vitreous (site of the embryonic hyaloid artery)
➢ The strongest attachment of the vitreous is to the retina and pars plana in the area of the vitreous base.

Functions of the vitreous:

❖ Stabilizes the volume of the globe.
❖ Being a hydrophilic gel, serves optical functions
❖ Pathway for nutrients to reach the lens and retina
❖ Acts as a cushion for the retina.
 ❖ One of the optical media of the eye.

Embryology:
➢ Vitreous body (secondary vitreous) is secreted by neuroectoderm of optic cup
➢ Secondary vitreous is mesenchymal in origin
➢ Tertiary vitreous is developed from neuroectoderm in the ciliary region

Liquefaction (synchysis).

➢ Most common degenerative change in vitreous

➢ This results in the formation of fluid lacunae inside the vitreous gel.
➢ These may rupture through the cortical vitreous and cause separation of the cortical vitreous from the
inner retinal surface (posterior vitreous detachment).

Causes of liquefaction include:

➢ Age related liquefaction

➢ Degeneration
➢ Post inflammatory
➢ Trauma to vitreous
➢ Thermal effects(Diathermy, photocoagulation and cryocoagulation)
➢ Radiation effects

The patient may complain of

❖ Flashes of light (photopsia)

❖ Vitreous floaters.
❖ black dots, rings or other shapes moving in his/her field of vision (Musca volitantes).

On slit lamp biomicroscopy, synchysis is characterized by absence of normal fine fibrillar structure and visible pockets
of liquefaction associated with appearance of coarse aggregate material which moves freely in free vitreous

Vitreous Hemorrhage

Causes:
 1. Proliferative retinopathies, as diabetic retinopathy.

2. Retinal breaks.

3. Central retinal vein occlusion.

4. Trauma.

5. Blood diseases as anemia, leukemia and purpura.

6. Intraocular tumors.

VITREOUS DETACHMENT

Vitreous detachment occurs in three forms:

❖ posterior
❖ basal
❖ anterior

Posterior Vitreous Detachment

❖ occurs posterior to the vitreous base

❖ senile phenomenon

Symptoms:

❖ sudden onset of photopsiae(due to vitreoretinal adhesions and are provoked by ocular movement)
❖ floaters.
❖ ring-like opacity, Weiss ring or Fuchs ring(detached attachment of the vitreous to the edges of the optic
nerve head).

Anterior and Basal Vitreous Detachments

❖ These occur secondary to trauma and are often accompanied by vitreous haemorrhage

Complications of PVD:
❖ Retinal breaks
❖ Vitreous hemorrhage
❖ Retinal hemorrhage
❖ Cystoid maculopathy
❖ Retinal detachment

Management OF PVD:
❖ Uncomplicated PVD – no treatment
❖ Retinal tear complicating PVD – Photocoagulation
❖ Vitreous hemorrhage complicating PVD – conservative treatment, treatment of cause and Vitrectomy
❖ Retinal detachment complicating PVD – urgent treatment

VITREOUS OPACITIES:
 ➢ Vitreous is a transparent structure, any relatively non transparent structure present in it will form an opacity
and cause floaters
➢ Vitreous opacities cast a shadow on the retina and appear as black spots moving in and out of the visual
field, especially when reading.
➢ They are commonly mistaken for small flying insects, and are termed muscae volitantes or floaters.
➢ Most floaters are merely compressed cells or strands of the vitreous gel which have clumped together so
that they are less transparent than the rest of the vitreous.

They may be due to the following conditions:

1. Developmental opacities which are located in the canal of Cloquet and are remnants of the hyaloid system
2. Persistent Hyperplastic Primary Vitreous (PHPV)
3. Inflammatory Vitreous opacities:
▪ Anterior uveitis
▪ Posterior uveitis
▪ Pars plantis
▪ Pan uveitis
▪ endophthalmitis
4. Degenerative changes:
❖ Asteroid hyalosis:
• Characterized by the unilateral appearance of spherical or disc-shaped white bodies in the vitreous cavity.
• These are calcium-containing lipid complexes attached to the collagen fibrils and suspended throughout
the vitreous.
• They may be commonly seen in diabetes.
• It is unilateral in the majority of cases and affects both sexes, is asymptomatic but may make examination of
the fundus difficult with the ophthalmoscope.
• Treatment is rarely required unless vision is affected, in which situation a vitrectomy may be considered.

❖ Synchysis scintillans(Cholesterolosis bulbi):

• This degenerative condition leads to deposition of cholesterol crystals in the vitreous.
• These are also found in the anterior chamber and subretinal space.
• It affects damaged eyes which have been subjected to trauma or inflammatory disease in the past.
• The crystals are multicoloured, glittering particles which settle in the lower part of the vitreous cavity due
to gravity but can be thrown up by eye movements to form a shower of iridescence.
• The vitreous in such cases is liquefied and no treatment is indicated.

❖ Amyloid degeneration:
• Amorphous amyloid material is deposited in vitreousas a part of generalized amyloidosis
• The clinical features consist of diplopia, diminution of vision, external ophthalmoplegia, vitreous opacities,
retinal haemorrhages and exudates.
• Both eyes are involved and the vitreous becomes opaque.
• The earliest lesion originates in the wall of a retinal vessel which has a cloudy margin and this slowly
invades the vitreous body from behind forwards.
• Diagnosis is confirmed by biopsy of the conjunctiva, rectum, skin or sternal marrow.
• The vitreous opacities themselves are linear with footplate attachments to the retina and posterior surface
of the lens and this is a helpful diagnostic feature.
• Vitreous amyloidosis may be treated surgically by pars plana but the prognosis must always be guarded.
5. Red cell opacities
6. Tumor cell opacities

VITREOUS SURGERY

An abnormality leading to opacification of the vitreous body or the development of vitreoretinal scar tissue may
require vitreous surgery.

Common indications for vitreous surgery include :

• vitreous haemorrhage
• complications from diabetic retinopathy such as tractional retinal detachment
• complicated retinal detachment
• preretinal membrane fibrosis
• injury with or without an intraocular foreign body, macular hole, endophthalmitis and complications of
prior intraocular surgery.

The aims of vitreous surgery are:

• To remove any vitreous abnormalities, e.g. haemorrhage, traction bands
• To restore retinal anatomy by removal of epiretinal membranes or drainage of subretinal fluid
• To treat abnormal retinal vessels or breaks by endophotocoagulation or cryotherapy
• To provide tamponade to maintain chorioretinal apposition, internally by silicon oil and gases, or externally by
an encirclage or plomb (buckle)
• To obtain tissue for biopsy.

Procedure:

➢ A vitrectomy is performed through a surgical microscope allowing coaxial illumination and fine movements by
X–Y coupling.
➢ Special planoconcave lenses are placed on the cornea to provide a clear image of the posterior third of the
eye.
➢ Microscope attachments allow re-inversion of the image seen.
➢ All these provide the surgeon with a magnified, binocular view of the retina and vitreous.
➢ Three sclerotomies of 20, 23 or 25 gauge size are made at the pars plana, 3–3.5 mm away from the limbus.
➢ In one an infusion line is inserted for balanced salt solution.
➢ In the second, a fibreoptic light source provides endoillumination and through the third, a vitrectomy
instrument for suction and cutting of the vitreous (Figs 21.4 and 21.5) is passed into the vitreous cavity.
➢ Any abnormalities in the vitreous can be cleared bimanually under direct vision using the vitrectomy
instrument and the endoilluminator as support when needed.
➢ It is necessary to completely clear all the central vitreous and also the region of the vitreous base to prevent
later fibrovascular proliferation.
➢ Once the visibility of the retina is restored, the cause for the vitreous disturbance is treated.
➢ Endophotocoagulation with a fibre optic probe delivering diode laser may be required to seal a retinal break
or treat areas of retinal neovascularization.
➢ Endodiathermy can be utilized to coagulate bleeding vessels.
➢ Vitrectomy is seldom carried out as an isolated procedure, but is often associated with surgery for
vitreoretinal proliferation, complicated retinal detachments or foreign bodies in the eye.
➢ In the presence of vitreoretinal proliferation it is important to relieve all traction on the retina.
➢ Vitreous bands can be cut using the vitrectomy instrument or special miniature vitreoretinal scissors.
➢ Epiretinal membranes are removed by gentle peeling with a vitreoretinal pick and forceps, or by cutting them
with vitreoretinal scissors, to allow the retina to fall back into place.
➢ Small foreign bodies are dissected of their fibrous capsule with a vitreoretinal pick or forceps and then
removed by intravitreal foreign body forceps.
➢ An intravitreal magnet is occasionally employed.
➢ Maintenance of chorioretinal apposition to allow chorioretinal adhesions to occur and to prevent recurrence
of fibrovascular proliferation in the vitreous necessitates an internal tamponade with gases or liquids.

➢ Visual prognosis after vitreous surgery is often guarded and depends upon the basic disease process and the
degree of damage to the retinal receptors.
➢ Meticulous surgery has greatly increased the chances of anatomical success.
➢ Open sky vitrectomy leads to instability of the entire vitreous and anterior segment while making the patient
aphakic. It is indicated only when the cornea is not transparent.
 DISEASES OF RETINA

What we will learn here?

• Anatomy of Retina
• Hypertensive retinopathy
• Retinal Artery Occlusion
• Retinal Venous Occlusion
• Retinopathy of Blood disorders
• Retinopathy of prematurity
• Retinal dystrophy and degeneration
• Macular degeneration
• Macular disorders
• Retinal Detachment

Retina is innermost layer of the eyeball Highly developed tissue of the eye ball

It consist of light sensitive cells rods and cones

Its extends from the optic disc to ora serrata

It consists of two regions posterior pole and peripheral retina by the retinal equator

RETINAL EQUATOR which lie in line with the exit of four vena verticosa
Posterior pole consists of two regions MACULALEUTEA and OPTIC DISC

Optic disc is pink coloured area lies 3.4mm to nasal fovea

All the layers of retina terminate at optic disc except the nerve fibres which passes through lamina cribrosa

to run into optic nerve

Thus the area reffered to as optic nerve head

Due to the absence of photoreceptor cells it produces absolute scotoma in the visual field called 2frica22ival2 blind spot
Macula lutea is the yellow spot

Fovea centralis is the central depressed part of the macula

It has lowest threshold for light and high visual activity It has highest number of cones

Pheriperal retina is the area bounded posteriorly by the retinal equator anteriorly by the ora serrata. Ora serrata is the peripheral margin where
retina ends

MICROSCOPY OF RETINA

It consist of ten layers

Fuctinally it has two components Pigment epithelium Neurosensory retina

Functinally retina is divided into nasal retina and temporal retina

BLOOD SUPPLY OF RETINA

outer four layer is supplied by choroidal vascular system supplied by anterior and posterior cilliay arteries

Inner six layer is supplied by central retinal artery branch of opthalamic artery

Central retinal vein which drains directly into the cavernous sinus
CONGENITAL AND DEVELOPMENTAL DISORDERS OF RETINA

Congenital disorders classified into ANOMALIES OF OPTIC DISC

Crescents Site inverses

Congenital pigmentation Coloboma

Drusen and hypoplasia of optic disc

ANOMALIES OF VASCULAR ELEMENTS:

Persistent hyaloid artery

Congenital tortuosity of retinal vessels

ANOMALIES OF NERVE FIBRES:

Medullated nerve fibres

ANOMALIES OF RETINA PROPER:

Albinism

Congenital retinal blindness Oguchis disease Congenital retinal cyst

Congenital retinal detachment Coloboma of the fundus

ANOMALIES OF MACULA:

Hypoplasia, aplasia, coloboma

HYPERTENSIVE RETINOPATHY

Occurs at BP over 140/90Hg

Pathogenesis

[Link]

[Link]

[Link] vascular permeability

It may occur under four circumstances

[Link] hypertension without sclerosis

Young patients

Retinal signs-constriction of arterioles ,flame shaped hemorrhages, cotton wool spots

[Link] with involuntary sclerosis

Vasoconstriction , thickening of vessel wall, deposition of hard exudates, hemorrhages without

edema

Nipping and perpendicular placement of veins at arteriovenous crossing: Gunn sign

[Link] sclerosis

In young patients arterioles respond to HT by proliferative and fibrous changes

In kidneys- chronic glomerulonephritis

Retinal signs-multiple hemorrhages edema cotton patches hard exudates

[Link] hypertension

Accelerated progression of hypertensive stage in young arterioles undefended by sclerosis

Associated with renal insufficiency

Retina – oedema , marked disc oedema, multiple cotton patches hard exudates
Prognosis -grave

Classification

Grade 1 – barely detectable arterial narrowing or sclerosis

Grade 2-moderate to marked narrowing of arterioles exaggeration of light reflex ,changes in AV

crossings

Grade 3 – grade 2+ retinal hemorrhage

Grade 4 - grade3+ pappiloedema

Management –blood pressure control

Pregnancy induced

Occurs in late pregnancy (6th -9th month)

Retinal changes :

Narrowing of nasal branches of arterioles

Spasm of vessels causes hypoxia characterized by ‘cotton wool spots’ and ‘superfcial hemorrhages’

Retinal edema and exudation

Profuse exudation may cause retinal detachment

Management : preorganic stage –maintenance of pregnancy in close observation

Inflammatory disease of retina:

Retinitis:

Nonspecific retinitis:

Caused by pyogenic organisms.

Acute purulent retinitis:

Occurs as Metastatic infections in patients with pyemia.

As endophthalmitis and panophthalmitis

Subacute retinitis of Roth:

Occurs in patients with subacute bacterial endocarditis (SABE)

Characterized by

Multiple superficial hemorrhages in posterior part of fundus. With white spot at the centre
(rothspots).

Blurring of vision due to involvement of macular region.

Specific retinitis:

Bacterial infections – tuberculosis ,syphilis,leprosy,actinomycosis.

Cytomegalo virus retinitis – cytomegalo virus.

Progressive outer retinal necrosis (PORN) – varicella zoster virus.

Acute retinal necrosis (ARN) – herpes simplex ll in patients under the age of 15 years and herpes
simplex l in older individuals . ( More chances in AIDS patients).

RETINAL VASCULITIS

Inflammation of the retinal vessels’ wall - Primary (Eales’ disease) or Secondary to uveitis.

EALES’ DISEASE : ( Periphlebitis retinae)

Idiopathic inflammation of the peripheral retinal veins

Classical triad – Young males ( more common in India), spontaneous vitreous hemmorhage
,recurrences are common.

Etiology – Unknown but seen commonly in TB patients (considering to be a hypersensitivity to

tubercular proteins)

Clinical features:

Sudden painless loss of vision ( due to vitreous hemmorhage)

Sudden appearance of floaters( black spots in front of eye)

Bilateral but assymetrical

Systemic neurological features and mild uveitis present

Clinical course :

[Link] of active inflammation – peripheral veins are congested ,perivascular exudates and
sheathing present along the surface,sheets of hemorrhages near veins

[Link] of vascular occlusion- obliterated vessels and areas ofcapillary non- perfusion in the
periphery is seen on fundus flourescin angiography.

[Link] of retinal neovascularisation- Abnormal fragile vessels at the junction of perfused and non-
perfused retina.(Bleeding from these vessels causes hemorrhage)

[Link] of sequelae – Development of complications( proliferative vitreoetinopathy,fractional

retinal detachment,rubeosis iridis,neovascular glaucoma.

{Occlusion – hypoxia – VEGF stimulus-Neovascularisation}

Treatment :
 [Link], corticosteroids + Antitubercular therapy

[Link] photocoagulation to reduce the neovascular stimulus.

[Link] surgery for nonresolving hemorrhage

[Link] VEGF inhibitors.

RETINAL ARTERY OCCLUSIONS

ETIOLOGY : Common in old age males >40 years and patients with HT,DM and cardiovascular
diseases.

EMBOLI (from carotid artery and cardiac valves) –

- Most common cause

- Most common site – Narrowest site of CRA where it pierces the dural sheath of optic
nerve,posterior to lamina cribrosa.

- Types : # Hollenhorst plaque – Cholesterol EMBOLI at retinal vessel bifurcation ( refractive

,orange and from atheroma in carotid artery)

# Calcium emboli – close to optic disc(white and from valves)

# Platelet fibrin emboli – full white and arises from atheroma in carotid artery)

[Link] RELATED THROMBOSIS

[Link] ARTERITIS ( Giant cell arteritis) and periarteritis (associated with polyarteritis nodosa,SLE,
Wegener’s granulomatosis , scleroderma)

[Link] (associated with amaurosis)

[Link] IOP

[Link] DISORDERS

[Link] SYNDROME – CRAO (+) Sensorineural hearing loss (+) encephalopathy.

[Link] DISORDERS ( oral contraceptives,polycythemia,antiphospholipid

syndrome)

Rare causes – retinal migraine, sickling hemoglobinopathies.

CLINICAL FEATURES: Clinically RAO presents as Central retinal artery occlusion(CRAO -60%) OR
Branch artery occlusion(BRAO-35%) OR Cilioretinal artery occlusion(5%)

CRAO – occurs due to obstruction at the level of lamina cribrosa

 [Link] sudden painless loss of vision ( painful in GCA)

[Link] of Amaurosis fugax in the past

[Link] acuity reduced ( except with those having patent cilioretinal artery supplying
macula )

[Link] puppilary reflex -absent ,RAPD positive

[Link] fundus examination,

- Marked narrowing of retinal arteries and mild narrowing of retinal veins.

- Milky white retina due to ischemic retinal edema ( except with those with
patent cilioretinal artery)

- Cherry Red Spot – seen in the centre of macula due to vascular choroid shining
through the thin retina in the foveal region,in contrast to the surrounding pale retina.

DD for Cherry red spot in macula

Cherry Trees Never Grow Tall in SAND ,Mud and Grime

1.C RAO [Link](Blunt) [Link]- Pick disease 4.GM1 gangliosides [Link]-Sach’s disease
[Link]’s disease [Link] leukodystrophy, Multiple sulfatase deficiency [Link]’s
disease( only type2).

- Cattle tracking/Box caring fundus – segmentation of blood column of veins and

arteries.

- Atrophic changes in the form of attenuated thread like arteries and consecutive
optic atrophy in chronic cases.

- Fundus flourescin angiography shows delay arterial filling(early filling in case of

patients with those with patent cilioretinal artery)

BRAO – Sudden and profound painless sectoral visual field loss(goes unnoticed when central
vision is spared)

[Link] following lodgement of embolus at a birfurcation

[Link] white edematous retina with narrowed arterioles

MANAGEMENT:

[Link] of supine posture.( To improve ocular perfusion)

[Link] of IOP :

- Ocular massage (to improve perfusion and dislodging the embolus or thrombus)

-Anterior chamber paracentesis

-Intravenous azetazolamide,mannitol,topical apraclonidine

[Link] – sublingual isosorbide dinitrate and inhalation of carbogen(95% oxygen and

5%carbondioxide)- 9frica99 angiospasm.
 4. Fibrinolytic therapy

[Link] steroids are indicated in patients with GCA

[Link] photodisruption of the embolus

[Link]-up for associated systemic conditions.

Complication – Neovascular glaucoma.

RETINAL VENOUS OCCLUSION

Etiology and risk factors:

• Older age
• Hypertension
• Diabetes mellitus
• Hyperviscosity – polycythemia,Hyperlipidemia,leukemia, multiple
myeloma,macroglobulinemia
• Periphlebitis retinae – associated with sarcoidosis,syphilis,SLE.
• Raised. Intra ocular pressure

Local causes -Orbital cellulitis,orbital tumors,facial erysipelas,Cavernous sinus thrombosis.

Use of contraceptives in young females.

Classification:

[Link] retional vein occlusion – non ischemic and ischemic

[Link] retinal vein occlusion.

CENTRAL RETINAL VEIN OCCLUSION:

Pathology:

Venous occlusion due to systemic or local factors causes stasis of bloodflow (nonischemic type)
Hypoxia of the involved retina Damage of capillary endothelial cell and leakage from neovascularized
vessel. (Ischemic type)

NOTE:

Occlusion usually occurs posterior to lamina cribrosa due to sharing of common adventitia by retinal
artery and vein.

15% of nonischemic type leads to ischemic occlusion in 4 months

Clinical features :

Non ischemic CRVO Ischemic CRVO

Most common (75%cases) Less common
 Sudden,painless, loss of vision(partial) Sudden,painless,complete loss of vision

RAPD – Absent or mild Marked

Mild hemorrhage in the periphery Severe hemorrhages involving periphery and posterior
pole – giving rise to Tomato ketchup
/Tomatosplash/Blood and thunder 11frica1111iv.

Cotton wool spots and tortuosity of vessels Extensive cotton wool spots and tortuosity of vessels

Loss of vision due to macular edema. Lossbof vision due to macular ischemia.

Doesnot occur Neovascularization at iris (NVI) occurs after 100 days

and causes glaucoma secondary to CRVO known as 100
day glaucoma

In FFA<10 disc area of nonperfusion. In FFA>10 disc area of nonperfusion

ERG- Normal ERG – amplitude of b wave <60%

Treatment – Treatment –
Laser photocoagulation notdone. Intravitreal PRP/ scatter photocoagulation done only on
triamcinolone 2 injections (1mg). 11frica1111iv of NVI/NVD.
0.7 mg dexamethasone intravitreal implant. Prophylactic PRP not done.
Intravitreal anti VGEF drugs –
ranibizumab,aflibercept

Branch retinal vein occlusion:

More common than central retinal vein occlusion

Occurs as Hemispheric occlusion – at the main branch of the disc

Quadrantic Occlusion – at the level of AV crossing

Small branch occlusion – either macular or peripheral occlusion.

Clinical features:

Retinal edema and hemorrhage

Loss of vision is due to macular edema

Neovascularization occurs.

Treatment:
 It may benefit from laser photocoagulation contrary to nonischemic type of venous occlusion.

Nasal cycle and nasal resistance. Mechanism of sinonasal allergy and mucociliary clearance
mechanism.

NASAL CYCLE:

Nasal mucosa undergoes rhythmic cyclical congestion and decongestion- controls the airflow
through nasal chambers.

When one nasal chamber is working, the total nasal respiration equal to that of both nasal chambers
is carried out by it.

Variation- every 2-4 hours in an individual

Congestion and decongestion of the nasal venous cavernous tissue is under the control of the ANS

Factors influencing nasal cycle:

Physiological factors:

• Age
• Sleep
• Posture
• Exercise

Pathological factors:

[Link] upper respiratory tract infection (URTI)

[Link] rhinitis

[Link] septal deviation

NC and drugs:

[Link] decongestants were shown to influence the NC.

2. The administration of nasal topical vasoconstrictor on the congested side is able to cause a
prompt cycle reversal.

[Link] it has been demonstrated that decongestants have little action on the patent side, they
cause a significant increase in airflow on the naturally congested side with the least sympathetic
nervous activity.

NASAL RESISTANCE:

Nasal vestibule is the first component of nasal resistance.

The nasal vestibule is composed of compliant walls that are liable to collapse from the negative
pressures generated during inspiration.

The vestibule is termed as the external nasal valve.

It contributes to 1/3rd of the nasal resistance

The remaining 2/3rd is contributed by the nasal septum.

Inferior and middle turbinates contain erectile tissues, the anterior end of it has a major influence on
the nasal resistance and functions as the internal nasal valve.

Factors influencing nasal resistance:

• Age
• Nasal cycle
• Exercise
• Respiration
• Nasal reflexes
• Skin and temperature
• Emotional and psychological response

MECHANISM OF MUCOCILIARY CLEARANCE:

Nasal mucosa-rich in – goblet cells, secretory glands ( both serous and mucous)

Their secretion forms a continuous sheet called mucous blanket ( spread over the normal mucosa)

Mucous blanket consists of:

Superficial mucus layer+ deep serous layer, floating on top of the cilia which are constantly beating
to carry it like a “conveyer belt” into the nasopharynx.

It moves at a speed of 5-10 mm/min

Complete sheet of mucus is cleared into pharynx every 10-20 min.

Inspired bacteria, viruses and dust particles →entrapped on the viscous mucous blanket→ carried to
nasopharynx→ swallowed.

Presence of turbinates- doubles the surface area yo perform this function.

About 600-700 ml of nasal secretion is produced in 24 hours.

Cilia beat 10-20 times per sec in room temperature.

Two strokes:

Rapid “effective stroke”- extended cilia reach the mucus layer

Slow “recovery stroke”- cilia bend and travel slowly in the reverse direction in the thin serous layer,
thus moving the cilia in one direction.
Factors affecting the movements of cilia:

Drying

Drugs (adrenaline)

Excessive heat or cold

Smoking

Infections and noxious fumes like sulfur dioxide and carbon dioxide.

Disorders of cilia:

Immotile cilia syndrome:

Cilia are defective and cannot beat effectively→stagnation of mucus in the nose, sinuses and
bronchi→chronic rhinosinusitis and bronchiectasis.

MECHANISM OF SINONASAL ALLERGY:

Aetiology:

Inhalent allergens (pollens,dust)

Genetic predisposition

Pathogenesis:

Inhaled allergens→ produce specific IgE antibody→ antibody becomes fixed to the blood basophils
or tissue mast cells by its Fc end.

Subsequent exposure→ antigen combines with IgE antibody in the Fab end→ degranulation of mast
cells→ release of several chemical mediators.

Mediators -responsible for the symptomatology of allergic disease.

They cause vasodilation, mucosal edema, infiltration with eosinophils, excessive secretion from nasal
glands or smooth muscle contraction.

“Priming effect”- mucosa earlier sensitized to an allergen will react to smaller doses of subsequent
specific allergen.

Allergic response occurs in two phases:

Acute or early phase- occurs 5-30 min after exposure to specific allergen.

Characterised by-sneezing, rhinorrhea nasal blockage and bronchospasm due to histamine.

Late or delayed phase: Occurs 2-8 hours after exposure to allergen without additional exposure.

It is due to the infiltration of inflammatory cells- eosinophils, neutrophils, basophil, monocytes and
CD4+ T cells at the site of antigen deposition.

Characterised by- Swelling, congestion and thick secretion.

In the event of repeated or continuous exposure to allergen, acute phase symptomatology overlaps
the chronic phase.

Complications:

• Recurrent sinusitis
• Formation of nasal polyp (2% of cases)
• Serous otitis media
• Orthodontic problems
• Bronchial asthma

Treatment:

Avoidance of allergen

Treatment with drugs ( anti-histamines, sympathomimetic drugs ,corticosteroids, sodium

cromoglycate, anticholinergics, leukotriene receptor agonists, Anti-IgE)

Immunotherapy.

Retinopathy of Blood disorder

Sickle cell retinopathy

Retinal changes in patient suffering from sickle cell hemoglobinopathies

When deoxygenated it becomes insoluble and distorts the normally discoid RBCs into characteristic
sickle shape. It obstructs the capillaries supplying retina and causes infraction especially in the
periphery of retina.

Pathogenesis:

Glutamic acid is replaced with valine in 6th position

This causes changes in the RBC Morphology and

Thus sickle cells are formed.

The Damaged RBC gets slowed down in the movement across the miocrovessels

High expression of adhesins by sickle cells causes increased stickiness to the endothelium
Aggregation of sickle cells in the vessel leading to blockage of vessel

Thus there occurs a lysis of RBC which causes release of free Hb.

Causes inactivation of NO

Narrows the blood vessels.

Microvascular Stasis

Clinical Manifestation:

• Retinopathy
• Angioid Streaks
• Glaucoma
• Pappilary edema
• Cataract
• Circumscribed dilation and constriction of conjunctival cappilaries.

Fundus:

Proliferative changes B. Non proliferative changes.

Proliferative changes:

Stage 1:

Peripheral artery occlusion and ischemia

Stage 2:

Peripheral arterio venous anomalies of dilated pre existing capillary channels.

Stage 3:

Sprouting of new vessels from pre existing anamolies

SEA-FANS Configuration

They involute spontaneously as a result of auto infraction.

They appear as greyish fibrovascular lesions.

Stage 4:
Neovascular tufts continues to proliferate and bleed into the vitreous.

Stage 5:

Extensive fibrovascular proliferation and retinal detachment.

Non Proliferative Retinopathy:

Asymptomatic lesions:

Venous tortuosity

Salmon patches

Black sunburst spots

Macular depression

Peripheral retinal holes

Symptomatic lesions:

Macular arteriolar occlusion

Acute central retinal artery occlusion

Choroidal vascular occlusion (Particularly in children).

Treatment:

Pan Retina photocoagulation: Regresses neovascularization.

Pars Mena vitrectomy.

Vitrearetinal surgery.

Anaemic Retinopathy:

Retinal changes are liable to occur when Hb levels falls by 50% and consequently present when it is
below 35% (5gm%)

Retinopathy increases as severity of anemia increases.

Pathogenesis:

Anemia

Retinal Hypoxia

Vascular dilation

Infraction of nerve fiber layer

Increased transmural pressure

Hypoproteinemia
Retinal Edema and Hemorrhage

Characteristic Features:

Fundus Background – Pale.

Retinal Arterioles – Pale.

Retinal Veins – Tortuous and dilated.

Retinal Hemorrhage – Superficial flame shaped and preretinal (Suhyloid) may be seen in the
posterior half of the fundus.

Roth Spot: Hemorrage with white Centre and platelet fibrin emboli.

Cotton wool spots: Seen in the patient with co-existing thrombocytopenia + Aplastic anemia.

Retinal Edema – Microtrauma of vessel wall secondary to increased transmural pressure.

Hard exudate – Seen due to resolved retinal edema when these are severe and located at the
macula – “Macular Star” is seen.

Optic nerve Changes – Edema or in later stages of optic neuropathy, Optic disc pallor is seen.
 Retinal Changes
seen in special
situations like

IDA Vit B12 Deficiency Sickle cell Anemia

Central Retinal Conjunctival

Optic Neuropathy
vein occlusion sickling sign

Retinal artery
Disc Pallor Choroidal infract
occlusion

atropy and
Disc Edema
neovascularisation

Anterior ischemic
optic neuropathy
 Retinal Changes seen
in special situations
like

Myeloproliferative
Thalasemia Malaria
Disorders

Retinal Pigment
Roth Spots Anemia
Epithelial Changes

leukemia infilterates
Increased ICP
in Retina

Choroidal infilteration
with 20 degree Retinal changes - Disc
serous retinal Edema
detachment.

Vascular sheathing

Symptoms:

Most cases are asymptomatic

At Macula – Hemorrhages, Edema ana Hard Exudates – patient can complain of loss of vision.

Investigation and Treatments:

Ocular investigations are indicated only if treatment is planned.

Fibro angiography demonstrates delay in arteriovenous transit time which indicates venous
occlusion

Optical Coherence tomography (OCT) is used to demonstrate vascular occlusion and macular edema.

Blood Investigations :

PBS examination

Complete blood count.

Bone Marrow Biopsy indicated in some cases.

Treatment:

Vascular occlusion and macular edema must be treated first

Laser hyaloidectomy is indicated in case of subhyoidal hemorrhage.

RETINOPATHY OF PREMATURITY

Bilateral proliferative retinopathy

occurs in premature infants with

low birth weight

exposed to high concentration of O2

Earlier it was known as retrolental fibroplasia

ETIOPATHOGENESIS:

➢ Primary Factors:
➢ Low gestation age, especially less than 32 weeks
➢ Low birth weight (less than 1500g, especially less than1250g)
➢ Supplemental O2 therapy
➢ Other risk factors:
➢ Vitamin E deficiency
➢ Respiratory distress syndrome
➢ Asphyxia
➢ Shock
➢ Acidosis

PATHOGENESIS

Normal development of retina

VEGF
 Retinal vessels

Reach 1 month after delivery

8thMonth Reach

Nasal periphery Temporal Periphery

Premature birth

VEGF Downregulated

Vessel Migration halted

Increased metabolic demands

with growing age

Activation of (excess production)

O2 regulated VEGF’s Non O 2 regulated

insulin like growth factors (IGF-1)

Neovascularization

Retinopathy of prematurity (ROP)

CLINICAL FEATURES:

Can be divided into

Active ROP Cicatricial ROP

International classification of ROP:

Staging of ROP:

Stage 1

Demarcation line formation at the edge of vessels dividing the vascular from avascular retina

Stage 2

Line structure of stage 1 acquire a volume to form a ridge with height & width

Stage 3

Ridge with extra retinal fibrovascular proliferation into the vitreous.

Stage 4

Stage 4 a) – Subtotal retinal detachment not involving macula.

Stage 4 b) – Subtotal retinal detachment involving macula.

Stage 5

Total retinal detachment

(b)Zones of ROP:

Divided into 2 zones

Centre of the retinal map is the optic disc

ZONE 1

Any ROP in the zone –

Very severe – Because of a large peripheral area of avascular retina

ZONE 2

Area between ZONE 1 & the boundary contributes ZONE 2

ZONE 3

Temporal are of retina left beyond the radius of ZONE 2 is ZONE 3

Extent of involvement

It is denoted by the clock hours of retinal involvement in particular zone.

CLINICALLY IMPORTANT TERMS

1)PLUS DISEASE- Dilatation and tortuosity of posterior pole vessels in at least 2 quadrants at the
posterior pole with any stage of ROP

2)PRE PLUS DISEASE- Normal < Venous dilation< <Defined plus disease.

3) Aggressive posterior ROP

Also called Rush disease

Require immediate treatment

ROP – location Zone I

Posterior ZONE 2

Flat proliferation with vascular loops and haemorrhages

4)Threshold disease

Stage 3 + ROP

Plus disease located -> Zone 1 or 2

Involves 5 continuous or 8 discontinuous clock hours

Requires Laser therapy in less than 42 hours

Pre-threshold disease

(has two types)

Type I or high-risk pre-threshold disease desire (requires photocoagulation)

Type 2 or low risk pre-threshold disease (which requires weekly follow up)
Differential diagnosis:

Familial exudative vitreoretinopathy (FEVR)

Incontinentia pigmenti in girls

Persistent fetal vasculature

Advanced retrolental fibroplasia

Management

1)Prophylaxis:

Premature new borns should not be placed in incubator with an O2 concentration of more than 30%.

Infections and attacks of apnoea must be avoided.

Early diagnosis and treatment to prevent blindness in high risk cases.

SCREENING PROTOCOL

All premature babies < 34 weeks of gestational age & those weighing 1750g or less must be
screened.

1st EXAMINATION

Indirect ophthalmoscopy:

Infants < 28 weeks of gestation < 1200gm : at 2-3 weeks of age

Infants born between 28-34 weeks of gestation / 1175gm: at 3-4 weeks of age

Infants between 34-36/7 weeks of gestation or between 1750-2000 gm should be screened

only if exposed to high rank factors.(prolonged O2 therapy, mechanical ventilation)

Further line of action – depends on the status of retina

Subsequent Follow Up Examinations

Spontaneous regression of disease occurs in about 80% of the cases

Patients should be examined till regression occurs

TREATMENT PROTOCOL

Laser is preferred over Cryotherapy

Laser treatment:
Photocoagulation using diode laser lesions with laser indirect ophthalmoscope

carried out in patients with high risk pre threshold, threshold & aggressive posterior ROP

Post-laser treatment & follow-up

Antibiotic & steroid eye drops prescribed for a week.

Treatment- Surgery
Surgical Management of Stage 4 ROP

ROP

Stage 4a Stage 4b

Lens sparing vitrectomy

Focal Generalized Generalized

traction traction traction

No RD No RD with RD

Followup Followup/ Buckling/Lens

Buckling sparing

Vitrectomy

Leukemic Retinopathy
Ocular involvement – more common with acute leukemia

Leukemia

Acute Chronic

• Myeloid • Myeloid
• Lymphoid • Lymphoid

Clinical Manifestation

Primary Secondary
(Direct Infiltration of neoplastic Cells) (Indirect involvement from non-viable or dysplastic cells or
chemotherapy)
Manifestation Include

Retinal involvement
Non Retinal involvement

Background is pale and orangish • Iris Infiltration

• Ocular Haemorrhages
Retinal veins – Tortuous and Dilated Sub Conjunctival
Retinal Arterioles – Pale and Narrow Haemorrhage and hyphaema
(bleeding of anterior
Perivascular Leukemic Infiltrates- chamber)
Grayish white lines along the course of veins, Roth’s Spots • Pseudohypopyon
Collection of White cells in
Subhyaloid Hemorrhages (Large pre-retinal Hemorrhage) the anterior chamber.
 Investigations

Complete blood count with platelets/differential (Significantly high or low WBC should be
considered)
Peripheral Blood Smear > 20% blast cells (Acute Leukemia).

Treatment – The key is to treat the malignancy

Induction Phase – Reduce the tumor burden by clearing the leukemic cells in the bone marrow using
chemotherapeutics.
Consolidation Phase – Eliminate all the Leukemic cells that remain viable.
Maintenance Phase – Chemotherapeutics and steroids are given to prevent relapse.

Opportunistic infection and side effects due to chemotherapy

Bacterial Virus Fungus Parasite

• Pseudomonas • HSV • Candida • Toxoplasma

(starts as • VZV • Aspergillus gondii (ocular
blephro • CMV (Cause • Focal, Toxoplasmosis
conjunctivitis necrotizing white, deep )
and spread to retinitis and lesions in
cause orbital retinal the vitreous
cellulitis detachment.

Ocular adverse effects of chemotherapeutic drugs:

Busulfan – Posterior subcapsular cataract.

Vincristine – Optic atrophy, corneal hyposthesia, transient cortical blindness, nystagmus.
Dexamethasone – Increased intra ocular pressure, sub capsular posterior cataract.
Fludarabine – Visual disturbances (15% of patients)
Cytarabine – Corneal toxicity and Hemorrhagic cystitis
Anthracyclines – Discoloration of tears and conjunctivitis.
Imitanib – Peri- orbital edema, blurred vision, conjunctival hemorrhage.

Hematopoitic stem cell transplantation

 Graft v/s Host disease

Kerato- Conjunctivitis, Corneal ulceration, Ischemic retinopathy

PRIMARY RETINAL TELANGIECTASIA

Idiopathic congenital or acquired retinal vascular malformation
Characterized by:
Dilation of capillary bed
Segmental dilation of neighbouring venules and arterioles

1o retinal telangiectasia includes

Idiopathic juxtafoveolar retinal telangiectasia
Also known as idiopathic macular telangiectasia
Mild decrease in visual acuity due to exudation from the juxtafoveal telangiectatic retinal capillaries.

Types
Type 1: - Unilateral disease characterized by parafoveal dilation of capillaries. Microaneurysms,
leakages and lipid deposition.
Type 2: - (Most Common form)
Bilateral juxtafoveal telangiectasia
Minimal exudates
Type 3: - (Extremely Rare)
Occlusive telangiectasia

Pathogenesis
Abnormalities in parafoveal muller cells
Muller cells – Important for the health of retinal capillary endothelium and surrounding retina.
Muller cell dysfunction – endothelial degeneration – Retinal capillary proliferation and telangiectasia

Clinical Presentation
Parafoveal graying of retina
Superficial crystalline deposits
Subfoveal cystoid cavities
Parafoveal cystoid cavities
Right angle vessels
Reduced visual acuity
Hyperplasia of retinal pigment epithelium

Investigations
Fluorescein angiography
Highlights parafoveal telangiectasia vessels
Demonstrate early hyperfluorescence with leakage
Optical coherence Tomography
Subfoveal cystoid space (without cystoid macular edema)
Advanced stages:
Photoreceptor dysfunction and outer retinal atrophy
Fundus autofluorescence
Pathognemonic of Type-II
Loss of Physiologic hypoauto fluorescence i.e., increased autofluorescence in the fovea.

Differential Diagnosis

Diabetic macular Pseudophakic Macular hole Retinal vein

edema macular edema occlusion

Treatment
Chemotherapeutic drug like (bevacizumab, ranibizumab)
Oral carbonic anhydrase inhibition
Focal grid laser, photodynamic therapy, intravitreal triamcinolone
Parafoveal telangiectasia.
If only the capillaries of fovea are involved, then it’s called Parafoveal telangiectasia.
Characterized by:
Microaneurysmal saccular dilation
Capillary non-perfusion of parafoveal capillaries
Parafoveal telangiectasia can be considered as having 2 basic forms:
Coat’s disease – A developmental or congenital vascular anomaly which may be the largest part of a
spectrum
Presumably an acquired form found in middle aged or older patients.

COAT’s DISEASE
Also known as exudative retinopathy of coats
Severe form of retinal telangiectasia (Idiopathic congenital retinal vascular malformation)
Characteristic Features:
Affects one of the eyes of boys in the 1 st decade of life
Early Stages – Large areas of intra and sub retinal yellowish exudates and hemorrhages associated
with “OVERLYING DILATED AND TORTUOUS RETINAL BLOOD VESSELS” and a number of
small aneurysms near the posterior pole and around the disc.
It might present with VISUAL LOSS, STRABISMUS or LEUCOCORIA (whitish pupillary reflex)
and thus it should be differentiated from retinoblastoma tones.

Progression
Produce exudative retinal detachment and a retrolental mass
Late stages – Complicated cataract, uveitis and secondary glaucoma and end in phthisis bulbi
(shrunken, nonfunctional eye)
Stages
Stage 1
Retinal telangiectasia only (dilation of capillaries in the retina)
Stage 2
Telangiectasia and exudation (escape of fluids and material from blood vessels into surrounding
tissues)
Extrafoveal exudation
Foveal exudation (exudation of fovea)
Stage 3 – Exudative Retinal Detachment
Subtotal Foveal and Subtotal Extrafoveal (partial detachment)
Total retinal detachment.
Stage 4
Total retinal detachment and glaucoma
Stage 5 – Advanced end stage disease
Blind, non-painful eye with total retinal detachment with cataract and phthisis bulbi
Investigation
Fundus Fluorescein Angiography – Highlights abnormal vessels, leakage and areas of capillary
drop out.
Treatment
Laser photocoagulation- Uses laser to shrink or destroy blood vessels
Cryotherapy – A procedure that uses extreme cold to destroy abnormal blood vessels
Anti-vascular endothelial growth factor (Anti-VEGF) injection
In more advanced stages,
Retinal detachment –Vitrectomy
Scleral buckling to correct the detached retina and external drainage of fluids.

LEBER’S MILIARY ANEURYSMS

Less severe form of Coat’s disease presenting in adults.
Characterized by:
Decreased vision.
Local area of fusiform and vascular aneurysmal dilation of venules and arterioles associated with
local exudation.
Investigation
Fundus Fluorescein Angiography (FFA)
Leakage as well as capillary drop out.
Late hypofluorescence.
Treatment
Direct photocoagulation of abnormal vessels.
 OCULAR ISCHAEMIC SYNDROME
Rare condition
Results due to chronic ocular hypoperfusion secondary to > 90% stenosis of carotid artery
Carotid Stenosis
Atherosclerotic occlusive carotid artery disease
Associated with – ulceration at the bifurcation of common carotid artery
Risk Factors:
Male (2:1)
Old age (60-90)
Smoking
Hypertension
Diabetes Mellitus
Hyperlipidaemia
Manifestations
Amaurosis fugax (transient retinal ischaemic attack)
Retinal artery occlusion (due to embolus)
Transient cerebral ischemic attack
stroke
Clinical features: (Symptoms)
Usually unilateral (80%)
Ocular discomfort
Pain around the orbit
Transient blackout (amaurosis fugax)
Delayed dark adaptation
Loss of vision, precipitated by exposure to bright light (bright light amaurosis)

SIGNS:
Cornea: Edema & striae
Anterior chamber: Reveal faint aqueous flare, with few cells (ischaemic pseudoritis)
Pupil: mid dilated and poorly reacting
Iris:
rubosis iridis (66%cases), atrophic patches
Iris neovascularization (90% of cases)
(Poor prognosis)
POSTERIOR SEGMENT: (fundus examination)
Venous dilation with or without tortuosity, peripheral retinal hemorrhages and micro aneurysms.
Easily induced retinal artery pulsations with gentle digital pressure
Retinal neovascularization (in 37% of cases)
Macular edema
COMPLICATIONS:
Anterior ischemic optic neuropathy in association with OIS- Due to inadequate perfusion pressure
within the deep capillaries of the optic nerve head.
Cataract – advanced cases.
Neovascular glaucoma – (as a sequelae to anterior segment neovascularization)
DIFFERENTIAL DIAGNOSIS:
Non- ischaemic Central retinal vein Occlusion (CRVO)
Diabetic retinopathy
Hypertensive retinopathy
Aortic arch disease
Atherosclerosis
Syphilis

INVESTIGATIONS:
Doppler ultrasound
Magnetic resonance angiography
Fluorescein fundus angiography
Delayed and patchy choroidal filling
Increased retinal arteriovenous circulation times
Leakage from retinal (new) vessels
Macular edema.
TREATMENT MANAGEMENT:
Treatment of neovascular glaucoma
Pan-retinal photo-coagulation
Glaucoma drainage device (i.e) artificial filteration shunt may control IOP.
Treatment of proliferative retinopathy by pan-retinal photocoagulation.
Treatment of pseudoiritis:
Topical steroid eye drops.
Treatment of carotid stenosis:
Anti-platelet therapy, oral anti- coagulants
Surgical – carotid endarterectomy

Retinal dystrophies and Degeneration

INTRODUCTION
Retina is the innermost nervous layer of the eye ball.

It extends from optic disc to ora serrata with surface area of 266 [Link].

Gross division:

1. Posterior pole - optic disc -beginning of optic nerve- devoid of rods and cones
(physiological blind spot)

- Macula lutea (yellow spot)- it has highest visual acuity. Fovea centralis is
central depressed part of macula with highest visual acuity as it contains only cones.

2. Peripheral retina –anterior to the retinal equator limited by ora serrata

Separated by retinal equator (imaginary line in line with exit of four vena
verticose).

Layers of Retina:

➢ Layers of rods and cones

➢ External limiting membrane
➢ Outer nuclear layer
➢ Outer plexiform layer
➢ Inner nuclear layer
➢ Inner plexiform layer
➢ Ganglion cell layer
➢ Nerve fibre layer
➢ Internal limiting membrane

Blood supply of retina:

Outer four layers are avascular and get their nutrition from choroidal vascular system formed by
anterior and posterior ciliary arteries.

Inner six layers are supplied by the central retinal artery, branch of ophthalmic artery

RETINAL DYSTROPHIES:
Hereditary dystrophies commonly affect the outer retina (RPE and photoreceptor)

Classsification:

General photoreceptor dystrophies:

They involve the entire retina (periphery more than the macula)

Typical retinis pigmentosa and its variants

Progressive cone dystrophy

Leber congenital amaurosis

Congenital stationary night blindness

Congenital monochromatism

Macular dystrophies:

Juvenile best macular dystrophy

Stargardt’s disease

Vitelliform dystrophy

RETINITIS PIGMENTOSA:

This is a slow, degenerative disease of retina.

Affecting both eyes

Beginning in childhood resulting in blindness in middle or advanced age.

The degeneration primarily affects rods and cones, rods first and cones later.

Commences in equator of eye then spreading gradually anteriorly and posteriorly.

Inheritance: Sporadic disorder include mutation of rhodopsin(40%)

Inherited disorder: AR-most common-intermediate severity

AD-next common-least severe

X linked –least common-most severe

Prevelance: Occurs 1 in 5000 of population, common in males (3:2).

Pathogenesis: Death of rod photoreceptor(apoptosis),later the cones die
Clinical features:

Visual symptoms(Due to loss of rods)

Night blindness
Dark adaptation: Light threshold of peripheral retina is increased
Tubular vision: Loss of peripheral vision with preservation of central vision.
Loss of central vision after many years.

Fundus change

Retinal pigmentary change : Small, jet-black spots resembling bone corpuscles with spidery outline
(the pigment of RPE migrates into retinal layer-epithelium becomes decolorized –choroidal vessels
are seen ,fundus appears tessellated)
Retinal arterioles become thread like
Thinning and atrophy of RPE at peripheral retina.
Optic disc: Has a pale, wax like yellowish appearance – ‘consecutive optic atrophy’
Progressive posterior cortical cataract is formed.

Visual field change

Annular or Ring shaped scotoma: Degenerated equatorial zone of retina.

Electrophysiological changes

Subnormal Electroretinogram(ERG) and Electrooculogram(EOG).

Assosiations:

Occular: Myopia
Primary open angle glaucoma
Microphthalmus
Posterior subcapsular cataract

General:
Laurence-Moon-Biedl-Bartum syndrome – retinitis pigmentosa , obesity, hypogonadism, mental
defect, polydactyl
Usher’s syndrome – retinitis pigmentosa, cardiac conduction defects and abetalipoproteinemia .
Refsum’s syndrome – retinitis pigmentosa , cerebellar ataxia and peripheral neuropathy

Atypical retinitis pigmentosa

Retinitis pigmentosa sine pigmento: Al symptoms are same , no pigmentary change in retina.
Retinitis punctate albicans: Numerous white dots scattered over the fundus.
Cone –rod dystrophy:
Cones are degenerated first
Symptoms:
Loss of central vision
Colour vision is defective

Defective vision in bright light

Sectorial retinitis pigmentosa: Segment of retina is affected.

Pericentric retinitis pigmentosa: Area around macula is affected

TREATMENT

Measures to stop progression-------vasodilators, placental extracts, light exclusion therapy, ultrasonic

therapy, acupuncture therapy

Correction of refractive error ------Glasses

Systemic acetazolamide ------- associated cystoid macular oedema

Low vision aids--------magnifying glasses, night vision device

Rehabilitation

Prophylaxis:------Generic counselling-no consaguinous marriage

-affected not to produce children

RETINAL DEGENERATION:
These acquired disorders of retina characterized by degenerative changes

Classification:

Peripheral retinal degeneration

Vitreoretinal degeneration

Macular degeneration

Peripheral retinal degeneration:

Occurs at the periphery in front of the equator.

1. Lattice degeneration:

-Characters:

White arborizing lines arranged in lattice pattern in upper peripheral fundus

Retinal thinning

Abnormal pigmentation

Typical lesion –spindle shaped

Mainly involves superior temporal region of fundus

Snail tract degeneration:

Variant of lattice-white lines replaced by snow flake areas-retina-white frost like appearance.
Acquired(senile) retinoschisis:

Splitting of retina at the level of outer plexiform layer

Common in hypermetropes

Occurs bilaterally

Involves lower temporal quadrant

Thin , transparent, immobile elevation of inner layers of retina

White without pressure:

Pale, discrete areas of retinal periphery due to vitreous traction

White with pressure:

Greyish translucent appearance of retina seen on scleral indendation

[Link] pigment clumps:

Small, irregular pigmentation seen in equatorial region associated with vitreous detachment or
retinal tear.

[Link] chorioretinal degeneration:

Common in myopic eyes

Choroid depigmented

Retina thin

Prone to tears

[Link] cystoid retinal degeneration:

Common in old people

May predispose to retinal detachment in very old people.

 Vitreoretinal degenerations:

Wagner’s syndrome

AD

Vitreous is liquefied with condensed membranes

Retina-narrow sheathed vessels,pigmented spots in periphery

Choroid -atrophied

Cataract-late complication

Stickler syndrome:

AD

Vitreous liquefied –optically empty vitreous cavity

Progressive myopia

Radial lattice like degeneration

Bilateral retinal detachment

Ectopia lentis

Pre senile cataract

Orofacial abnormalities – flattened nasal bridge , maxillary hypoplasia, cleft palate , high arched
palate…
Arthropathy

Deafness

Mitral valve prolapse

[Link] –goldmann syndrome:

AR

Vitreous shows syneresis

Retinoschisis

Pigmentary chnges present

ERG is subnormal

MACULAR DEGENERATION

Age related macular degeneration :

Leading cause of blindness in people over 65 years of age in developed countries.

Bilateral

Risk factors: hereditary factors , age , nutrition , sunlight , hyperopia , blue eyes, nuclear cataract

Two types:

Dry or atrophic

Wet or exudative

Dry or atrophic:

Thinning of macular tissue

Amorphous deposits and pigmentation in macula(drusens-yellowish white deposits)

Symptoms: Gradual diminution of vision, difficulty in reading due to central shadowing

Stages: Early stage: macular drusens (<20),focal hyper pigmentation ,

RPE atrophy

Intermediate stage: RPE atrophy with >20medium drusens

and one large drusen

Advanced stage: large atrophic areas with visible choroidal

Vessels and disappearance of drusen

Wet or exuadative type:

New leaky vessels forma choroidal neovascular membrane(CNV)

(sub-RPE --- greenish grey and subretinal---halo or pigment plaque)

Symptom: Sudden painless loss of vision

Typical lesion: drusen with RPE detachment , hemorrhagic pigment epithelium detachment ,
disciform subretinal scarring .

Diagnosis:

[Link] signs

2. Fundus fluorescein angiography and indocyanine green angiography----CNV

3. Optical coherence tomography–reveals subretinal fluid CNV,hemorrhages,intraretinal thickening

Treatment:

[Link] ARMD

Vitamin C , A and E supplements , zinc oxide , cupric oxide and other antioxidants

Smoking cessation

Amsler grid

Correction of refraction

Low vision aid

[Link] ARMD

Intravitreal anti-VEGF therapy-Bevacizumab,Ranibizumab,..

Photodynamic therapy

Transpupillary thermotherapy

Photocoagulation

Surgical treatment
[Link] MACULAR DEGENERATION:
Chorioretinal atrophic patches at macula with heaping up of pigment around them.

Foster-Fuchs’ spot seen at macula(dark red patch due to subretinal CNV)

[Link] HOLES:

CAUSES: Senile, traumatic,tractional forces associated with early PVD.

Symptoms: decreased vision, metamorphopsia,central scotoma.

Investigation: OCT, fundus fluorescein angiography.

Stages: Stage 1 : absent foveal reflex and yellow spot

Stage 2: small,l full thickness hole in centre or margin of ring

Stage 3: full thickness reddish spot surrounded by grey halo

Stage 4:Full thickness hole with Srf cuff and complete PVD.

Treatment: Stage 2 -4 : pars plana vitrectomy with posterior hyaloid removal ,ILM peeling and gas or
silicon tamponade with strict post-operative face down position for 7-14 days.

MACULAR DISORDERS
HEREDITARY MACULAR DYSTROPHIES

SOLAR RETINOPATHY

CENTRAL SEROUS CHORIORETINOPATHY

CYSTOID MACULAR OEDEMA

MACULA
Macula is an oval shaped pigmented area near the centre of retina of human eye. (5.5mm in
diameter)

It is responsible for central, high resolution, colour vision.

It is subdivided into umbo, foveola, foveal avascular zone, fovea, parafovea, and perifovea areas.
Macular disorders are classified into

Congenital anomalies

Hereditary dystrophies

Acquired maculopathies

HEREDITARY MACULAR DYSTROPHIES

They can be classified according to anatomical level of retinal involvement as

 Hereditary macular disorders

INNER RETINA PHOTORECEPTORS

RETINAL PIGMENT EPITHELIUM
• X LINKED • CONE-ROD
JUVENILE DYSTROPHY • BEST’S DISEASE
RETINOSCHISIS • STARGARDT’S DISEASE
• FUNDUS
FLAVIMACULATUS

X LINKED JUVENILE RETINOSCHISIS

Juvenile retinoschisis is characterized by bilateral maculopathy, with associated peripheral

retinoschisis in 50%.

The basic defect is mediated via the Muller cells, leading to splitting of the retinal nerve fibre layer
from the rest of the sensory retina. [Muller cells are located in the inner nuclear layer of retina and
maintains structural and functional stability of retinal cells.]

Implicated gene is RS1

Affects mainly young males

Signs:

Gradual progressive loss of vision during first or second decade of life

Symptoms:

The most common appearance is foveal schisis, appearing as spoke-like striae radiating from the
foveola.
Peripheral retinoschisis in 50% cases

Presence of vitreous veils in extreme cases- floating of retinal blood vessels

Investigations:

Fundus Fluorescein Angiography (FFA) – Normal posterior pole

Electroretinogram (ERG) – negative

Electrooculogram (EOG) – normal

Treatment:

Topical carbonic anhydrase inhibitors

Gene therapy

CONE ROD DYSTROPHY

(also known as cone dominant dystrophy)

Mostly sporadic but may e autosomal dominant, autosomal recessive or X linked.

Symptoms:

Reduced central vision which is more marked in bright light (Hemeralopia).

On fundus examination, fundus may be normal or in some cases, bilateral Bull’s eye pattern of
macular depigmentation maybe seen.

Investigations:

FFA – patchy areas of hypo and hyper fluorescence.

Bull’s eye pattern- zone of hypo fluorescence over a central non fluorescent part.

ERG- marked loss of cones and moderate loss of rods

 BEST’S DISEASE

(also known as Best vitelliform macular dystrophy)

Autosomal dominant. It is due to allelic variation in the BEST1 gene.

Clinical picture of Best’s diseases is divided into:

Pre- vitelliform stage – normal fundus, abnormal EOG

Vitelliform stage- egg yolk lesion at macula

Pseudohypopyon stage- partially absorbed egg yolk lesion

Vitelli eruptive stage- scrambled egg appearance of macula

Stage of scarring – hypertrophic or atrophic vascularised scar at macula

Investigations:

Normal ERG, abnormal EOG

Fundus auto fluorescence – intense hyper auto fluorescence of the yellowish lesions and hypo auto
fluorescence in the atrophied areas.

STARGARDT’S DISEASE AND FUNDUS FLAVIMACULATUS

Stargardt disease (juvenile macular dystrophy) and fundus flavimaculatus (FFM) are regarded as
variants of the same disease, and together constitute the most common macular dystrophy.

Stargardt disease is a recessive, progressive tapetoretinal dystrophy of the central retina and
develops between the ages of 8 and 14 years.

Increased vitamin A intake is associated with the progression of the disease.

The condition is characterized by the accumulation of lipofuscin within the RPE.

Symptoms:
Gradual impairment of central vision.

On fundus examination, Stargardt’s disease show beaten bronze or snail slime reflex in macular area
and fundus flavimaculatus shows yellowish white retinal flecks of variable size and shape distributed
over whole of posterior pole

snail slime lesion

Investigations:

ERG is usually normal for Stargardt’s disease but there will be changes in full field ERG for fundus
flavimaculatus.

SOLAR RETINOPATHY

(also known as photo retinitis, eclipse retinopathy, blue light retinal injury)

Causes of solar retinopathy:

Religious sun gazing, solar eclipse observing, telescopic solar viewing, sun bathing and sun watching
in psychiatric disorders.

Welding arc exposure

Lightening retinopathy

Retinal phototoxicity from ophthalmic instruments like operating microscope

Pathogenesis:

Photochemical reaction following exposure of retina to shorter wavelength in the visible spectrum.

Symptoms:

Persistence of negative after image of the sun

Decreased vision
Signs:

Small yellow spot with grey margin may be noted in the foveolar and para foveolar region

Typical lesion: central burnt-out hole in the pigment epithelium surrounded by aggregation of
mottled pigment

Through ophthalmoscope: bean-or kidney shaped pigmented spot with yellowish white centre in the
foveal region, macular holes in worse cases.

CENTRAL SEROUS CHORIORETINOPATHY

(also known as central serous choroidopathy, central serous retinopathy)

Central serous choroidopathy is a focal disease of the retinal pigment epithelium and
choriocapillaris.

Risk factors:

Males of 20-50 years are more at risk

Type A personality

Steroid intake

Emotional stress

SLE

Pregnancy

Cushing’s disease

Pathogenesis: Choroidal vascular hyperpermeability theory

Sympathetic drive,
sympathomimetics,
corticosteroids

Alter choroidal vascular

permeability
Affects auto regulation
 Increases tissue
hydrostatic pressure

Pigment epithelial defect

Breach in outer blood

retinal barrier

Leakage of fluid

Development of localised
serous detachment of
neurosensory retina
Symptoms:

Unilateral blurring, metamorphopsia, micropsia and mild dyschromatopsia

Signs:

Fundus examination shows:

Mild elevation of macular area, demarcated by a circular ring-reflex

Small, yellow grey elevations

Absence of foveal reflex

Subretinal deposits

Clinical Course

Acute classic CSCR (central serous chorioretinopathy): short clinical course with spontaneous
resolution within 3-6 months

Chronic CSCR: diffuse retinal pigment epitheliopathy

Bullous CSCR: rare, large and more numerous areas of serous detachments

Investigations:
in-point defect in Bruch’s membrane results in a smokestack or inkblot appearance in the late

phases.

FFA: Ink blot pattern: small hyperfluorescent spot which gradually increases in size

FFA: Smoke stack pattern: small hyperfluorescent spot which ascends vertically like a smoke-stack
and gradually spreads laterally to take a mushroom or umbrella configuration

Indocyanine angiography: multiple areas of hyper fluorescence (hyperpermeability of choroid)

Treatment:

Corticosteroid treatment should be discontinued if possible

Laser photocoagulation in chronic and recurrent cases

Photodynamic therapy (PDT)

Anti- VEGF

CYSTOID MACULAR OEDEMA

Accumulation of fluid in the outer plexiform and inner nuclear layers of the retina with the
formation of tiny cyst-like cavities.

Etiology:

Complication of ocular treatment (e.g.: ocular surgery)

Retinal vascular disorders (e.g.: diabetic retinopathy)

Intraocular inflammations (e.g.: pars planitis)

Retinal dystrophies (e.g.: retinitis pigmentosa)

Vitreomacular traction

Systemic disease

Fundus tumours (e.g.: retinal capillary haemangioma)

Drug-induced (e.g.: topical prostaglandin derivatives)

Pathogenesis:

Breakdown of inner
blood retinal barrier

Leakage of fluid
 Accumulation in
outer plexiform and
inner nuclear layer
of retina and
formation of cyst-
like changes

Symptoms:

Blurring, distortion and micropsia

Signs:

Loss of the foveal depression, thickening of the retina and multiple cystoid areas in the sensory
retina

Investigations:

Ophthalmoscopy reveals a typical Honey-comb appearance

Fundus fluorescein angiography: flower petal appearance

Treatment:

Treatment of the causative factor

Topical anti prostaglandin drops

Topical and systemic steroids

Systemic carbonic anhydrase inhibitors (CAIs) e.g., oral acetazolamide

Age Related Macular Degeneration (ARMD)

aka Senile macular degeneration

Bilateral disease affecting people above 50yrs of age

Most common cause of Irreversible visual loss in developed countries

Risk Factors:-

Age – Major risk factor

Race – More common in white individuals than other races

Heredity –

Risk of ARMD is 3x higher if a first degree relative has the disease

Variation in Complement factor H gene and ARMS2 gene increase risk

Smoking – Doubles the risk

Hypertension and CVS risk factors aggravate ARMD

Dietary factors – High fat intake and obesity promotes ARMD

Aspirin – Increases risk of neovascular ARMD

Other-

Cataract surgeries

Blue iris

High sunlight exposure

Female gender

Classification:-

Conventional classification

Clinical classification

Conventional classification:

[Link] exudative (or) Atrophic ARMD

aka Dry (or) Geographic ARMD

90% of cases

Symptoms – Gradual loss of vision, Distorted vision and Difficulty in reading

Lesions are described in 3 stages:

[Link] stage, characterized by:

# Small or medium sized Drunsens(They are well defined, yellowish white, slightly elevated spots)

#Focal pigmentation

#Pale area of Retinal Pigment Atrophy(RPE)

[Link] stage, shows:

#Sharply circumscribed areas of RPE atrophy

#Loss of Choriocapillaries with large/medium drunsen

[Link] stage, with:

#Enlargement of atrophic areas

#Choroidal vessels become visible

 #Pre-existing Drunsen disappear

[Link] ARMD

aka Wet (or) Neovascular ARMD

10% of cases

Major symptom is Rapidly progressing loss of vision

Chronological appearance of lesions :

Drunsen with Retinal Pigment Epithelial Detachment(PED)

Choroidal neovascularization

Haemorrhagic PES

Haemorrhagic detachment of neurosensory retina

Disciform sub-retinal scarring

Clinical classification:
Diagnosis:-

Above signs are detected using Slit Lamp Biomicroscopy

Fundus Fluorescence Angiography helps to detect Choroidal Neovascularization (CNC).

It’s of 2 types-

[Link] CNV – Seen as lacy hyperfluorescence

[Link] CNV – Seen as stippled hyperfluorescencec Optic Coherence Tomography(OCT) reveals

Subretinal fluid, Intraretinal thickening, CNV and haemorrhage in exudative ARMD

Treatment:-

[Link] for Non exudative ARMD:

Dietary supplements and antioxidants

Smoking cessation

Amsler grid is used to detect new or progressive metamorphosis

Refraction with increased near add is useful in early cases

Low vision aid is useful in advanced cases

[Link] for Exudative ARMD:

Intravitreal anti-VEGF therapy – First choice treatment. Improves vision in 30%-40% of cases

Photodynamic Therapy (PDT) – Treatment of choice after anti VEGF injections

Transpupillary thermotherapy(TTT)

Double frequency YAG 532nm photocoagulation

Surgical treatment

Macular Hole

It refers to a partial or full thickness hole in the Neurosensory Retina

Causes:-

[Link](83%) -More common in females than males(3:1 ratio)

[Link](5%)

[Link] causes – Cystoid Macular oedema, Vitreomacular traction, Post surgical

Pathogenesis:-

Caused by Tractional forces associated with early PVD(Post Vitreous Detachment)

Clinical Features:--
[Link] vision

[Link] (or) distortion of vision

[Link] scotoma

Signs:-

[Link] Grid testing – shows central scotoma

[Link] Allen test – shows a line appearing broken which indicates macular hole

[Link] Examination – basis for Gass classification of Macular hole

Gass classification of Macular hole:

Stage 1 (or) Impending hole

Absence of foveal reflex

Yellow spot/ring in foveal region

OCT reveals pseudocyst

Stage 2

Small full thickness hole seen centrally or eccentric

Less than 400 mm(micrometer)

Stage 3

Full thickness hole seen as round reddish spot

Grey halo surrounds it

No PVD

OCT shows macular hole greater than 400mm

Stage 4

Full thickness hole with SRF(Subretinal fluid) cuff

Complete PVD

OCT confirms large thick holes with PVD from disc and macula
Differential Diagnosis of fundus appearance:-

Macular pucker with pseudohole

Solar retinopathy

Intraretinal cyst

Vitreomacular traction syndrome

Investigation:-

[Link] fluorescein angiography

[Link]

Treatment:-

Stage 1 : Treatment not recommended. Close follow up and observation only required

Stage 2-4 : Treatment with

Pars plana vitrectomy with post hyaloid removal

Internal Limiting Membrane peeling

Gas or silicon oil tamponade with strict post-op

Prognosis:-

80%-90% show anatomical closure

Visual improvement reported in 70% of recent onset hole

Complications of surgery:-

Occurrence or progression of Cataract (common complication)

Other complications-Retinal breaks, detachment, phototoxicity, endophthalmitis.

RETINAL DETACHMENT:

Retinal detachment (RD) refers to separation of neurosensory retina from the retinal pigment
epithelium (RPE).

CLASSIFICATION:

1. Rhegmatogenous or primary retinal detachment,

2. Tractional retinal detachment, and

3. Exudative retinal detachment.

RHEGMATOGENOUS OR PRIMARY RETINAL DETACHMENT

PREDISPOSING FACTORS:

Age-Most common 40-60 years

Sex-Male: Female: 3:2

Myopia-40% cases

Aphakia or pseudophakia (previous cataract surgery)

• Retinal degenerations such as:

- Lattice degeneration (most common)

-Snail track degeneration

-White-with-pressure and white-without pressure lesions

-Diffuse chorioretinal degeneration

-Acquired (senile) retinoschisis.

6. Trauma

7. Senile posterior vitreous detachment (PVD).

[Link]. This is a condition where there is splitting of the neurosensory retina and
vitreous degeneration. It is of two types: -

-Typical Retinoschisis: Split at the level of Outer Plexiform Layer

- Reticular Retinoschisis: Split at the level of Nerve Fibre Layer.

PATHOGENESIS:

CLINICAL FEATURES:

PRODROMAL SYMPTOMS
Photopsia (flashes of light) due to vitreoretinal traction

Dark spots (floaters) in front of the eyes (muscae volitantes).

SYMPTOMS OF DETACHED RETINA

Localized relative loss in the field of vision of detachment retina, which is described by the patient as
a black curtain or veil in front of the eye.

Loss of vision in detachment involving macula area.

SIGNS

Hypotony: The liquefied vitreous in the subretinal space is absorbed through the RPE leading to
hypotony.

Shafer’s sign: Pigments in anterior vitreous (tobacco dusting) is a feature of fresh RD.

Detached retina gives grey reflex, is raised, thrown into folds which oscillate with the movements of
the eye.

Retinal breaks holes (round, horse-shoe-shape or slit like) look reddish and are most frequently
Round in the periphery (commonest in the upper temporal quadrant).

Thinning of detached retina, secondary intraretinal cysts, subretinal demarcation lines are signs of
old RD

COMPLICATIONS

Proliferative vitreoretinopathy

Complicated cataract

Uveitis

Phthisis bulbi

TREATMENT

Prophylactic laser barrage:

It is done in Symptomatic break (associated with photopsia and floaters), Horse shoe tear, Superior,
especially superotemporal tears, Aphakia, One eyed patient

Surgery for retinal detachment

Scleral buckling: In this procedure, the sclera is indented by attaching an explant known as a buckle.
This pushes the RPE inwards towards the neurosensory retina. Subretinal fluid is drained and the
break is closed by laser or cryotherapy

Pneumatic retinopexy: In this procedure, the neurosensory retina is pushed towards the RPE by
injecting an expansile gas in the vitreous cavity. The break is then sealed with laser. Th commonly
used are Sulphur Hexafluoride and Perfluoropropane (C3F8)

Pars plana vitrectomy

TRACTIONAL RETINAL DETACHMENT:

PATHOPHYSIOLOGY

Fibrovascular membranes in the vitreous due to long standing vitreous hemorrhage exert traction on
the retina. This pulls the retina forward leading to retinal detachment.

CAUSES

Proliferative diabetic retinopathy(PDR)

Central retinal vein occlusion

Eales’ disease

Retinopathy of prematurity (ROP).

SIGNS

Detached retina is concave in configuration with highest elevation at the site of the tractional band.
No breaks are seen

Minimal mobility

TREATMENT

Pars plana vitrectomy and endophotocoagulation.

EXUDATIVE RETINAL DETACHMENT

PATHOPHYSIOLOGY

Exudative fluid, mainly from choroid, collects in the sub retinal space leading to retinal detachment.

CAUSES

Inflammatory conditions like choroiditis, choroidal vasculitis, posterior scleritis

Choroidal tumor like melanoma, hemangioma, metastasis

Toxemia pregnancy

Malignant hypertension

Coat’s disease,

Symptoms

Floaters due to vitritis but no photopsia

Visual field defect

Loss of vision due to involvement of macula

SIGNS

Detached retina has a convex configuration. Surface is smooth. No break Is seen.

Shifting fluid is seen

TREATMENT
Systemic steroid

Treatment of the cause,

1. Classification:

A. Primary tumours

1. Neuroblastic tumours. : These arise from sensory retina (retinoblastoma and astrocytoma) and

Pigment epithelium (benign epithelioma and melanotic malignant tumours).

2. Mesodermal angiomata :e.g., cavernous haemangioma.

3. Phakomatoses:

Angiomatosis retinae (von Hippel-Lindau disease),

tuberous sclerosis (Bourneville’s disease),

neuro- fibromatosis (von Recklinghausen’s disease and

Encephalo-trigeminal angiomatosis (Sturge-Weber syndrome).

B. Secondary tumours

1. Direct extension: e.g., from malignant melanoma of the choroid.

2. Metastatic carcinomas from the gastrointestinal tract, genitourinary tract, lungs, and pancreas.

3. Metastatic sarcomas.

4. Metastatic malignant melanoma from the skin.

[Link]

Most common ocular tumour of childhood

INCIDENCE

rare, occurring in up to 1:18000 live births

most common primary intraocular malignancy of childhood

GENETICS

Mutations in retinoblastoma gene, which is RB 13q14

Deletion or inactivation of this gene by Hudson’s two hit hypothesis

May arise as hereditary or non hereditary forms

Hereditary or familial case

Mutation will occur in all germ cells

Accounts for 40% of all cases

Mostly bilateral

Mostly multifocal

Some have trilateral retinoblastoma

Non hereditary or sporadic cases

Mutation takes place in somatic cells

Accounts for60% of all cases

Unilateral and bifocal

Tumour is not transmissible

3. PATHOLOGY:

a. ORIGIN:

Malignant proliferation of immature retinal cells (retinoblasts)

HISTOPATHOLOGY:

Flexner -Wintersteiner rosettes

Homer Wright Rosettes

Pseudo rosettes

Fleurttees formation

Areas of necrosis and calcification

CLINICAL PICTURE:

4 STAGES

QUIESCENT STAGE

GLAUCOMATOUS STAGE

STAGE OF EXTRAOCULAR EXTENSION

STAGE OF DISTANT METASTASIS

[Link] STAGE (6months to 1 yr.)

Leukocoria or yellowish white papillary reflex(amaurotic cats eye appearance)

Squint

Nystagmus

Defective vision
Ophthalmoscopic features like endophytic and exophytjc retinoblastoma

[Link] STAGE (if left untreated)

Severe pain, redness, watering

Enlarged eyeball

Conjunctiva is congested

Cornea becomes hazy

IOP raised

[Link] OF INTRAOCULAR EXTENSION

Progressive enlargement followed by the burst through acler

Rapid fungation

Marked proptosis

[Link] OF DISTANT METASTASIS

Lymphatic spread

Direct extension

Metastasis by blood stream

[Link] DIAGNOSIS :

D/D of leukocoria

Retinoblastoma

Congenital cataract

Persistenthyperplastic primary vitreous (PHPV)

Coats disease

Toxacariasis

ROP

Endophthalmitis

Coloboma

Endophytic retinoblastoma

Exophytic retinoblastoma

[Link]
EXAMINATION UNDER ANAESTHESIA:Fundus examination,measurement of IOP,corneal diameter

PLAIN X RAYS OF THE ORBIT: Calcification present

LACTIC DEHYDROGENASE :level is raised in aqueous humour

ULTRASONOGRAPHY AND CT SCANNING

[Link]

[Link]

Cryotherapy

Laser photocoagulation

Transpupillary thermotherapy

SYSTEMIC

Chemotherapy

ENUCLEATION

RETINAL VASCULAR TUMOURS:

Capillary haemangioma

Von Hippel–Lindau disease

Cavernous haemangioma

Racemose haemangioma

Vaso proliferative tumour

CAPILLARY HAEMANGIOMA:

Early tumour-small red oval or round lesions

well-established tumour – round orange-red mass

juxta papillary site is common

TREATMENT:

Observation

Laser photocoagulation

Cryotherapy

Brachytherapy
Vitreoretinal surgery

VON HIPPEL LINDAU DISEASE:

Mutation in the VHL tumour suppressor gene

CLINICAL FEATURES:

CNS haemangioma

Phaeochromocytoma.

Renal carcinoma

Polycythaemia

Cysts of testes , kidney, ovaries, lungs,liver and pancreas

CAVERNOUS HAEMANGIOMA

Rare unilateral congenital hamartoma.

SIGNS

Clusters of saccular aneurysms resembling a ‘bunch of grapes’

‘menisci’

Haemorrhage and epiretinal membrane formation

TREATMENT :

Vitrectomy

CONGENITAL RETINAL ARTERIOVENUS COMMUNICATION (racemose haemangioma)

Vasoproliferative tumour

rare gliovascular lesion

can be primary (80%) or secondary

TREATMENT

Cryotherapy or brachytherapy

PRIMARY INTRAOCULAR LYMPHOMA

The main classification and ocular manifestations

Hodgkin disease.

Non-Hodgkin lymphoma can manifest with conjunctival involvement, orbital involvement, Mikulicz
syndrome and uveal infiltration.

CNS B-cell lymphoma may be associated with intermediate uveitis and sub-RPE infiltrates.

Primary vitreoretinal lymphoma (PVRL)

Primary uveal lymphoma

TREATMENT

Radiotherapy

Intravitreal methotrexate

Systemic chemotherapy

TUMOURS OF THE RETINAL PIGMENT EPITHELIUM

Congenital hypertrophy of the RPE

Congenital hypertrophy of the retinal pigment epithelium (CHRPE) used to encompass three entities
with distinct features and implications:

Solitary CHRPE, grouped CHRPE, Atypical CHRPE.

PHACOMATOSES

Phacomatoses or neurocutaneous syndromes refer to a group of familial conditions (having

autosomal AB dominant transmission) which are characterized by development of neoplasms in eye,
skin and central nervous system. Phacomatoses includes the following conditions:

1. Angiomatosis retinae (Von Hippel Lindau’s syndrome). This is a rare condition affecting males
more often than females, in the third and fourth decade of life. Angiomatosis involves retina, brain,
spinal cord, kidneys and adrenals. Clinical course of angiomatosis retinae comprises vascular
dilatation, tortuosity and formation of aneurysms which vary from small and 72frica7272 to balloon-
like angiomas

2. Tuberous sclerosis (Bourneville disease). It is characterized by a classic diagnostic triad of

adenoma sebaceum, mental retardation and epilepsy associated with hamartomas of the brain,
retina and viscera. The name tuberous sclerosis is derived from the potato-like appearance of the
tumors in the cerebrum and other organs.

3. Neurofibromatosis (von Recklinghausen’s disease). It is characterized by multiple tumours in the

skin, nervous system and other organs. Cutaneous manifestations are very characteristic and vary
from I-au-lait spots to neurofib romata. Ocular manifestations include neurofibromas of the lids and
orbit, glioma of optic nerve and congenital glaucoma.
 4. Encephalofacial angiomatosis (Sturge-Weber syndrome). It is 73frica7373ival73 by angiomatosis
in the form of port-wine stain (naevus flammeus), involving one side of the face which may be
associated with choroidal haemangioma, leptomeningeal angioma and congenital glaucoma on the
affected side.

ENUCLEATION

Enucleation refers to excision of the eyeball. It can be performed under local anaesthesia in
adults and under general anaesthesia in children. Indications

1. Absolute indications are retinoblastoma and malignant melanoma.

2. Relative indications are painful blind eye, nonresponsive to conservative measure mutilating
ocular injuries

3. Indication for eye donation from cadaver is presently the most common indication
 NEURO – OPHTHALMOLOGY

What will we learn here???

▪ Anatomy of visual pathway

▪ Physiology of vision
▪ Lesions of visual pathway
Optic nerve lesions
Chiasmal lesions
Retrochiasmal lesions
▪ Pupillary reflexes and their abnormalities
Light reflex
Near reflex
Abnormalities of pupillary reactions
Anisocoria
▪ Diseases of optic nerve
Optic neuritis
Leber’s hereditary optic neuropathy
Autosomal heredity optic atrophy
Toxic optic neuropathy
Anterior ischemic optic neuropathy
Traumatic optic neuropathy
Papilloedema
Optic atrophy
▪ Symptomatic disturbance of vision
Night blindness
Day blindness
Color blindness
Amaurosis
Amblyopia
Cortical blindness
Malingering
Disorders of higher visual functions
▪ Ocular manifestation of diseases of CNS
 ANATOMY OF VISUAL PATHWAY

The visual pathway starts from retina and ends in visual cortex

lateral
optic optic optic visual
retina optic tracts geniculate
nerves chiasma radiations cortex
bodies

Blood supply: (important)

• Surface layer of optic disc – capillaries from retinal arterioles

• Prelaminar region – centripetal branch of peripapillary choroid
• Lamina cribrosa – posterior ciliary arteries branches and arterial circle of Zinn
• Retrolaminar part – centrifugal branches of central retinal artery and centripetal
branches from pial plexus

PHYSIOLOGY OF VISION

Feature Somatic sensation Visual sensation

Sensory end organ Nerve endings in the skin Rods and cones
Neurons of 1st order Lie in posterior root Lies in bipolar cell layer of
ganglion the retina
Neurons of 2nd order Lies in nucleus gracilis or Lies in ganglion cells of the
cuneatus retina
Neurons of 3rd order Lies in thalamus Lies in geniculate body
 LESIONS OF THE VISUAL PATHWAY

lesions of visual
pathway

retrochiasmal
optic nerve lesions chiasmal lesions
lesions

OPTIC NERVE LESIONS

Lesions in distal part of optic nerve Lesions in proximal part of optic

nerve
Salient • Ipsilateral complete blindness • Ipsilateral blindness
features • Abolition of the direct light reflex • Contralateral hemianopia
and consensual of contralateral • Abolition of the direct light reflex
side and consensual of contralateral
• Accommodation reflex is present side
• Accommodation reflex is present
Common • Optic atrophy
causes • Trauma
• Indirect optic neuropathy
• Ischemic optic neuropathy
• Acute optic neuritis

CHIASMAL LESIONS
Causes:

• Intrinsic
→ Glioma and multiple sclerosis
• Extrinsic
→ Pituitary adenoma, craniopharyngiomas and meningioma
• Other causes
→ Metabolic, toxic, traumatic and inflammatory conditions
 Chiasmal syndrome

Chiasmal Features Causes

syndrome
Anterior • Junctional scotoma – a combination • Lesions affecting the ipsilateral
of central scotoma in one eye and optic nerve fibres and contralateral
temporal hemianopia defect in inferonasal fibres located in
another eye Willebrand knee
Middle • Bitemporal hemianopia and • Lesions involving the decussating
• Bitemporal hemianopic paralysis of fibres in the body of chiasma
pupillary reflex
Posterior • Paracentral bitemporal field defects • Lesions affecting caudal fibres in
• Contralateral homonymous chiasma
hemianopia
Lateral • Binasal hemianopia • Distension of 3rd ventricle
• Binasal hemianopic paralysis of • Atheroma of posterior
pupillary reflexes communicating arteries or carotids

RETROCHIASMAL LESIONS

Retrochiasmal
lesions

lesions of lateral
lesions of optic lesions of optic lesions of visual
geniculate
tract radiations cortex
nucleus

Lesions of optic tract

→ Causes
▪ Intrinsic lesions – demyelinating diseases and infarctions
▪ Extrinsic lesions – compressive lesions
▪ Other causes – syphilitic or tubercular meningitis

→ Characteristic features
▪ Incongruous homonymous hemianopia
▪ Wernicke’s reaction
▪ Descending type of partial optic atrophy
▪ Ipsilateral third nerve palsy and ipsilateral hemiplegia
Lesions of lateral geniculate nucleus
→ Characteristic features
▪ Homonymous hemianopia
▪ Descending type of partial optic atrophy

Lesions of optic radiations

→ Common lesions – vascular occlusions, tumours, trauma, temporal lobectomy for
seizures
→ Characteristic features

Depending on the site it could be

▪ Superior quadrantic hemianopia
▪ Inferior quadrantic hemianopia
▪ Complete homonymous hemianopia

Lesions of visual cortex

→ Characteristic features

Visual field defects

▪ Congruous homonymous hemianopia
▪ Congruous homonymous macular defects
▪ Bilateral homonymous hemianopia with macular sparing
▪ Bilateral homonymous macular defects
Other defects
▪ Cortical blindness
▪ Dyschromatopsia
▪ Visual hallucinations
▪ Palinopsia
▪ Visual anaesthesia
▪ Polyopsia
PUPILLARY REFLEXES AND THEIR ABNORMALITIES

LIGHT REFLEX
NEAR REFLEX
 ABNORMALITIES OF PUPILLARY REACTIONS
• Amaurotic light reflex – absence of direct light reflex on affected side and consensual
reflex on the normal side
• Efferent pathway defect – absence of both direct and consensual light reflex on the
affected side only
• Wernicke’s hemianopic pupil – lesion in optic tract. ipsilateral direct and
contralateral consensual reflex is absent
• Marcus Gunn pupil – due to relative afferent pathway defect.
• Argyll Robertson pupil – both pupils are small and irregular. light reflex absent. near
reflex present.
• Adies tonic pupil – light reflex absent. near reflex is slow and tonic

ANISOCORIA
Definition
Difference between the size of two pupils is known as anisocoria
Causes

• physiological
o minimal
• pathological
o due to abnormal miosis and mydriasis of one pupil

Evaluation

• pupil size
• pupillary light reflex
• pharmacological tests
 DISEASES OF OPTIC NERVE

diseases of
optic nerve

congenital inflammatory vascular

trauma degeneration tumours
anomalies conditions distrubances

OPTIC NEURITIS
Introduction:
An inflammation of the optic nerve is known as optic neuritis.

Etiology:

• Idiopathic
• Hereditary optic neuritis
• Demyelinating disorders
• Parainfectious optic neuritis
• Infectious optic neuritis
• Autoimmune disorders
• Toxic optic neuritis

Clinical profile:
Anatomical types

anatomic
classification

retrobulbar
papillitis neuroretinitis
neuritis
 ▪ Typical neuritis – optic neuritis associated with demyelinating disorders as in multiple
sclerosis
▪ Atypical neuritis – optic neuritis associated with causes other than demyelinating
disorders

Clinical features
Symptoms Signs
• Vision loss – monocular, sudden, • ↓ visual acuity
progressive and profound loss • ↓ colour vision
• ↓ dark adaptation • Marcus Gunn pupil
• Visual obscuration in bright light • Central or centrocaecal scotoma
• Impaired colour vision • ↓ contrast sensitivity
• Uhthoff’s symptom
• Pulfrich’s phenomenon

Differential diagnosis
▪ Papillitis
▪ Acute retrobulbar neuritis

Investigations
▪ Multifocal VEP
▪ MRI scan of brain and orbit

Treatment
▪ Treat the underlying cause
▪ Corticosteroid therapy
o Oral prednisolone therapy
o Methylprednisolone i.v.
▪ Interferon therapy
 LEBER’S HEREDITARY OPTIC NEUROPATHY

Introduction
▪ It is characterised by sequential subacute
optic neuropathy in males aged 11 – 30
years.

Etiology
▪ Point mutation in mitochondrial DNA – MT-
ND4 GENE.
▪ Transmitted by carrier females.

Clinical features
▪ Early cases – asymptomatic
▪ ↓ bilateral visual acuity
▪ Centrocaecal scotoma among others

Investigations
▪ Oct optic disc – peripapillary retinal thinning
▪ Fluorescein angiography
▪ Genetic testing

Treatment
▪ No known effective treatment
▪ Avoid smoking and alcohol
▪ Avoid dietary deficiency – vitamin B12
▪ Low vision aids
 AUTOSOMAL HEREDITY OPTIC ATROPHY

autosomal

recessive dominant

Autosomal recessive optic atrophy (infantile)

▪ Severe visual loss at birth or within 2 years of life
▪ Commonly associated with nystagmus

Autosomal dominant optic atrophy (juvenile)

▪ Associated with mutation of opa1 gene on chromosome 3
▪ Characteristic feature
o Onset – insidious
o Slowly progressive
o ↓ colour vision
o Temporal pallor of optic disc
o Centrocaecal scotoma in visual field

Wolfram’s syndrome – gene defect localised in chromosome 4

Consists of
▪ Diabetes mellitus
▪ Optic atrophy
▪ Deafness
 TOXIC OPTIC NEUROPATHY

Also known as nutritional optic neuropathy and toxic amblyopia

types

tobacco ethyl alcohol methyl alcohol quinine ethambutol

amblyopia amblyopia amblyopia amblyopia amblyopia

Tobacco – alcohol / nutritional amblyopia

Predisposing factors
▪ Pipe smokers
▪ Heavy drinkers
▪ Diet deficiency in proteins and vitamin b complex

Pathogenesis
Excessive tobacco smoking
↓ ↓ cyanide detoxification due to
↑ cyanide in blood ← alcoholic’s dietary deficiency of
↓ sulfur rich proteins
Degeneration of ganglion cells
particularly of the macular region
↓
Degeneration of Toxic
Papillo- macular bundle → Amblyopia
in the nerve
 Clinical features Treatment Prognosis

▪ Bilateral ▪ Complete cessation of tobacco and alcohol Good

centrocaecal consumption
scotoma ▪ Hydroxocobalamin
▪ Thiamine
▪ Peripapillary ▪ Folate
haemorrhage ▪ Care of general health and nutrition

Ethyl alcohol amblyopia

▪ Usually occurs in tobacco amblyopia
▪ Can occur in non-smokers, heavy drinkers suffering from chronic gastritis.
▪ Clinical features and treatment are similar to tobacco amblyopia
▪ Prognosis not good

Methyl alcohol amblyopia (methanol poisoning)

Etiology
▪ Intake of wood alcohol
Pathogenesis
▪ Methyl alcohol oxidised into formic acid and formaldehyde in tissues. They cause
edema followed degeneration of ganglion cells of retina resulting in complete
blindness.

Clinical features
General symptoms Ocular features
Headache Complete blindness
Nausea Mild disc edema
Vomiting Markedly narrowed blood vessels
Dizziness Bilateral primary optic atrophy
Delirium

Treatment
▪ Gastric lavage
▪ Administration of alkali
▪ Ethyl alcohol
▪ Eliminative treatment

Prognosis is poor
 ANTERIOR ISCHAEMIC OPTIC NEUROPATHY

Introduction
▪ It refers to ischemic damage to the optic nerve head from occlusion of the short
posterior ciliary arteries.

Types
▪ Arteritic anterior ischemic optic neuropathy (AAION)
▪ Non arteritic anterior ischemic optic neuropathy (NAAION)

AAION NAAION
Etiology ▪ Inflammatory and thrombic ▪ Unknown
occlusion of short posterior
ciliary arteries caused giant
cell arteritis
Clinical ▪ Headache ▪ Headache
features ▪ Tenderness ▪ Scalp tenderness
▪ Jaw claudication ▪ Jaw claudication
▪ Transient ischemic attacks ▪ Amaurosis fugax
▪ Central retinal artery ▪ Visual loss
occlusion ▪ Optic disc edema
▪ Diplopia
Investigations ▪ Fundus fluorescein ▪ ESR
angiography ▪ C reactive proteins
▪ Visual fields ▪ FFA
▪ ESR & c – reactive protein
levels
▪ Temporal artery biopsy
Treatment ▪ Corticosteroid therapy ▪ Addressing systemic
risk factors
▪ Aspirin
 TRAUMATIC OPTIC NEUROPATHY
Types
▪ direct
▪ indirect

Direct Indirect
Less common More common
Due to Direct anatomical disruption of optic Due to Shearing or avulsion of nutrient
nerve in cranio-orbital trauma vessels or by pressure transmitted along
bone to the optic canal

Characteristic features
▪ loss of vision
▪ pupil dilation
▪ loss of ipsilateral direct reflex and contralateral consensual light reflex
▪ Marcus Gunn pupil
▪ diminished light brightness sensitivity
▪ diminished contrast sensitivity
▪ central or centrocaecal scotoma

Investigations
▪ CT
▪ MRI

Treatment
▪ methylprednisolone i.v. in high doses
▪ surgical decompression of optic canal
 PAPILLOEDEMA

Papilloedema is referred to as disc swelling associated with bilateral asymmetrical

increased intracranial pressure

Etiopathogenesis
▪ Congenital conditions
▪ Intracranial space occupying lesions
▪ Intracranial infections and hemorrhages
▪ Obstruction of CSF absorption
▪ Tumours of spinal cord
▪ Idiopathic intracranial hypertension
▪ Systemic conditions
▪ Diffuse cerebral edema

Unilateral papilloedema is seen in Foster Kennedy Syndrome and Pseudo Foster Kennedy
Syndrome

Pathogenesis
Hayreh’s theory is the most accepted theory

alteration in pressure results in stasis of axoplasm

gradient across the lamina in prelaminar region of resulting in papilloedema
cribrosa optical disc

Clinical features
General features
▪ Headache
▪ Nausea
▪ Projectile vomiting
▪ Diplopia
Ocular features
Early Established Chronic Atrophic
Symptoms Absent Transient visual - -
obscuration
Visual Normal Normal ↓ Severely impaired
acquity
Ophthalmic ▪ Obscuration of ▪ Disc edema ▪ Dome of ▪ Greyish white
features disc margins ▪ Obliterated champagne discoloration
▪ Blurring of physiological cork and pallor of
peripapillary cup of optic appearance disc
nerve fiber disc ▪ Central cup ▪ ↓ prominence
layer ▪ Multiple obliterated of the disc
▪ Absence of cotton wool ▪ Presence of ▪ Narrowed
spontaneous spots and corpora retinal
venous superficial amylacea arterioles
pulsation in the hemorrhages ▪ Congested
disc ▪ Tortuous and veins
▪ Mild hyperemia engorged ▪ White
of disc veins sheathing
▪ Splinter ▪ Paton’s lines around blood
hemorrhages vessels
present
Pupillary Normal Normal Normal Impaired light
reactions reflex
Visual Normal Enlargement of Blind spot Concentric
fields blind spot enlarge and contraction of
visual field peripheral field
constrict

Treatment

▪ It’s a neurological emergency

▪ Requires immediate hospitalization
▪ If causative agent isn’t identified, cerebral decompression is done

Prognosis is bad
 OPTIC ATROPHY

▪ It refers to the degeneration of optic nerve which occurs as an end result of any
pathologic process that damages axons in the anterior visual system

ophthalmic
classification

primary consecutive glaucomatous post neuritic vascular

pathological features
Following 3 situations can occur
▪ Degeneration of nerve fibres associated with excessive gliosis
▪ Degeneration and gliosis may be orderly
▪ Degeneration of nerve fibres with negligible gliosis

Etiology
Type Etiology
Primary ▪ Multiple sclerosis
▪ Idiopathic retrobulbar neuritis
▪ Leber’s optic atrophy
▪ Intracranial tumours
▪ Trauma or avulsion
▪ Toxic amblyopia
▪ Tabes dorsalis
Consecutive Secondary to
o Diffuse chorioretinitis
o Retinitis pigmentosa
o Pathological myopia
o Occlusion of central retinal artery
Post neuritic ▪ As a sequela to long standing papilloedema or papillitis
Glaucomatous ▪ Long standing raised ICT
Vascular ▪ Giant cell arteritis
▪ Severe hemorrhage
▪ Severe anemia
▪ Quinine poisoning
Clinical features
▪ Loss of vision
▪ Semi-dilated pupil
▪ Sluggish or absent direct light reflex
▪ Presence of Marcus Gunn pupil

Differential diagnosis
FEATURE PRIMARY SECONDARY CONSECUTIVE
APPEARANCE Chalky white Dirty grey white Waxy pallor
MARGINS Well defined Ill defined Well defined
LAMINA CRIBROSA Well seen Obscured Well seen
VESSELS Normal Peripapillary Allenuation
sheathing
SURROUNDING Healthy Hyaline bodies / Pathology seen
RETINA drusen

Treatment
▪ Treat the underlying cause
▪ Once there is complete atrophy, vision cannot be recovered

SYMPTOMATIC DISTRUBANCES OF THE VISION

NIGHT BLINDNESS

Another name: nyctalopia

Etiology:
▪ Rod dysfunction – vitamin a deficiency, retinitis pigmentosa, congenital high myopia,
oguchi’s disease
▪ Advanced POAG
▪ Media opacities – paracentral lenticular and corneal opacities
 DAY BLINDNESS
Another name: hemeralopia
Causes
▪ Congenital deficiency of cones
▪ Central lenticular opacities
▪ Central corneal opacities

COLOR BLINDNESS
• Normal color vision- trichromate (see 3 primary colors i.e. Red, blue and green)
• Absence of one or more primary colors is defective or absent

dyschromatopsia
congenital
color blindness achromatopsia
acquired

Congenital color blindness – males > females

Dyschromatopsia [color confusion due to deficient to perceive colors]

Anomalous The mechanism to Protanomalous – defective red color
trichromacy appreciate all the three appreciation
colors is present but is
defective in one or two of Deuteranomalous – defective green
them color appreciation

Tritanomalous – defective blue color

appreciation
Dichromacy The ability to perceive one Protanopia – complete red colour
of the 3 primary colours is defect
absent
Deuteranopia – complete green color
Such individuals are known defect
as dichromates
Tritanopia – complete blue color defect
Blue cone Complete absence of red
monochromatism and green cone function
Achromatopsia
• rod monochromatism
• extremely rare
• autosomal recessive
• Male=female

Characteristics:
▪ Total color blindness
▪ Day blindness (6/60 visual acuity)
▪ Nystagmus
▪ Fundus is usually normal

Acquired color blindness

▪ Following macular and optic nerve damage
▪ Associated with central scotoma and decreased visual acuity
▪ Blue yellow impairment: retinal lesion by CSR, macular edema, shallow retinal
detachment
▪ Red green deficiency: optic nerve lesions such as optic neuritis, Leber’s optic
atrophy, compression of optic nerve
▪ Acquired blue color defect: in old age due to increased sclerosis of lens;
physical absorption of blue rays by increased amber coloured pigments

Tests for color vision:

• Pseudo chromatic charts: most commonly used test using ishihara’s plates; quick
method to screen red color defect
• Hardy rand rittler plates: more sensitive than ishihara’s plates
• Edridge green lantern test: name various colors shown to him by lantern
• Farnsworth munsell 100 hue test: most sensitive test both congenital and acquired
High score= poor vision
• Farnsworth d 15 hues
• City university color vision test
• Nagel’s anomaloscope
• Holmgren’s wools test
currently, there is no treatment for color blindness
 AMAUROSIS

Complete loss of sight in one or both in absence of ophthalmoscopic or other marked

examination

Amaurosis fugax:
Sudden temporary painless monocular loss of vision due to transient failure of retinal
circulation.

Causes:
▪ Carotid transient ischemic attacks
▪ Embolization of retinal circulation
▪ Papilloedema
▪ Giant cell arteritis
▪ Raynaud’s disease
▪ Migraine
▪ Hypertensive
▪ Venous stasis retinopathy

Clinical characteristics:
▪ Typical present as curtain that descends from above or ascends from below to
occupy upper or lower half of visual fields
▪ Lasts for 2 to 5 mins
▪ Resolves in reverse pattern of progression
▪ Shortly after the attack, fundus may normal or show signs of retinal ischemia as
edema, hemorrhage or emboli

Uraemic amaurosis:
▪ Sudden, bilateral complete loss of sight due to toxic materials upon cells of visual
centre in patients with acute nephritis, eclampsia of pregnancy, renal failure.
▪ Presentation: loss with dilated pupil responses to light, fundus normal except
hypertensive retinopathy
▪ Vision returns in 12 to 48 hrs
 AMBLYOPIA
▪ Partial loss of sight in one or both eyes in absence of ophthalmoscopic or other
marked signs
▪ May be congenital or acquired (functional or organic)
▪ Functional amblyopia: from psychical suppression of retinal image, it may be
anisometric/strabismic/stimulus deprivation

CORTICAL BLINDNESS
▪ Bilateral occipital lobe lesion

Causes:
▪ Bilateral occipital infarction by vascular causes
▪ Head injury involving bilateral occipital lobes
▪ Tumors among others

Clinical features:
▪ Bilateral loss of vision
▪ Normal pupillary light reflexes
▪ Visual imagination
▪ Anton syndrome: denial of blindness by the patient who obviously cannot see
▪ Riddoch phenomenon: able to perceive kinetic but not static targets.

Management: thorough neurological and cardiovascular examination to find cause

Treatment: based on the cause

MALINGERING
▪ Person poses to be blind but he is not
▪ He does to gain advantage. He does not show any objective sign. Usually one eye is
said to be blind

Differential diagnosis: to rule out condition with normal anterior segment and fundus.
▪ Amblyopia
▪ Cortical blindness
▪ Retro bulbar neuritis
▪ Cone rod dystrophy
▪ Chiasmal tumors
 Tests for malingering:
▪ Convex lens test:
Place low convex/concave lens (0.25) before blind eye and high power(10d) in
front of normal eye if the patient reads distant words, malingering is proved

▪ Prism base down test:

Place the prism base in normal eye, if the patient says seeing two lights
confirms malingering.

▪ Prism base out test:

Ask to see light source, place the prism of 10d is placed before blind eye. If
patient eye moves inwards proves malingering.

▪ Snellen’s colored types test:

It has letters printed on red and green. Ask the patient to see through red glass
if he reads all letters it confirms malingering because normally red letters only
can be read through red glass.

Hysterical blindness
o It is a form of psychoneurosis, commonly seen in attention seeking females

Characteristic features
o Sudden bilateral loss of vision
o Lacrimation
o Blepharospasm
o Visual fields are concentrically contracted
o Treatment
o Psychological support and reassurance
o Placebo tablets
 DISORDERS OF HIGHER VISUAL FUNCTIONS

Visual agnosia
▪ Definition
It refers to a rare disorder in which ability to recognise the objects by sight is
impaired while the ability to recognise by touch, smell or sound is intact

▪ Types
Prosopagnosia – can’t identify familiar faces
Object agnosia – can’t identify familiar objects

▪ Site of lesion – bilateral inferior occipitotemporal junction

▪ Associated features
Bilateral homonymous hemianopia
Dyschromatopsia

Visual hallucinations
▪ Definition

It refers to conditions in which patient alleges of seeing something not evident

to others in the same environment

▪ Types
o Elementary – colours, flashes, etc
o Complex – includes objects, peoples or animals

▪ Causes
o Occipital and temporal lobe lesions
o Drug induced
o Charles bonnet syndrome
o migraine
o Psychiatric disorders
Alexia and agraphia
▪ Alexia – inability to read
▪ Agraphia – inability to write

Causes
▪ Alexa associated with agraphia – lesions of angulate gyrus of the dominant
hemisphere
▪ Alexa without agraphia – lesions that destroy the visual pathway in left occipital
lobe and associated fibres from right occipital lobe

Visual illusions
▪ E.g.: palinopsia, optic anaesthesia, etc can also occur.
▪ It mostly occurs in lesions in occipital, occipitoparietal or occipitotemporal regions

OCULAR MANIFESTATIONS OF DISEASES OF CNS

Intracranial infections
o Meningitis
o Encephalitis
o Brain abscess
o Neurosyphilis

Intracranial aneurysms
▪ they produce complications by following mechanisms
o Pressure effects
o Aneurysm of circle of Willis
o Posterior communicating artery aneurysm
o Vertebrobasilar artery aneurysms
o Production of arteriolar venous fistula
o Subarachnoid hemorrhage
o Intracranial hemorrhage

▪ They include primary and secondary tumors

 ▪ Clinical features

General effects of False localising signs Focal signs of intracranial mass

↑ ICP lesions
▪ Headache ▪ Diplopia ▪ Prefrontal tumors – Foster
▪ Vomiting ▪ Sluggish pupillary Kennedy syndrome
▪ Papilloedema reflexes ▪ Chiasmal tumours – chiasmal
▪ Giddiness ▪ Unilateral mydriasis syndrome
▪ Hypertension ▪ Bitemporal hemianopia ▪ Cerebellar tumours – corneal
▪ Homonymous anaesthesia
hemianopia

Demyelinating diseases
Ocular manifestations
▪ Multiple sclerosis – unilateral optic neuritis, internuclear ophthalmoplegia and
vestibular or cerebellar nystagmus
▪ Devic’s disease – bilateral optic neuritis
▪ Schilders disease – optic neuritis, cortical blindness, ophthalmoplegia and nystagmus

Ocular signs in head injury

Concussion injuries to brain
▪ Hutchinson’s pupil – initially ipsilateral miosis, later dilatation with no light reflex –
indicates immediate cerebral compression
▪ papilloedema – if it appears with 48 hours, it indicates extra or intracerebral
hemorrhage. If it appears after a week it is due to cerebral edema

Fractures of base of skull

▪ Cranial nerve palsies
▪ Optic nerve injury
▪ Subconjunctival hemorrhage
▪ Ipsilateral dilated pupil
 OCULAR MOTILITY & STRABISMUS

OCULAR MANIFESTATION

Binocular Single Vision

Definition :

It is the co-ordinated use of both eyes so as to produce a single mental impression

i.e in normal individual the image is formed on fovea of both eyes, but the individual
perceives a single image.

Development of BSV:

• It is a conditioned reflex
• acquired after 6 months
• normal retinal correspondence is prerequisite for BSV

Important milestones:

Motor mechanism Straight eyes – starting from neonatal period

precise coordination for all directions of gaze
Sensory mechanism Reasonably clear vision in both eyes for similar
images in both retina
Mental process Ability of visual cortex to produce BSV

Grades of BSV:

There are 3 grades

Grade 1: Simultaneous Perception - Power to see 2 dissimilar objects
simultaneously

Grade 2:Fusion - It consist of power to superimpose two incomplete but

similar images to form one complete image

Grade3:Stereopsis - Ability to perceive the third dimensions i.e depth

perception. Tested with stereopsis slides in synoptophore

Anomalies of Binocular Single Vision

1. SUPPRESSION

2. AMBLYOPIA

3. ABNORMAL RETINAL CORRESPONDENCE

4. CONFUSION
 5. DIPLOPIA

SUPRESSION

• temporary active cortical inhibition of image formed on retina of squinting eye

• occurs only during both eyes open

• when normal eye is( fixating eye) is covered the squinting eye is fixed (suppression
disappears)

• test to detect suppression

1. worth’s 4 dot test

2. 4 dioptre base out prism test

3. red glass test

4. synoptophore test

AMBLYOPIA

Partial reversible loss of vision in one or both eyes, for which no cause can be found by
physical exam. i.e Absence of any organic disease to ocular media, retina, visual pathway

Pathogenesis:

• amblyogenic factors @ critical period of visual development Birth – 6to 7

years

• At this stage (a) visual pathway develops

(b) brain learns to interpret signals from eyes

• If the child cannot use one or both eyes for any reason the vision is not
developed

• this condition is termed amblyopia

AMBLYOGENIC FACTORS:

1. Visual deprivation eg; anisometropia

2. Light deprivation eg; congenital cataract

3. Abnormal binocular interaction eg; strabismus

TYPES OF AMBLYOPIA
1. STRABISMIC AMBLYOPIA

. due to uniocular suppression with unilateral constant squint who fixate with normal eye

. Squint is most common amblyopia

2. STIMULUS DEPRIVATION AMBLYOPIA

. also amblyopia ex anospia

. one eye is totally excluded from seeing early in life in congenital or traumatic 3frica33,
complete ptosis, Dense central corneal opacity

3. ANISOMETROPIC AMBLYOPIA

. occurs in the eye having higher degree of refractive error than the other

. most common in anisohypermetropic children

. 1-2D hypermetropic anisometropia cause amblyopia but 3D myopic anisometropia does not

4. ISOAMETROPIC AMBLYOPIA

bilateral amblyopia in children with bilateral uncorrected hidh refractive error

5. MERIDIONAL AMBLYOPIA

occurs in uncorrected astigmatic refractive error

Selective amblyopia for specific for specific visual meridian

CLINICAL CHARACTERISTICS

1. Visual acuity:

- decreases

- recognition acuity affected more than resolution

6. Effect of neutral density filtor:

visual acuity is

- amblyopia is improved

-decreases in organic lesion

7. Crowding phenomenon :

visually acuity is less when tested with multiple letter charts- snellen’s charts.

8. Fixation pattern :

central/ eccentric

Degree of amblyopia in eccentric fixation is proportional to the distance of the eccentric point
from the fovea

9. Colour vision :
 usually normal but affected in deep amblyopia

TREAMENT

must be started as early as possible (<3 yrs)

10. Occlusion therapy

. occlusion of normal eye forcing the use of amblyopia eye is the main treatment

. Before starting ensure,

- opacity in the media (if any should be removed, eg:cataract)

- refractive errors corrected completely

. Simplified schedule for occlusion therapy upto 2 years ->2:1 (2 days normal eye 1 day
amblyopic eye)

3rd year->3:1(3 days normal eye 1 day amblyopic eye)

4th year->4:1

5th year ->5:1

6th year ->6:1

Duration of occlusion should be until the visual acuity develops fully, or there is no further
improvement of vision after 3 months of occlusion.

11. Penalization

blurring of vision of normal eye 2methods

- use of atropine-> atropine penalization

- use of over plus lens->optical penalization

12. Pleoptic exercise

re-establish foveal fixation

13. Pharmacological manipulation

use of levodopa/carbidopa as adjunct

Perceptual learning

adjunct to occlusion therapy

14. Computerised vision therapy

.useful for treatment of amblyopia with 4frica44ival4 result

. works on the concept of operant conditioning i.e psychological treatment

ABNORMAL RETINAL CORRESPONDENCE

 In a state of normal binocular single vision, there exists a precise physiological relationship b/w
the corresponding points of the two retinae. This the fovea of corresponding points and have the
same visual direction. This is normal retinal correspondence

Definition:

In squint , there occurs an active cortical adjustment in the directional values of the two retinae.
Hence, fovea of normal eye& extra foveal point on the retina of the squinting eye acquire a common
visual direction.

This is abnormal retinal correspondence(ARC)

Test to detect ARC;

1. Worth’s four dot test

2. litmus stereo test

3. Bagolini striated glasss test

4. Synoptophore test

DIPLOPIA:

refers to formation of images on the dissimilar points of the two retinae. There are 2

-UNIOCULAR

-BINOCULAR

BINOCULAR VISION:

occurs on formation of image of dissimilar points of the 2 retinae

causes;

1. paralysis of extraocular muscles

2. displacement of one eyeball

3. mechanical restrictions of ocular movement like pterygium, symblepharon, thyroid

ophthalmopathy

4. deviation of ray of light in one eye

5. anisometropia ->disparity of image size b/w 2 eyes as in high anisometropia

TYPES ;

1. Uncrossed

2. Crossed

Uncrossed:- (harmonious)

-false image is on the same side as deviation

-occurs in convergent squint as in lateral rectus paralysis

Crossed:- (unharmonious)

-false image is seen on the opposite side

- occurs in divergent squint as in the medial rectus paralysis

UNIOCULAR VISION:

an object appears double from the affected eye even when the normal eye is closed

causes:

1. Subluxated clear lens

2. subluxated intreocular lens

3. double pupil due to congenital anomaly/pheriperal iridectomy/iridodialysis

4. Incipient 6frica66-> polyopia

5. Keratoconus -> diplopia due to changed refractive power of cornea in different parts

Treatment of diplopia;

1. Treat the causative disease

2. Temporary relief by occluding the ajjected eye

STRABISMUS

Contents:

• Definition
• Heterophoria
• Concomitant strabismus

DEFINITION

• A misalignment of the visual axes of the two eyes is called squint or strabismus
• The visual axis passes from the fovea, through the nodal point of the eye, to the
point of fixation.

Pseudo strabismus:

• The visual axis passes from the fovea, through the nodal point of the eye, to the point of
fixation
PSEUDOESOTROPIA PSEUDOEXOTROPIA

• Apparent convergent squint • Apparent divergent squint

• Prominent epicanthal folds • Hypertelorism (wide separation of 2
eyes)
• Negative angle kappa • Positive angle kappa

• Angle kappa is the angle, usually about 5°, subtended by the visual and anatomical axes.
 • The angle is positive(normal) when the fovea is temporal to the centre of the posterior
pole resulting in a nasal displacement of the corneal reflex, and negative when the converse
applies.

CLASSIFICATION OF STRABISMUS

STRABISMUS

MANIFEST
SQUINT
LATENT SQUINT
(heterotropia)
(heterophoria)

CONCOMITANT INCOMITANT
SQUINT SQUINT
 HETEROPHORIA

• Heterophoria implies a tendency of the eyes to deviate when fusion [correct blending of
images of both eyes] is blocked (latent squint).
• Orthophoria implies perfect ocular alignment in the absence of any stimulus for fusion;
this is uncommon.
Types of heterophoria:
ESOPHORIA (latent convergent EXOPHORIA (latent divergent HYPER CYCLOPHORIA
squint) squint) PHORIA (Latent torsional deviation)

Tendency of eye ball to deviate Tendency of eye ball to deviate Tendency of eye ball Tendency of eye ball to rotate
inward outward to deviate upward around anteroposterior axis
[downwards:
hypophoria]
Types: Types: Types:
• Convergence excess • Convergence weakness • Incyclophoria: When 12’o
type (esophoria more type (exophoria more clock meridian of cornea
for near fixation than for near fixation) rotates nasally
distant) • Divergence excess type • Excyclophoria: When 12’o
• Divergence weakness (more for distant clock meridian of cornea
type (more for distant fixation) rotates temporally)
fixation) • Nonspecific type
• Nonspecific type
Aetiology:
[Link] factors:
• Orbital symmetry
• Abnormal interpupillary distance (wide: exophoria, small: exophoria)
• Faulty insertion of extraocular muscles
• A mild degree of extraocular muscle weakness
• Abnormal innervation
• Anatomical variation in the position of the macula

[Link] factors:

• Age: esophoria more common in younger age, exophoria more common in

elders
• Role of accommodation: increased accommodation: esophoria, decreased:
exophoria
• Role of convergence: increased convergence: esophoria, decreased
convergence: exophoria
• Dissociation factor: e.g.: prolonged constant use of one eye results in
exophoria

Symptoms:
 • Compensated heterophoria: Compensation of heterophoria depends upon the reserve
neuro-muscular power to overcome the muscular imbalance and individual’s desire for
maintenance of binocular vision
• Decompensated heterophoria: they are grouped as:
Symptoms of muscular fatigue Symptoms of failure to Symptoms of defective
maintain binocular singular postural sensations
vision
• Headache and eye • Blurring • Problems in
ache • Intermittent diplopia judging distances
• Difficulty in changing • Intermittent squint and positions of
the focus moving objects
• Photophobia

Examination:

[Link] for vision and refractive error

[Link]- uncover test:

• Cover one eye with an 9frica9 and the other is made to fix on an object
• Deviation of eye undercover is observed

[Link] of heterophoria:

• Prism cover test:

[Link] of increasing strength with apex towards the deviation are
placed in front of one eye and the patient is asked to fixate an object
with the other.
[Link] cover-uncover test is performed till there is no recovery
movement of the eye under cover.
[Link] will tell the amount of deviation in prism dioptres. Both
heterophoria as well as heterotropia can be measured by this test.
• Maddox- rod test: Maddox rod consists of a series of fused cylindrical
red glass rods that convert the appearance of a white spot of light in the
centre of the Maddox tangent scale into a red streak. When the
glass rods are held horizontally, the streak will be vertical and vice
versa.
• Maddox wing test: Maddox wing is an instrument by which the amount
of phoria for near (at a distance of 33 cm) can be measured.
Right eye sees a vertical white arrow and a horizontal red arrow and the
left eye sees a vertical and a horizontal line of numbers.
The number seen by the patient on horizontal line with white arrow
gives amount of horizontal phoria and that on vertical line with red
arrow gives vertical phoria
The cyclophoria is measured by asking the patient to align the red arrow
with the horizontal line of numbers.
[Link] of convergence and accommodation

• Measurement of near point of convergence measurement ( NPC- the

nearest point on which the eyes can maintain binocular fixation) using
RAF rule A target is slowly moved along the rule towards the patient’s
eyes until one eye loses fixation and drifts laterally
 • Measurement of near point of accommodation (NPA- the nearest point
on which the eyes can maintain clear focus using RAF rule
15. Measurement of fusional reserve:
• Fusional reserve is the maximum amount the eyes can converge or diverge
• Vertical fusional reserve: 1.5°-2.5°
• Horizontal negative fusional reserve (abduction range): 3°-5°
• Horizontal positive fusional reserve (adduction range): 20°-40°

Treatment

• Correction of refractive error

• Orthoptic treatments (non- computerised exercises using synoptophore, prisms etc or
computerised exercises)
• Prescription of prism in glasses
• Surgical treatment

CONCOMITANT STRABISMUS

• It is a type of manifest squint in which the amount of deviation in the squinting eye remains
constant (unaltered) in all the directions of gaze; and there is no associated limitation of
ocular movements.

Aetiology:

The obstacles in the development of binocular vision and coordination of ocular movements are:

Sensory obstacles Motor obstacles Central obstacles

• Refractive errors • Abnormal shape and size • Deficient
• Anisometropia of orbit development of fusion
• Prolonged use of • Abnormalities of faculty
14frica1414ival14 extraocular muscles • Abnormalities of
spectacles • Abnormalities of cortical control of
• Corneal opacities accommodation, ocular movements
• Lenticular opacities convergence and their
• Diseases of macula ratio
• Optic atrophy

General features of concomitant strabismus

• Ocular deviation
• Ocular movements are not limited
• Refractive error (may or may not be present)
• Suppression and amblyopia (decreased eyesight due to abnormal visual development)
• A-V patterns in horizontal strabismus

Types of concomitant squint

• Convergent squint (esotropia)

• Divergent squint (exotropia)
• Vertical squint (hypertropia)
CONVERGENT SQUINT

• Concomitant convergent squint or esotropia denotes inward deviation of one eye.

• It is more common than divergent type
• The deviation is not always purely horizontal; in many cases the eye deviates upwards as
well as inwards.

Clinico-etiological types:
1. Infantile esotropia
2. Accommodative esotropia (refractive, non-refractive and mixed)
3. Acquired non accommodative esotropia
4. Sensory esotropia
5. Consecutive esotropia

1. Infantile esotropia:

• Age of onset: 2-4 months

• Angle of deviation >35 degrees
• Fixation in most infants is alternating in the primary position
• There is cross fixating in side gaze, so that the child uses the left eye in right gaze and the
right eye on left gaze
 • Amblyopia develops in 25-40 % cases
• Surgery is the treatment of choice

2. Accommodative esotropia

Refractive accommodative esotropia Non-refractive Mixed esotropia

accommodative
esotropia

AC/A (accommodative AC/A ratio: large High AC/A ratio with

convergence/accommodation ratio: hypermetropia
normal with high hypermetropia
For near and distance Greater for near
Fully correctable by use of spectacles It is fully corrected by Esotropia for
bifocal glasses adding distance is corrected
+3 DS for near vision. by correction of
 hypermetropia; and
the residual
esotropia for near is
corrected by an
addition of +3 DS
lens.

3. Acquired non accommodative esotropias

It includes:

• Essential acquired or late onset esotropia

• Acute concomitant esotropia
• Cyclic esotropia
• Nystagmus blockage syndrome
• Esotropia in myopia and microtropia

Essential acquired or late onset esotropia is of 3 types:

Basic type Convergence excess type Divergence insufficiency type

Deviation is equal at distance Deviation is large for near and Greater deviation for distance
and near small for distance than near

4. Sensory esotropia
• Sensory or secondary esotropia is caused by a unilateral reduction in visual
acuity that interferes with or abolishes fusion; causes can include cataract,
optic atrophy or hypoplasia, macular scarring or retinoblastoma.
5. Consecutive esotropia
• Consecutive esotropia follows surgical overcorrection of an exodeviation

DIVERGENT SQUINT

• Concomitant divergent squint (exotropia) is characterised by outward deviation

of one eye while the other eye fixates

Clinico- etiological types:

• Congenital exotropia
 • Primary exotropia (intermittent and constant)
• Sensory exotropia
• Consecutive exotropia

1. Congenital exotropia
• Presentation is often at birth.
• Signs – Normal refraction
-Large and constant angle.
• Neurological anomalies are frequently present, in contrast
with infantile esotropia.
• Treatment is mainly surgical and consists of lateral rectus
recession and medial rectus resection.
2. Primary exotropia
• Intermittent exotropia: most common type. Age of onset 2-5 years
Deviation is present at times and remains latent at others
• If untreated, intermittent exotropia may decompensate into constant exotropia

Types:

• Convergence insufficiency type (exotropia greater for near than distance)

• Divergence excess (exotropia greater for distance than near)
• Basic non-specific type (exotropia equal for near and distance).

3. Sensory exotropia
• Secondary (sensory) exotropia is the result of monocular or binocular visual
impairment by acquired lesions, such as cataract or other media opacity.
4. Consecutive exotropia
• Consecutive exotropia develops spontaneously in an amblyopic eye, or more
frequently following surgical correction of an esodeviation.
EVALUATION OF A CASE OF CONCOMITANT STRABISMUS

• History:

• Examination:
• Inspection
• Ocular movements
• Pupillary reactions
• Media and fundus examination
• Testing of vision and refractive error
• Cover tests
▪ Direct cover test: 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.
 ▪ Cover- uncover test (mentioned in examination for heterophoria)
▪ 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).
• Estimation of angle of deviation can be done by
▪ Hirschberg corneal reflex test:
the patient is asked to fixate at point light held at a
distance of 33 cm and the deviation of the corneal light
reflex from the centre of pupil is noted in the squinting
eye. Roughly, the angle of squint is 15o and 45o when the
corneal light reflex falls on the border of pupil and limbus,
respectively
▪ The prism and cover test (refer examination of
heterophoria)
▪ Modified Krimsky corneal reflex test:

It involves placement of prisms in

front of the fixating eye until the
corneal light reflections are
symmetrical. This test reduces the
problem of parallax and is
 more commonly used than the
prism reflection test.

▪ Measurement of deviation with

synoptophore:

All types of heterophorias and heterotropias

(both objective and subjective angle of squint)
can be measured accurately with it.
• Tests for grade of binocular vision and sensory function:
o Worth’s four dot test: patient wears goggles with red lens in front
of the right and green lens in front of the left eye and views a box
with four lights – one red, two green and one white
Results are:
Normal binocular vision: All 4 lights in the absence of
a manifest squint

Abnormal retinal All 4 lights even in the

correspondence: presence of a manifest
squint

Left suppression: 2 red lights

Right suppression: 3 green lights

 Alternating suppression: 3 green lights and 2 red lights
alternatively

Diplopia: 2 red lights and 3 green lights

o Tests for fixation: It can be tested with the help of a visuoscope

or fixation star of the ophthalmoscope. Patient is asked to cover
one eye and fix the star with the other eye. Fixation may be
centric (normal on the fovea) or eccentric (which may be
unsteady, parafoveal, macular, paramacular, or peripheral

o After- image test: In this test the right fovea is stimulated with a
vertical and left with a horizontal bright light and the patient is
asked to draw the position of after-images. Results are:
Normal retinal correspondence Draws cross

Esotropic patient with abnormal retinal Draws vertical image to the left
correspondence: of horizontal

Exotropic patient with abnormal retinal Draws vertical image to the right
correspondence: of horizontal

o Sensory function tests with synoptophore: Synoptophore (major

amblyoscope) consists of two tubes, having a right-angled bend,
 mounted on a base. Each tube contains a light source for
illumination of slides and a slide carrier at the outer end, a
reflecting mirror at the right-angled bend and an eyepiece of +6.5
D at the inner end. Uses are:
1. Estimation of grade of binocular vision
2. Detection of normal/ abnormal retinal correspondence

o Neutral density filter test: visual acuity is measured without and

with neutral density filter placed in front of the eye. In cases with
functional amblyopia visual acuity slightly improves while in
organic amblyopia it is markedly reduced when seen through the
filter.

TREATMENT OF STRABISMUS:

1. Spectacles with full correction of refractive error

2. Occlusion therapy. It is indicated in the presence of amblyopia. After correcting the refractive
error, the normal eye is occluded and the patient is advised to use the squinting eye.
3. Preoperative orthoptic exercises.
4. Squint surgery:
• In operating for squint with a general or local anaesthetic it is important
to remember that the position of the eyes varies in different stages of
anaesthesia so that it gives no indication of the final position after the
anaesthetic has worn off.

5. Postoperative orthoptic exercises.

REFERENCES:

1. A K KHURANA Comprehensive ophthalmology

2. Kanski’s Clinical Ophthalmology
 3. Parsons’ Diseases of the Eye
4. Oxford handbook ophthalmology

CONCOMITANT SQUINT

Concomitant Strabismus

It is a type of heterotropia (manifest squint) in which the amount of deviation varies in different
directions of gaze. It includes following conditions:
1. Paralytic squint.
2. ‘A’ and ‘V’ pattern heterotropias.
3. Restrictive squint.

Paralytic strabismus

It refers to ocular deviation resulting from complete or incomplete paralysis of one or more
extraocular muscles.
Etiology
1. Neurogenic lesions.
2. Myogenic lesions.
3. Neuromuscular junction lesions.

Neurogenic lesions
1. Neurogenic lesions may occur at the level of nerve nucleus, nerve root, or any part of the in its
course.
2. Nuclear ophthalmoplegia refers to paralysis of extraocular muscles due to lesions of 3rd cranial
nerve. They are more often bilateral.
Causes of neurogenic lesions:
16. Congenital.
Hypoplasia or absence of nucleus is a known cause of third and sixth cranial nerve palsies. Birth
injuries may mimic congenital lesions.
17. Inflammatory lesions.
These may be in the form of encephalitis, meningitis, neurosyphilis or peripheral neuritis
(commonly viral). Nerve trunks may also be involved in the infectious lesions of cavernous sinus and
orbit.
18. Neoplastic lesions.
These include brain tumours involving nuclei, nerve roots or intracranial part of the nerves; and
intraorbital tumours involving peripheral parts of the nerves.
4. Vascular lesions.
(a) These are known in patients with hypertension, diabetes mellitus and atherosclerosis. These
may be in the form of haemorrhages, thrombosis, embolism, aneurysms or vascular occlusions.
Cerebrovascular accidents are more common in elderly people.
(b) Ophthalmoplegic migraine or episodic ophthalmoplegia is a well-known vascular condition
characterized by recurrent attacks of headache associated with paralysis of 3rd (most common), 4th or
6th cranial nerve.
I The condition is often unilateral, persists for days or weeks and even tends to become
permanent, in some cases.
5. Traumatic lesions.
These include head injury and direct or indirect trauma to the nerve trunks. Head injury is common
cause of 6th nerve palsy.

19. Toxic lesions.

 These include carbon monoxide poisoning, effects of diphtheria toxins (rarely), alcoholic and lead
neuropathy.
20. Demyelinating lesions.
Ocular palsy may occur in multiple sclerosis and diffuse sclerosis.
II. Myogenic lesions
21. Congenital lesions.
These include absence, hypoplasia, malinsertion, weakness and musculofacial anomalies.
22. Traumatic lesions.
These may be in the form of laceration, disinsertion, hemorrhage into the muscle substance or
sheath and incarceration of muscles in blow out fractures of the orbital walls (floor or medial wall).

Eye injury

23. Inflammatory lesions.

Myositis is usually viral in origin and may occur in influenza, measles and other viral fevers.
24. Myopathies.
These include thyroid myopathy, carcinomatous myopathy and that associated with certain drugs.
Chronic progressive ophthalmoplegia (CPO) is a bilateral myopathy of extraocular muscles; which may
be sporadic or inherited as an autosomal dominant disorder.
It is the most common (75% cases) type of mitochondrial myopathy. It is characterized by:
25. Bilateral ptosis with slowly progressive ophthalmoplegia
is typical presentation.
(2). Diplopia is usually not a complaint since all eye movements are reduced equally.
 (3).Other associated symptoms of CPO include exercise intolerance, hearing loss, ataxia, sensory
axonal neuropathy, parkinsonism, and clinical depression.
III. Neuromuscular junction lesion
It includes myasthenia gravis. The disease is characterized primarily by fatigue of muscle groups,
usually starting with the small extraocular muscles, before involving other large muscles.

Clinical features
Symptoms
26. Diplopia.
It is the main symptom of paralytic squint. It is more marked in the field of action of paralyzed
muscle. It may be crossed (in divergent squint) or uncrossed (in convergent squint). It may be
horizontal, vertical or oblique depending on the muscle paralyzed.
Diplopia occurs due to formation of image on dissimilar points of the two retinae. The false image
(seen by the squinting eye)
is less distinct than the true image (seen by the other eye).

27. Confusion.
It occurs due to formation of image of two different objects on the corresponding points of two
retinae.
28. Nausea and vertigo.
These result from diplopia and confusion and may cause vomiting also.
29. Ocular deviation is typically a sudden onset.

Signs
30. Primary deviation.
It is deviation of the affected eye and is away from the action of paralysed muscle, e.g., if lateral
rectus is paralysed the eye is converged. Angle of deviation varies in different directions of
gaze (incomitant).
2. Secondary deviation.
(1) It is deviation of the normal eye seen under cover, when the patient is made to fix with the
squinting eye. It is greater than the primary deviation.
(2) This is due to the fact that the strong impulse of innervation required to enable the eye with
paralysed muscle to fix is also transmitted to the yoke muscle of the sound eye resulting in a greater
amount of deviation. This is based on Hering’s law
of equal innervation of yoke muscles.
31. Restriction of ocular movement
It occurs in the direction of the action of paralysed muscles.
4. Compensatory head posture.
(1) It is adopted to avoid diplopia and confusion. Head is turned towards the direction of action
of the paralysed muscle, e.g., if the
right lateral rectus is paralysed, patient will keep the head turned towards right.
(2) Ocular torticollis refers to tilting of head and chin depression occurring to compensate for the
vertical diplopia. It needs to be
differentiated from the true torticollis occurring due to undue contracture of sternocleidomastoid
muscle.
32. False projection or orientation.
It is due to increased innervational impulse conveyed to the paralysed muscle. It can be
demonstrated by asking the patient
to close the sound eye and then to fix an object placed on the side of paralysed [Link] will
locate it further away in the same direction.

Varieties of Ocular Paralysis

33. If one muscle alone is affected it is generally the lateral rectus or the superior oblique, since each
of these is supplied by an
independent nerve.
 (2) Affection of several muscles simultaneously extrinsic and intrinsic muscles of one or both eyes
may be paralysed called total ophthalmoplegia.
(3) If only the extrinsic muscles are affected the condition is called external ophthalmoplegia;if
only the intrinsic muscles (sphincter pupillae and ciliary muscle) are affected it is termed as internal
ophthalmoplegia.

Pathological sequelae of an extraocular muscle palsy

In all cases of extraocular muscle palsy, certainsequelae take place after some time. These occur
more in paralysis due to lesions of the nerves than the lesions of muscles. These include:
1. Overaction of the contralateral synergistic muscle.
2. Contracture of the direct antagonist muscle.
3. Secondary inhibitional palsy of the contralateral antagonist muscles.

Pathological sequelae of the right lateral rectus muscle paralysis

Clinical varieties of ocular palsies

34. Isolated muscle paralysis.

Lateral rectus and superior oblique are the most common muscles to be paralysed singly, as they
have separate nerve supply. Isolated paralysis of the remaining four muscles is less common, except
in congenital lesions.
35. Paralysis of the third cranial nerve.
It is of common occurrence. It may be congenital or acquired.
Clinical features of third nerve palsy include:
(1) Ptosis due to paralysis of the LPS muscle.
(2) Deviation. Eyeball is turned down, out and slightly intorted due to actions of the lateral rectus
and
superior oblique muscles. Ocular movements are restricted in all the directions except outward.
 (3) Pupil is fixed and dilated due to paralysis of the sphincter pupillae muscle.
(4) Accommodation is completely lost due to paralysis of the ciliary muscle.
(5) Crossed diplopia is elicited on raising the eyelid.
(6) Head posture may be changed if pupillary area remains uncovered.
3. Double elevator palsy
It is also known as monocular elevationan and is a deficiency is a congenital condition caused by
third nerve nuclear lesion. It is characterised by paresis of the superior rectus and the inferior oblique
muscle of the involved eye.
36. Total ophthalmoplegia.
In this condition, all extraocular muscles including LPS and intraocular muscles, viz., sphincter
pupillae, and ciliary muscle
are paralysed. It results from combined paralysis of third, fourth and sixth cranial nerves. It is a
common feature of orbital apex syndrome and cavernous sinus thrombosis.
37. External ophthalmoplegia.
In this condition, all extraocular muscles are paralysed, sparing the intraocular muscles. It results
from lesions at the level of motor nuclei sparing the Edinger-Westphal nucleus.
38. Internuclear ophthalmoplegia.
In this condition, there is lesion of the medial longitudinal
Fasciculus (MLF). It is the pathway by which various ocular motor
nuclei are linked.
Internuclear ophthalmoplegia is characterised by:
Defective action of medial rectus on the side of lesion, horizontal nystagmus of the opposite
convergence is normal, as the pathway of convergence runs directly into the midbrain without
involving the MLF.
 A patient with third cranial nerve paralysis showing:
A, ptosis; B, divergent squint

Examination of case of paralytic squint

History Taking and Preliminary Clinical Examination

Visual acuity examination
Following common devices should be used to assess the vision:
1. Snellen’s visual acuity chart (can be used with patients of all ages, who are literate)
2. Illiterate E chart (used with illiterate patients)
3. Catford Drum – Based on Osscillatory movements
4. Teller’s acuity cards – for children from 6 months to 2 years
5. Cardiff vision chart – Based on vanishing optotypes (for children from 2-3 years)
6. Sheridan Gardiner cards (useful in case of children above 3 years)
7. Angular visual acuity cards can be used to avoid crowding phenomenon
8. Near vision should be assessed by near vision charts for each eye separately.

Tests for paralytic squint

[Link] charting.
 (1) It is indicated in patients complaining of confusion or double vision. In it patient is asked to wear
red and green diplopia
charting glasses. Red glass being in front of the right eye and green in front of the left.
(2) Then in a semi-dark room, he is shown a fine linear light from a distance of 4 ft. and asked to
comment on the images in primary position and in other positions of gaze.
(3) Patient tells about the position and the separation of the two images in different fields.

Diplopia charting in a patient with right lateral rectus palsy

2. Tests to Help Identify the Affected Muscle
I. Park 3-step test
Step 1: Identify the hypertropic eye in the primary (straight ahead) position. This implies that either
one of the two depressors of the hypertropic eye or one of the two elevators of the hypotropic eye is
weak.
Step 2: Ask the patient to look horizontally right and then left and see in which position the deviation
is more. Considering that the deviation increases in the direction of action of the paralysed muscle,
identify which two of the four muscles are likely to be affected. Step 3: Tilt the patient’s head towards
each shoulder and see in which direction the vertical squint increases. Remembering that on tilting
the head towards one shoulder the eye on the same side intorts and the other eye extorts, the
ipsilateral synergist of the paralysed muscle will try to intort or extort the globe as the case may be,
and since the muscle also has a vertical action, that vertical effect will be more prominent in the
paralysed eye.
39. Bielschowsky head tilt test
It is based on the same principle as the third step of the Park 3-step test and is useful for diagnosing
superior rectus palsy. In a case of right superior oblique palsy, for example, the right hypertropia will
become more prominent when the head is tilted to the right shoulder and will disappear when the
head is tilted to the left shoulder.
40. Hess chart
Hess screen/Lees screen test tells about the paralysed muscles and the pathological sequelae of
the paralysis, viz., overaction, contracture and secondary inhibitional palsy.
Procedure
(1) It consists of a tangent screen marked in red lines on a black cloth with red spots at the
intersection of the l5° and 30° lines with themselves and with the horizontal and vertical lines
(2) Over it three green threads are suspended in such a way that they can be moved over the screen
in any direction by a pointer.
(3) The patient, wearing red-and-green glasses, is asked to place the junction of the three threads
over the red spots in turn.
(4) Through the red glass he can only see the red markers and through the green, thegreen threads,
so that he indicates the point at which one eye islooking when the other fixes a spot.
(5) The position on which the indicator appears to coincide with the spot gives a permanent record
of the primary and secondary deviation.
Inference
The smaller chart belongs to the eye with paretic muscle and the larger to the eye with overacting
muscle.

Hess chart of a recent right lateral rectus paralysis

41. Field of binocular fixation.

It should be tested in patients with paralytic squint where applicable, i.e., if patient has some field
of single vision. This test is
performed on the perimeter using a central chin rest.
42. Forced duction test (FDT).
 It is performed to differentiate between the incomitant squint due to paralysis of extraocular
muscle and that due to mechanical restriction of the ocular movements.
Inference
FDT is positive (resistance encountered during passive rotation) in cases of incomitant squint due
to mechanical restriction and negative in cases of extraocular muscle palsy.
Management
1. Treatment of the cause: An exhaustive investigative work-up should be done to find out the cause
and, if possible, treat it.
2. Conservative measures: These include: wait and watch for self-improvement to occur for a period
of 6 months, vitamin B-complex as neurotonic; and systemic steroids for non-specific inflammations.
3. Treatment of annoying diplopia:It includes use of 38frica38 on the affected eye, with intermittent
use of both eyes with changed headposture to avoid suppression amblyopia.
4. Chemodenervation of the contralateral muscle with botulinum toxin may be useful during the
recovery period.
A’ and ‘V’ Pattern Heterotropia
The terms ‘A’ or ‘V’ pattern squint are 38frica3838 when the amount of deviation in squinting eye
varies by more than 10° and 15°, respectively, between upward and downward gaze.
The ‘A’ and ‘V’ phenomena should be assessed by the cover test in 25° upward and downward
gaze. This test should be carried out for near and distance fixation.

‘A’ Esotropia
In the absence of vertical muscle anomaly, resection of the lateral recti with displacement of the
insertions downwards should be effective in patients with a greater deviation for distance than for
near.
In those with ‘A’ esotropia associated with convergence excess, recession of the medial recti with
shifting of the insertions upwards is effective. Large degrees of esotropia in small children, with gross
overaction of the superior obliques, may respond to bilateral weakening of the muscle.
 ‘A’ esotropia

‘A’ Exotropia
Smaller degrees may be helped by resection of the medial recti with elevation of the insertions
but the results are disappointing. Large degrees in small children with overaction of the superior
obliques respond to bilateral weakening of this muscle.

‘A’ exotropia

Causes
1. Primary superior oblique overaction is usually associated with exodeviation in the primary
position of gaze.
2. Inferior oblique underaction/palsy with subsequent superior
oblique overaction.
43. Inferior rectus underaction.
Treatment
Patients with oblique dysfunction are treated by superior oblique posterior tenotomy. Treatment
of cases without oblique muscle
dysfunction is as follows:
1. ‘A’ pattern esotropia is treated by bilateral medial rectus recessions and upward transposition
of the tendons.
2. ‘A’ pattern exotropia is treated by bilateral lateral rectus recessions and downward
transposition of the tendons.

‘V’ Esotropia
In the absence of vertical muscle anomaly, recession of the medial recti with displacement of the
insertions downwards is effective. If overaction of the inferior obliques is present, this responds to
bilateral anteroposition of this muscle with recession of the medial rectus muscles. If the overaction
is gross, the anteroposition should be combined with recession of the inferior oblique.

V pattern Esotropia

‘V’ Exotropia
In the absence of marked vertical muscle anomaly, recessions of the lateral recti with
displacement of the insertions upwards is effective.
If overaction of the inferior obliques is present, bilateral anteroposition of the muscle is effective,
with or without recession of the muscle, depending on the degree of overaction. Recession of the
lateral recti may be performed at the same time.
 V pattern Exotropia

Causes of ‘v’ pattern heterotropia

[Link] oblique overaction associated with fourth nerve palsy.

2. Superior oblique underaction with subsequent inferior oblique overaction, seen in infantile
esotropia as well as other childhood esotropias. The eyes are often straight in upgaze with a marked
esodeviation in downgaze.

[Link] rectus underaction.

4. Brown syndrome.
[Link] anomalies featuring shallow orbits and down-slanting palpebral fissures.
Treatment
Treatment is by inferior oblique weakening or superior oblique strengthening when oblique
dysfunction is present. Without
oblique muscle dysfunction treatment is as follows:
44. ‘V’ pattern esotropia can be treated by bilateral medial rectus recessions and downward
transposition of the tendons.

2.‘V’ pattern exotropia can be treated by bilateral lateral rectus recessions and upward
transposition of the tendons.

Strabismus Surgery
The most common aims of surgery on the extraocular muscles are to correct misalignment to
improve appearance.
Surgical techniques
1. Muscle weakening procedures include recession, marginal myotomy and myectomy.
2. Muscle strengthening procedures are resection, tucking and advancement.
3. Procedures that change direction of muscle [Link] include:
(a) Vertical transposition of horizontal recti to correct ‘A’ and ‘V’ patterns,
(b) Posterior fixation suture (Faden operation) to correct dissociated vertical deviation, and
ITransplantation of muscles .
Weakening procedures
Recession
Recession slackens a muscle by moving it away from its [Link] can be performed on any muscle
except the superior oblique.
Steps of recession :
1. Muscle is exposed by reflecting a flap of overlying conjunctiva and Tenon’s capsule.
2. Two vicryl sutures are passed through the outer quarters of the muscle tendon near the insertion.
3. The muscle tendon is disinserted from the sclera with the help of tenotomy scissors.
4. The amount of recession is measured with the callipers and marked on the sclera.
5. The muscle tendon is sutured with the sclera at the marked site posterior to original insertion.
6. Conjunctival flap is sutured back.

Technique of recession

Disinsertion
 1. Disinsertion (or myectomy) involves detaching a muscle from its insertion without reattachment.
2. It is most commonly used to weaken an overacting inferior oblique muscle, when the technique
is the same as for a recession except that the muscle is not sutured.
[Link] occasionally, disinsertion is performed on a severely contracted rectus muscle.

Strengthening procedures
Resection shortens a muscle to enhance its effective pull. It is suitable only for a rectus muscle and
involves the
following steps:
. 1. Muscle is exposed as for recession and the amount to be resected is measured with callipers
and marked.
2. Two absorbable sutures are passed through the outer quarters of the muscles at the marked
site.
3. The muscle tendon is disinserted from the sclera and the portion of the muscle anterior to
sutures is excised.
4. The muscle stump is sutured with the sclera at the original insertion site.
5. Conjunctival flap is sutured back.

Technique of resection

Posterior fixation suture

 The principle of this (Faden) procedure is to suture the muscle belly to the sclera posteriorly so as
to decrease the pull of the muscle in its field of action without affecting the eye in the primary
position. The Faden procedure may be used on the medial rectus
to reduce convergence in a convergence excess esotropia and on the superior rectus to treat DVD.
When treating DVD, the superior
rectus muscle may also be recessed. The belly of the muscle is then anchored to the sclera with a
non-absorbable suture about
12 mm behind its insertion.

Transposition
Transposition refers to the relocation of one or more extraocular muscles to substitute for the
action of an absent or severely
deficient muscle. The most common indication is severe lateral rectus weakness due to acquired
sixth cranial nerve palsy other applications include CCDD (e.g. Duane syndrome), alphabet patterns
and monocular elevation deficit.

Transposition of the superior and inferior rectus muscles in lateral rectus palsy

Adjustable sutures
Indications
 The results of strabismus surgery can be improved by the use of adjustable suture techniques on
the rectus muscles. These are particularly indicated when a precise outcome is essential and when
the results with more conventional procedures are likely to be
unpredictable; for example, acquired vertical deviations associated with thyroid myopathy or
following a blow-out fracture of the
floor of the orbit.
Other indications include sixth nerve palsy, adult exotropia and re-operations in which scarring of
surrounding tissues may make the final outcome unpredictable. The main contraindication is
inability to tolerate postoperative suture
adjustment (e.g. young children).

Postoperative adjustment
This is performed under topical anaesthesia, usually a few hours after surgery when the patient is
fully awake.
[Link] accuracy of alignment is assessed.
2. If ocular alignment is satisfactory the muscle suture is tied off and its long ends cut short.
[Link] more recession is required, the bow is pulled anteriorly along the muscle suture, thereby
providing additional slack to the recessed muscle and enabling it to move posteriorly

45. If less recession is required, the muscle suture is pulled anteriorly and the knot tightened against
the muscle stump
46. Once alignment is satisfactory, the main knot is secured, the sliding loop removed and the
conjunctiva closed.

Nystagmus

• Definition –
o It is the term applied to the rapid oscillatory movements of the eyes, independent of
normal eye movements.
o Oscillations are involuntary
o Lateral (Usually)/ Vertical/ Rotatory/ Mixed
o Almost always bilateral

• Classification
 Based on Aetiology
Physiological Pathological
1. End gaze Congenital Acquired
2. Optokinetic a)Infantile manifest a)Secondary to visual loss
3. Vestibulo-ocular reflexes b)Infantile latent b)Toxic and Metabolic
c) Infantile manifest- c)Neurological disorders
latent
d)Nystagmus blockage
syndrome

Physiological Nystagmus –

• Optokinetic Nystagmus –
o Jerky nystagmus
o Induced by moving repetitive visual patterns across the visual field.
o Slow phase – direction of moving pattern
Fast phase – opposite direction
o Rail road nystagmus
o Clinical Application – Testing visual acuity in infants or young children and for
detecting malingering.

• End-Gaze Nystagmus –
o Fine jerk horizontal nystagmus
o Seen in extreme gaze positions

• Vestibulo-ocular Nystagmus –
o Jerk Nystagmus
o Involves semicircular canals
o Can be produced physiologically by- rotation in specially designed chair or syringing
the ears
o Conjugate movement to opposite side induced by syringing one ear with cold water
o COWS {Cold – OPPOSITE; Warm – SAME} – one ear
o CUWD {Cold – UP; Warm – DOWN} – both ears
o Vestibular nystagmus + Interstitial keratitis = Cogan Syndrome
Pathological Nystagmus –

1) Early onset Nystagmus

✓ Infantile nystagmus syndrome
✓ Fusion mal-development nystagmus syndrome
✓ Spasmas nutans syndrome

• Infantile nystagmus syndrome –

o Idiopathic/ Associated with sensory deprivation due to albinism, aniridia, Leber’s
congenital amaurosis, Macular disease etc.
o Jerky type and horizontal, absent during sleep
o Persists throughout life
o Visual prognosis dependent on integrity of sensory system
o Progression : Pendular-> Jerk
o Family history : Often positive

• Latent Manifest Nystagmus –

o Fusion mal-development nystagmus syndrome
o Bilateral jerky, horizontal nystagmus
o Elicited by covering one eye – fast component towards the uncovered eye
o No nystagmus when both eyes are open but appears when one eye is covered
{LATENT}
o Visual acuity – normal when both eyes are open; rapidly decreases when one eye is
covered
o Associated with Strabismus
o Intensity decreases with age

• Spasmus Nutans Syndrome

o Occurs in the first year of life
o Associated with nodding movements of the head – anteroposterior/ Lateral/
Rotatory
o Fine and rapid nystagmus; more marked in one eye
o Disappears over time on its own

2) Acquired Nystagmus
✓ Late onset or acquired nystagmus
✓ Usually characterized by Oscillopsia and other neurological abnormalities
✓ [Oscillopsia – is the perception of the environment appearing to oscillate horizontally,
vertically or torsionally]

• Nystagmus due to disorders of visual fixation

o Visual loss nystagmus
✓ Diseases of the retina
✓ Diseases of the Optic nerve
 ✓ Diseases affecting the optic chiasma
✓ Diseases affecting the post chiasmal visual system

• Vestibular Nystagmus

❖ Peripheral Vestibular Nystagmus

o Conjugate horizontal jerk nystagmus with fast phase away from the side of the
lesion
o Improves with fixation
o Worsens with gaze towards fast phase
o Associated with destructive lesions of the vestibular system, labyrinthitis, vestibular
neuritis
❖ Central Vestibular Nystagmus

I. Up beat Nystagmus
o Fast phase in upward direction
o Cause: Phenytoin sodium intoxication/ vermis of cerebellum – lesions

II. Down beat Nystagmus

o Jerky nystagmus, with fast phase downwards
o Cause: Lesion at the cervicomedullary junction at the foramen magnum
o Arnold Chiari Malformation

III. See-Saw Nystagmus

o One eye rising and intorting while the other eye falls and extorts
o Cause: Chiasmal lesion (bitemporal hemianopia)

IV. Periodic alternating Nystagmus

o Jerky nystagmus with rhythmic changes in amplitude and direction (60-
90 seconds)
o Congenital or acquired
o Cause: Demyelinating disease of the brainstem/ blindness/ lesions at
cervicomedullary junction

• Nystagmus due to disorders of gaze holding

❖ Gaze evoked nystagmus
o Slow, conjugate horizontal jerk nystagmus in the direction of gaze
o Occurs in smaller angles than physiological end-gaze nystagmus
o Cause: Neurological lesions of brain stem and posterior fossa/ Drug
intoxication- alcohol, barbiturates

❖ Dissociated or conjugated nystagmus

o Ataxic Nystagmus
o Nystagmus of abducted eye
o Unilateral or asymmetric
 o Cause: Internuclear ophthalmoplegia

❖ Convergence retracted syndrome

o Jerk nystagmus with bilateral fast component to the medial side
o Associated with retraction of the globe in convergence
o Cause: Pineal gland tumors, stroke, trauma, MS
o Parinaud Syndrome or Sylvian aqueduct syndrome
➢ Features –
Retraction nystagmus
Vertical Nystagmus
Difficult voluntary vertical gaze
Defective convergence
Adduction movements with attempted vertical gaze
Pupillary abnormalities
Pathological lid retraction

❖ Brun’s Nystagmus
o Low frequency, large amplitude nystagmus when the patient looks towards the
side of the lesion – GAZE EVOKED
o High frequency, small amplitude nystagmus when the patient looks towards
the side opposite to the lesion – VESTIBULAR IMBALANCE
o Cause: Tumors in cerebro-pontine angle

❖ Centripetal and rebound nystagmus

o Patient – gaze-evoked nystagmus -> attempts to look eccentrically for a
sustained period of time -> Nystagmus-↓amplitude -> May Reverse direction ->
CENTRIPETAL NYSTAGMUS
o Eyes returned to centre -> Short lived nystagmus with slow drifts in the
direction of the prior eccentric gaze occurs -> REBOUND NYSTAGMUS
o Centripetal and Rebound nystagmus – attempt by brainstem and cerebellar
mechanisms to correct the drift of gaze evoked by nystagmus.
o Causes: Cerebellar diseases, Lateral Medullary infarction, Tumors confined to
flocculus.

• Acquired pendular Nystagmus –

o Usually disconjugate with horizontal, vertical and torsional components
o May be associated with involuntary, repetitive movements of palate, pharynx and
face – oculopalatal myoclonus

• Differential diagnosis –
o Ocular bobbing –
✓ Neoplasms involving pontine brainstem – poor prognosis
✓ Loss of caloric response
o Flutter-like oscillations
 ✓ Interruptions of cerebellar connections into the brainstem
✓ Overshooting/ Undershooting the target
o Opsoclonus
✓ Wild, chaotic movements
✓ Frequent myoclonic movement of face, arms and legs
✓ Follows an episode benign encephalitis
✓ Good prognosis
• Treatment –
o Proper history must be taken and the exact cause must be identified before
prescribing suitable treatment
o Optical aids such as spectacles, prisms and contact lenses
o Medications for specific conditions
o Biofeedback – Training mechanisms to reduce nystagmus

Surgery – correct nystagmus and head posture.

 DISORDERS OF EYELIDS

What will we learn here???

Applied anatomy

Congenital anomalies of eyelid

Edema of eyelids
Inflammatory edema
Solid edema
Passive edema

Inflammatory disorders of eyelids

Blepharitis
External hordeolum
Chalazia
Internal hordeolum
Molluscum contagiosum

Eyelash disorders
Trichiasis
Distichiasis
Madarosis
Trichomegaly
Poliosis

Anomalies in the position of lid margin

Entropion
Ectropion
Symblepharon
Ankyloblepharon
Blepharophimosis
Lagophthalmos
Blepharospasm
Ptosis
Lid retraction

Tumours
Benign
Pre malignant
Malignant
 APPLIED ANATOMY

GROSS ANATOMY

Introduction
o Mobile tissue curtains placed in front of eyeballs
o Protect eyes from injuries and excessive light
o Spread tear film over cornea and conjunctiva
o Drainage of tears by lacrimal pump system

Parts
Divided by horizontal sulcus
• Orbital part
• Tarsal part

Position: when eye is open

• Upper lid – covers 1/6th of cornea
• Lower lid – just touches the limbus

Canthi:
• The region where the two eyelids meet – medial and lateral angles

Palpebral aperture:
• Elliptical space between the upper and lower lid (10-11mm vertically in the centre;
28-30mm horizontally)

Lid margin:
• 2mm broad – divided by punctum – medial lacrimal portion (rounded and devoid of
lashes) and lateral ciliary portion (rounded anterior border sharp posterior border
and an intermarginal strip between the two borders)
 STRUCTURE
⑦ layers

1) Skin – elastic and thinnest in

the body

2) Subcutaneous areolar
tissue – loose connective tissue
containing no fat; readily distended
by edema or blood

3) Layers of striated muscle –

orbicularis muscle [Orbital part
(encircles orbital margin), Preseptal
part, Pretarsal part (Horner’s
muscle), Levator palpebrae
superioris muscle

4) Submuscular areolar tissue

– layer of loose connective tissue-
nerves and vessels lie in this layer;
anesthetic injections given in this
plane

5) Fibrous tissue – Central Tarsal plate, Peripheral Septum orbitale – Framework of

eyelid

6) Layer of non-striated muscle - Palpebral muscle of Muller – supplied by

sympathetic fibres and paralysis leads to Horner’s Syndrome

7) Conjunctiva – Palpebral conjunctiva lines the eyelids

 GLANDS OF EYELIDS
o Meibomian glands
✓ Tarsal glands
✓ Upper lid – 30 to 40; Lower lid – 20 to 30
✓ Modified sebaceous glands
✓ Oily layer of tear film
o Glands of Zeis
✓ Sebaceous glands
✓ Open into follicles of eyelashes
o Glands of Moll
✓ Modified sweat glands situated near hair follicle
✓ Open into ducts of Zeis glands
o Accessory lacrimal glands of Wolfring

BLOOD SUPPLY
o Arteries – Marginal arterial arcades; another- Superior arterial arcade in the
upper eyelid alone
o Veins – Two plexuses – Post-tarsal -> Ophthalmic veins; Pre-tarsal ->
Subcutaneous veins
o Lymphatics – Pre-tarsal and Post-tarsal - Lateral half -> Preauricular lymph
nodes; Medial half -> Submandibular lymph nodes

NERVE SUPPLY
o Motor nerve – facial nerve (orbicularis muscle); Oculomotor (LPS Muscle);
Sympathetic fibres (Muller’s muscle)
o Sensory nerve – Branches of trigeminal – lacrimal, supraorbital, supratrochlear
for upper eyelid; Infraorbital and Infratrochlear branch for lower eye lid.
 CONGENITAL ANOMALIES OF EYELIDS

CONGENITAL PTOSIS:
• Congenital weakness of Levator palpebral superiors
• Abnormal drooping of eyelids

CONGENITAL COLOMBOMA:
• Full thickness triangular gap in tissue of lids
• Usually occurs near nasal side & involves upper lid

EPICANTHUS:
• Semicircular fold of skin covers medial canthus

DISTICHIASIS:
• Extra row of cilia occupies the position of meibomian glands which open into their
follicles as ordinary sebaceous gland

CRYPTOPHTHALMOS:
• Lids fail to develop and skin passes continuously from the eyebrow

MICROBLEPHARON:
1. Eyelids are small
2. Associated with microphthalmos or Anophthalmus
• May be very small or absent as like ablepharon

EPIBLEPHARON:
• Horizontal fold of tissue rises above lower eyelid margin.
• Usually disappears with growth of face

EURYBLEPHARON:
• Unilateral or bilateral horizontal widening of palpebral fissure
• Associated with lateral canthal malposition & lateral ectropion.

CONGENITAL ANKYLOBLEPHARON:
• also known as ankyloblepharon filiforme adnatum (AFA)
• single or multiple strands of connective tissue join the upper and lower lid margins
except in medial and lateral canthi
 OEDEMA OF EYELIDS

INFLAMMATORY OEDEMA
Inflammation of lid Inflammation of eyeball Inflammation of orbit
• Dermatitis • Acute iridocyclitis • Orbital cellulitis
• Stye • Endophthalmitis • Orbital abscess
• Insect bites • Panophthalmitis • Pseudotumor
• Cellulitis
• Lid abscess

Inflammation of Inflammation of conjunctiva Inflammation of lacrimal

paranasal sinus • Such as acute, Purulent, sac
• Maxillary sinus Pseudomembranous • Acute dacryocystitis
conjunctiva • Lacrimal abscess

Inflammation of lacrimal
gland
• Acute dacryoadenitis

SOLID OEDEMA OF THE EYELIDS

• Chronic irritation of lids, follows recurrent attack of erysipelas.
• Hard in consistency & is inflammatory

PASSIVE OEDEMA Of THE EYELIDS

Local:
o Cavernous sinus thrombosis
o Head injury
o Angioneurotic oedema
General:
o Congestive heart failure
o Renal failure
o Hypoproteinemia
o Severe anaemia
 INFLAMMATORY DISORDERS OF EYELIDS

inflammatory
disorders

external internal molluscum

blepharitis chalazion
hordeolum hordeolum contagiosum

BLEPHARITIS
Clinical types:
• Bacterial blepharitis
• Seborrheic / squamous blepharitis
• Mixed staphylococcal with seborrheic blepharitis
• Posterior blepharitis/ meibomitis
• Parasitic blepharitis

Bacterial blepharitis
• also known as Chronic anterior / staphylococcal / ulcerative blepharitis
• Chronic infection of anterior part of lid margin
• Occurs usually in childhood and continues throughout life

Etiology:
• Mostly coagulase +ve staphylococci
• Rarely streptococci, Moraxella, etc.

Clinical features:
Symptoms: Signs:
• Chronic irritation • Yellow crust at root cilia
• Itching • Small ulcers that bleed on crust removal
• Mild lacrimation • Red, thick margins with dilated blood vessels
• gluing of cilia • associated with Mild papillary conjunctivitis and
• Mild photophobia conjunctival hyperthermia
Complications & sequelae:
• Lash abnormalities
• Madarosis
• Trichiasis
• Poliosis
o Tylosis
o Eversion of punctum
o Eczema of skin and ectropion
o Recurrent styles
• Marginal keratitis
• Tear film instability
• Secondary inflammatory changes & mechanical changes in conjunctiva or cornea

Treatment:
• Lid hygiene – warm compresses, crust removal, avoid rubbing of eyes
• Antibiotics – ointment or drops – erythromycin or doxycycline in unresponsive
patients
• Topical steroids - Fluorometholone
• Ocular lubricants – artificial tear drops

Seborrheic/ squamous blepharitis:

• Also called primary anterior blepharitis

Etiology
• Associated with seborrhea of scalp
• Zeis gland secretes excessive neutral lipid which are split by cornybacterium acne
into free fatty acid

Clinical features
Symptoms: Signs:
• Whitish scales in lid margin • Accumulation of white dandruff like
• Mild discomfort scales
• Irritation • Lash fall out easily
• Occasional Watering • Lid margin is thickened
• H/O falling eyelashes • Signs of bacterial blepharitis
Complications:
• Similar to bacterial blepharitis

Treatment:
• Balanced diet
• Associated seborrhea should be treated
• Lukewarm solution of 3% sodium bicarbonate used to remove scales
• Antibiotics – similar to bacterial blepharitis

Meibomitis (posterior blepharitis)

• Meibomitis – inflammation of meibomian glands

Chronic meibomitis:
• Chronic dysfunction of meibomitis gland. those especially with seborrhea dermatitis

Pathogenesis:
• Bacterial lipase plays main role

Clinical features:
• Chronic irritation
• Itching
• Burning
• Grittiness
• Mild lacrimation

Signs:
• White frothy secretion – meibomian seborrhea
• Thick secretion released from openings of meibomian gland – toothpaste appearance
• Vertical yellowish streaks through conjunctiva
• Hyperemia and telangiectasia
• Oily & foamy tear film

Acute meibomitis:
• Due to staphylococcal infection
• Painful swelling around the gland
• Pressure on it releases serosanguinous discharge
Treatment of meibomitis:
• Lid hygiene – warm compresses
• Topical antibiotics
• Systemic tetracyclines – doxycycline drug of choice. erythromycin can be used if
doxycycline is contradicted
• Ocular lubricants – artificial tear drops
• Topical steroids – fluorometholone

Parasitic blepharitis (lash infection)

Etiology:
Includes
• Phthiriasis palpebrarum - infestation by phthirus pubis (crab louse) occurs in adults.
It is also acquired as sexually transmitted disease.
• Pediculosis – infestation by pediculus humanus corporis or capitis (head louse)
• demodex blepharitis

Clinical features:
Ingestion of lash with lice causes chronic blepharitis or chronic follicular conjunctivitis

Symptoms:
Chronic irritation, itching, burning and mild lacrimation
Signs:
• Lid margins are red and inflamed
• Life anchoring lashes may be seen on slit lamp examination
• Conjunctival congestion and follicles are seen.
• Nits (eggs) are seen as opalescent pearls

Treatment:
• Mechanical removal of lices and nits
• Application of antibiotic ointment and yellow mercuric oxide 1%
• Delousing of the patient, family members and accessories.
 EXTERNAL HORDEOLUM (STYE)
Acute suppurative infection of lash follicle and its associated Zeis or moll gland

Etiology:
Predisposing factor
• Age – more common in children and young adults
• Habitual rubbing of eyes
• Metabolic factors – excessive intake of carbohydrates and alcohol

Causative organism - staphylococcus aureus

Clinical features
Symptoms:
• Acute pain with a swelling
• mild watering
• photophobia

Signs:
• Stage of cellulitis – localized, red, firm, tender swelling associated with marked
edema
• Stage of abscess formation – visible pus point on lid margin in relation to affected
cilia

Treatment:
• Hot compress 2-3 times a day
• Evacuation of pus
• Surgical incision
• Antibiotic eyedrops
• Systemic anti-inflammatory analgesics and systemic antibiotics
 CHALAZION
• also known as Tarsal or meibomian cyst.
• Chronic non- suppurative lipogranulous inflammation of meibomian glands

Etiology:
Predisposing factors – similar to hordeolum externum

Pathogenesis

non infective lipo

mild grade proliferation of infiltration and retention of enlargement of acts as irritant
granulomatous
infection epithelium blockage of ducts secretion gland and causes
inflammation

Clinical features
Symptoms: Signs: Clinical course and complications:
➢ Painless swelling • Nodule is slightly • Complete spontaneous resolution
in eyelid noted • Slightly increase in size
➢ Mild heaviness • Projection of main bulk • Fungating mass of granulation
of the lid of the swelling tissue may be formed
➢ Blurred vision • Marginal chalazion • Secondary infection may occur
➢ Watering of eyes present as reddish grey • calcification
(epiphora) nodule. • Malignant change into meibomian
adenocarcinoma

Treatment:
➢ Conservative treatment – hot fomentation, topical antibiotic eye drops and oral anti-
inflammatory drugs
➢ Intralesional infection of long acting steroids - triamcinolone
➢ Incision and curettage
Surface anesthesia given. incision is made, contents are curetted out. Carbolic acid
cautery with methylated spirits for neutralization. Patching of eye is done and post-
operative treatment to decrease the discomfort.
➢ Diathermy
➢ Oral tetracyclines – as prophylaxis in recurrent chalazia
 INTERNAL HORDEOLUM
Suppurative infection of meibomian gland associated with blockage of duct.

Etiology:
Predisposing factors:
Similar to external HORDEOLUM
Causative organism:
• Occur as primary staphylococcal infection.
• Secondary infection in chalazion

Clinical features:
Symptoms:
• Acute pain
• Swelling
• Watering
• Photophobia

Signs:
• Localized, firm, red, tenderness and oedema of eyelids.
• Internum and externum can be differentiated by the point of maximum tenderness
and swelling away from Lid margin and pus usually points on the tarsal conjunctiva
and not on root of cilia

Treatment:
• Similar to externum.
• Pus formation alone can be drained by vertical incision from tarsal conjunctiva
 MOLLUSCUM CONTAGIOSUM
Etiology:
• Viral infections affecting children
• Usually caused by large pox virus.

Clinical features:
Typical lesion is
▪ Multiple
▪ Pale
▪ Waxy
▪ Umbilicated swelling around the skin of lid margin.

Complications:
▪ Chronic follicular conjunctivitis
▪ Superficial keratitis

Treatment:
Skin lesion can be incised and interior cauterized with tincture of iodine or pure carbolic
acid.
 DISORDERS OF EYELASHES

TRICHIASIS

• It refers to inward misdirection of cilia with normal position of the lid margin (which rub
against the eyeball)

Pseudotrichiasis:
The inward turning of lashes along lid margin (sun in entropion) is called pseudo trichiasis

Etiology:
• Cicatrizing trachoma
• Ulcerative blepharitis
• Healed membranous conjunctivitis
• Hordeolum externum
• Mechanical injuries
• Burns
• Operative scar on the lid margin

Clinical features:
Symptoms: Signs:
• Foreign body sensation • Misdirected cilia one or more touching the cornea
• Photophobia • Reflex blepharospasm and photophobia occur
• Irritation when cornea is abraded
• Pain • Conjunctiva may be congested
• Lacrimation • Signs of causative disease: trachoma, blepharitis
may be present

Complications:
• Recurrent corneal abrasions
• Superficial corneal opacities
• Corneal vascularization
• Non healing corneal ulcer
Treatment:
Epilation:
• Mechanical removal with forceps
• It is temporary measures as recurrence occurs within 3-4 weeks
Electrolysis:
• Method of destroying the lash follicle by electric current
Procedure:
→ Infiltration anesthesia is given to the lid
→ A current of 2ma is passed for 10 secs through a fine needle inserted into the
lash root
→ The loosened cilia with destroyed follicles are then removed with epilation
forceps
Cryoepilation:
• It is also an effective method
• after infiltration anaesthesia, cryoprobe (-200 C) is applied for 20 to 25 seconds to
external lid margin by double freeze thaw technique
• disadvantage – depigmentation of skin
Surgical correction:
When many cilia are misdirected operative treatment similar to cicatricial entropion should
be employed.

DISTICHIASIS
Congenital distichiasis:
• Rare anomaly in which an extra row of cilia occupies the position of meibomian
glands which open into their follicles as ordinary sebaceous glands.
• These cilia are usually directed backwards and if rubs the cornea, it should be
electroepilated or cryoepilated.
Acquired distichiasis:
• Metaplastic lashes
• Occurs due to metaplasia and differentiation
• The meibomian glands are transformed into hair follicles
 • The most important cause is late stage of cicatrizing conjunctivitis associated with
chemical injury, stevens Johnson syndrome, ocular cicatricial pemphigoid.

MADAROSIS
• Partial or complete loss of eyelashes
Causes
Local causes: Systemic causes:
1. Chronic blepharitis 1. Alopecia
2. Cicatrizing conjunctivitis 2. Psoriasis
3. Complication of cryotherapy 3. Hypothyroidism
4. Radiotherapy or surgery 4. Leprosy

TRICHOMEGALY
→ excessive growth of eyelashes
→ causes: congenital, familial, topical prostaglandin analogues, phenytoin, malnutrition,
hypothyroidism, porphyria, AIDS

POLIOSIS
→ greying of eyelashes and eyebrows

Causes
Ocular Systemic

Chronic anterior blepharitis Waardenburg syndrome

Sympathetic ophthalmitis Vitiligo
Idiopathic uveitis Marfan syndrome, etc.
 ANOMALIES IN THE POSITION OF LID MARGIN

ENTROPION

Definition
→ Inward rolling and rotation of the lid margin toward globe.

Etiological types:

types

congenital cicatricial senile mechanical

congenital entropion
▪ rare condition – since birth
▪ more common – upper eyelid
▪ lower eyelid congenital entropion
→ caused by improper development of the lower lid retractors.
▪ upper eyelid congenital entropion
→ usually secondary to mechanical effects of microphthalmos.

Cicatricial entropion
• common
• involves upper eyelid
• caused by cicatricial contraction of palpebral conjunctiva with or without associated
distortion of tarsal plate.
• common causes are:
1. trachoma
2. membranous conjunctivitis
3. chemical burns
4. pemphigus
5. stevens-Johnson syndrome

Senile entropion
 • Affects only the lower lid in elder people.

Etiological factors:
• horizontal laxity – due to weakening of orbicularis muscle
• vertical lid instability – due to weakening of dehiscence of capsulopalpebral fascia
• overriding of pretarsal orbicularis
• laxity of orbital septum

Mechanical entropion
• occurs due to lack of support provided by globe to the lids.
• occurs in patients with:
1. phthisis bulbi
2. enophthalmos
3. after enucleation / evisceration operation

Clinical features:
Symptoms: occurs due to rubbing of cilia over cornea and conjunctiva similar to trichiasis
• Foreign body sensation
• Irritation
• Lacrimation
• Photophobia

Signs:
Inturning of lid margins are found
▪ Depending upon degree of inturning it can be divided into three grades.
• Grade i entropion – posterior lid in rolled
• Grade ii entropion – inturning upto inter marginal strip
• Grade iii entropion – whole lid inturned

Signs of causative disease:

• scarring of palpebral conjunctiva in cicatricial entropion
• horizontal lid laxity in involutional entropion

Signs of complication:
• recurrent corneal abrasions
 • superficial corneal opacities
• corneal vascularization
• corneal ulceration

TREATMENT:
Congenital entropion.
• resolve with time without need of any intervention
• or may require excision of a strip of skin and muscle with plastic reconstruction of lid
crease (HOTZ PROCEDURE)

Cicatricial entropion:
• alteration of direction of lashes or
• transplanting lashes or
• straightening the distorted tarsus

SURGICAL PROCEDURES:
1. anterior lamellar resection
2. tarsal wedge resection
3. transposition of tarsoconjunctival wedge
4. posterior lamellar graft
Anterior lamellar resection:
• simplest operation
• to correct mild degree of entropion
• procedure: an elliptical strip of skin and orbicularis muscle is resected 3mm
away from the lid margin.
Tarsal wedge resection:
• It corrects moderate degree of entropion associated with strophic tarsus.
• PROCEDURE:
o In addition to elliptical resection of skin and muscle, a wedge of tarsal
plate is also removed

Transposition of tarsoconjunctival wedge:

Also known as Modified ketssey’s operation
• This is indicated to treat mild to moderate amount of cicatricial entropion.
 • It basically involves tarsal fracture and eversion of distal tarsus.
• A horizontal incision is made along the whole length of sulcus subtarsalis
involving conjunctiva a tarsal plate
• the lower end is undermined up to lid margin.
• Mattress sutures are then passed from upper cut end of the tarsal plate to
emerge on the skin 1mm above lid margin
• When sutures are tied entropion is corrected by transposition of
tarsoconjunctival wedge.
Posterior lamellar graft
INDICATIONS: severe entropion with upper eyelid retraction
Procedure:
• The deficient or keratinized conjunctiva and the scarred and contracted
tarsus are replaced by composite posterior lamellar graft.
• Tarsus may be replaced by preserved sclera or ear cartilage or hard palate
along with conjunctival or mucous membrane graft.

Senile entropion:
1. Transverse everting suture
2. Weis operation
3. Plication of lower lid retraction
4. Quickest procedure
Transverse everting suture:
• Temporary cure (upto 18 months)
• Indicated in very old patients
• Transverse suture – applied through full thickness of lids
• To prevent over riding of preseptal muscles
• Everting sutures tighten the lower lid retractors, similar to transverse
sutures except these passes at lower part of inferior fornix and emerge out
from skin near lash line.
Weis operation:
▪ Transverse lid split and everting sutures
▪ Indicated for long term cure in patients with little horizontal laxity.

Procedure:
• Incision (involving skin orbicularis & tarsal plate along whole length of
eyelid
 • Mattress sutures are then passed through the lower cut end of the tarsus
to emerge on skin 1mm below lid margin and are firmly tied
• The entropion is corrected by prevention of overriding of preseptal
muscle by horizontal scar tissue barrier
• Transferring of pull of eyelid retractors to upper border of tarsus by
everting sutures

Plication of lower lid retractors (jones operation)

• It is performed in severe cases or when recurrence occurs when
recurrence occurs after the above described operations.
Procedure:
• The lower lid retractors are exposed via horizontal skin incision at lower
border of tarsal plate shortened and sutures are used to create a barrier
to prevent overriding of the preseptal muscles.
Quickest procedure:
• Indication – horizontal lid laxity
Procedure:
• Transverse lid split to create barrier for overriding of preseptal
muscle, everting sutures to transfer pull of lower lid retractor to upper
border of tarsus and horizontal lid shortening to correct the laxity.
• Quickest procedure: horizontal lid shortening + Weis procedure

Lateral tarsal strip (LTS)

▪ Lateral canthal tightening is done by excising of lateral tarsal strip
▪ Useful in marked lid laxity of lateral tarsal strip
 ECTROPION
Out rolling or outward turning of lid margin is called ectropion.

Etiology types

types

congenital involutional cicatricial paralytic mechanical

Congenital ectropion:
• Very rare, may be seen in down’s syndrome & blepharophimosis syndrome.
• It may occur in both upper and lower lids and is due to congenital shortage of skin

Involutional entropion:
• Involves lower lids
• Commonest
• Occurs due to age related changes
1. Horizontal laxity of eyelid
2. Medial canthal tendon laxity
3. Lateral canthal tendon laxity
4. Disinsertion of lower lid retractors.

Cicatricial ectropion:
• It occurs due to scarring of skin scarring of skin and can involves both the lids
• Common causes of skin scarring
1. Thermal burns
2. Chemical burns
3. Lacerating injuries
4. Skin ulcers

Paralytic ectropion
• Due to paralysis of seventh nerve
• Occurs in lower lids
• Common causes of facial nerve palsy are
 1. Bell’s palsy
2. Head injury
3. Infection
4. Infections of the middle ear
5. Operation of the middle ear
6. Operations on parotid gland

Mechanical ectropion
• Occurs in condition where either lower lid is pulled down (as in tumors)
• Pushed out and down (as in proptosis and marked chemosis of conjunctiva)

Clinical features:
Symptoms:
• epiphora – main symptom
• Irritation
• Discomfort
• Mild photophobia
Signs:
• Lid margin is out rolled
→ Grade I – only punctum is everted
→ Grade II – lid margin is everted and palpebral conjunctiva is visible
→ Grade III – the fornix is also visible
• Signs of etiological condition
Skin scars in cicatricial ectropion
Seventh nerve palsy in paralytic ectropion
• Involvement ectropion
Signs:
1. Horizontal lid laxity – by positive snap test
2. Medial canthal tendon laxity – severe – inferior punctum moves till pupil
3. Lateral canthal tendon laxity – rounded appearance of lateral canthus 72mm.

Complications:
• Dryness and thickening of conjunctiva and corneal ulceration
• Eczema and dermatitis of lower lid
Treatment
Congenital ectropion:
• Mild – no treatment
• Moderate & severe – cicatricial ectropion with horizontal lid tightening full thickness
skin graft to vertically lengthen anterior lamella.
Involutional ectropion:
• Medial conjunctivoplasty:
o Used in mild case involving punctum area.
o Consists of excising spindle shaped piece of conjunctiva and subconjunctiva
tissue from below the punctal area.
• Horizontal lid shortening:
o Performed by full thickness pentagonal excision in patients with moderate
degree of ectropion.
• Byron smith’s modified kuhnt-szymanowski operation.
o Severe degree of ectropion, More marked in lateral lid
o base up pentagonal full excision of lateral third of eyelid + combined triangular
excision of skin from area just Lateral canthus to elevate the lid.
• Lateral tarsal strip technique.
For generalized ectropion with horizontal lid laxity

Paralytic ectropion:
Resolves spontaneously within 6 months when its due to bell’s palsy.
Temporary measures: Permanent measures
1. Topical lubricants 1. Horizontal lid tightening
2. Taping temporal side of eyelid 2. Palpebral sling operation
3. Suture tarsorrhaphy

Cicatricial ectropion:
Depending on degree
➢ V-y operation – mild ectropion
V shaped incision is given skin is sutured in Y shaped pattern.
➢ Z-Plasty (Elschnig’s operation) - mild to moderate ectropion
➢ Excision od scar tissue and full thickness skin grafting – in severe ectropion
Mechanical ectropion:
It is corrected by treating underlying mechanical force causing ectropion.
 SYMBLEPHARON
• Adhesion between palpebral and bulbar conjunctiva thus resulting in adhesion of
globe to eyelid
Etiology – results from healing of the kissing raw surfaces upon palpebral and bulbar
conjunctiva
▪ Common causes
• Thermal heat
• Chemical injury
• Membranous conjunctivitis
• Injuries and conjunctival ulceration
• Ocular pemphigus
• Stevens Johnson syndrome

Clinical features - Restricted ocular movements, Diplopia, Lagophthalmos, cosmetic

disfigurement

Types: -
• Anterior symblepharon- Adhesion only in anterior part
• Posterior symblepharon- Adhesion present upto the fornices
• Total symblepharon- Adhesion involving whole of the eyelid. Completely adherent

Complications: - Dryness, thickening, keratinistation of conjunctiva, corneal ulceration.

Treatment:
• Prophylaxis to prevent adhesion during the stage of raw surfaces - Glass rod is kept in
the fornix to prevent adhesion. Done several times a day. Therapeutic soft contact
lens.
• Curative – symblepharectomy –
• mobilizing the surrounding conjunctiva
• Conjunctival/buccal mucosa graft
• Amniotic membrane transplantation (AMT).
 ANKYLOBLEPHARON
• Adhesion between margins of upper and lower eyelid.
Etiology
• Congenital
• Acquired – chemical burns, thermal burns, ulcers, trauma.

Types - Complete/ Incomplete

Associated with symblepharon
Treatment:
• Separate the adhesions by excision - it should be kept apart during the healing
process.
• if adhesion extend to angles - Epithelial graft to prevent recurrences

BLEPHAROPHIMOSIS
• Decreased extent of palpebral fissure
• Eyelid appears contracted at outer canthus
Etiology:

❖ Congenital – Blepharophimosis syndrome – Congenital ptosis+

Blepharophimosis + Telecanthus + Epicanthus inversus
❖ Acquired – Epicanthus lateralis (due to formation of vertical skin fold at lateral
canthus following eczematous contraction)

Treatment:

❖ mild cases- No treatment

❖ severe cases- Canthoplasty operation.

LAGOPHTHALMOS
- Inability to close eyelids voluntarily
Etiology – Orbicularis oculi paralysis, Symblepharon, Severe ectropion, Proptosis, Coma.
- Physiological lagophthalmos – some people sleep with their eye open – nocturnal
lagophthalmos
C/F: - Incomplete closure of palpebral aperture leads to
 1. Corneal and conjunctival xerosis
2. Exposure keratitis

Treatment - Aim to prevent exposure keratitis and treat cause of lagophthalmos

1. Frequent instillation of Artificial tear drops + Antibiotic eye drops (during
sleep)
2. Soft-bandage contact lens
3. Measure to treat the cause of lagophthalmos
4. Tarsorrhaphy - Operation in which adhesions are created between the
eyelids to close the palpebral aperture.

Temporary tarsorrhaphy Permanent tarsorrhaphy

Indications Indications
• Recovering VII cranial nerve palsy • VII nerve palsy (non-recovering)
• to assist healing of indolent corneal ulcer • Neuroparalytic keratitis with
severe corneal sensation loss.
• to assist healing of skin grafts in correct position.
Steps
Steps ▪ Performed at the lateral canthus
▪ Incision of about 5mm marked on corresponding to create permanent adhesions.
parts of upper and lower lid margins which are ▪ The eyelids are overlapped after
3mm from midline on either side. excising a triangular flap of skin
▪ 2mm deep incision is made on the marked grey and orbicularis from lower lid
line. and corresponding triangular
▪ marginal epithelium is excised. tarsoconjunctival flap from
▪ care is taken not to damage the ciliary line upper lid
anteriorly and sharp lid border posteriorly.
▪ the raw surfaces are Sutured with double armed
6-0 silk sutures passed through rubber bolster.
 BLEPHAROSPASM
• Involuntary, sustained, forceful closure of eyelid.

Etiology
1. Essential or spontaneous blepharospasm – Rare idiopathic, age 45-60
2. Reflex blepharospasm - Reflex sensory stimulation through branches of V
cranial nerve due to conditions such as
▪ Phlyctenular keratitis
▪ Interstitial keratitis
▪ Corneal foreign body
▪ Corneal ulcer and iridocyclitis
▪ Hysterical patients
▪ Dazzling light causing excessive stimulation of retina

C/F – Persistent epiphora, edema of eyelid, spastic entropion (elderly) and ectropion
(children and young adults), Blepharophimosis.
Treatment
1. Essential blepharospasm – Botox (subcutaneously – relieves spasm), Facial denervation
in severe cases
2. Reflex blepharospasm – Treat causative disease and associated complications.

LID RETRACTION
normal: the upper eyelid covers 1/6th of the cornea (about 2mm)
lid retraction: when the lid margin is either at or above the level of superior limbus

Causes:
• Congenital: Down’s syndrome, Duane’s retraction syndrome
• Thyroid eye disease
• Mechanical causes: Surgical overcorrection of ptosis, Scarring of upper eyelid skin
• Neurogenic causes: Facial palsy, third nerve misdirection, Marcus Gunn-jaw winking
syndrome
• Systemic causes: Uraemia
 PTOSIS

Definition: abnormal drooping of upper eyelid is called ptosis

▪ Normally upper lid covers 2mm of cornea, when its more than 2mm it is referred to
as ptosis

Clinic-etiological types

▪ Congenital
▪ Acquired

Congenital ptosis

Etiology – maldevelopment of the levator palpebrae superioris muscle

Characteristic features Associated features

Drooping of one or both upper Simple congenital ptosis

lids Congenital ptosis with associated weakness of superior
Lid crease rectus muscle
Lid lag on downward gaze Blepharophimosis syndrome
Functioning of LPS muscle may Congenital synkinetic ptosis – Marcus Gunn jaw
vary winking ptosis

Acquired ptosis

Depending on the cause it can be

▪ Neurogenic
▪ Myogenic
▪ Aponeurotic
▪ Mechanical

Neurogenic ptosis Acquired myogenic Aponeurotic ptosis Mechanical ptosis

ptosis
Caused by Occurs due to LPS Develops due to Due to excessive
innervational muscle disorders defect of levator weight in upper lid
defects aponeurosis when
 Myasthenia gravis the muscle function Lid tumors
3rd nerve palsy Dystrophia myotonica is normal Multiple chalazia
Horner’s syndrome Ocular myopathy lid edema
Ophthalmoplegic Thyrotoxicosis Senile ptosis Cicatricial ptosis
migraine Post op ptosis
Multiple sclerosis Trauma

Clinical evaluation

1. History
2. Examination
a. Exclude pseudoptosis
b. observe following points
i. Unilateral or bilateral ptosis
ii. Function of orbicularis oculi muscle
iii. Eyelid crease +/-
iv. Jaw- winking phenomenon +/-
v. Any associated weakness of extraocular muscle
vi. Bell’s phenomenon
c. Measurement of degree of ptosis
i. Mild – 2mm
ii. Moderate – 3mm
iii. Severe – 4mm
d. Margin reflex distance
e. Assessment of levator function
i. Normal – 15mm
ii. Good >= 8mm
iii. Fair – 5 – 7 mm
iv. Poor < = 4mm
f. Special investigations
i. Tensilon test
ii. Phenylephrine test
iii. Neurological investigations
g. Photographic record
Treatment

Congenital

- Almost always need surgical correction

1. Tarso conjunctivo mullerectomy
2. Levator resection
a. Done in moderate and severe cases

Moderate ptosis
i. Good function = 16 – 17 mm
ii. Fair function = 18 – 22 mm
iii. Poor function = 23 – 24 mm

Severe ptosis = 23 – 24 mm

b. Techniques
i. Conjunctival approach
ii. Skin approach

3. Frontalis sling operation

Acquired

• Treat the underlying cause

• Conservative treatment
• Surgical procedures
• Horner’s syndrome – fasanella servat operation
• Neurogenic ptosis in 3rd nerve palsy – frontalis sling operation
 TUMOURS OF EYELID

CLASSIFICATION

tumors of eyelid

benign pre malignant malignant

BENIGN TUMOURS PREMALIGNANT MALIGNANT TUMOURS

TUMOURS

• PAPILLOMAS • KERATOSIS • BASAL CELL CARCINOMA

• XANTHELASMA • XERODERMA • SQUAMOUS CELL
• HEMANGIOMA PIGMENTOSA CARCINOMA
• NEUROFIBROMA • SEBACEOUS GLAND
• KERATOCANTHOMAS CARCINOMA
• NAEVI • MALIGNANT MELANOMA

BENIGN TUMOUR
1. PAPILLOMAS:
• Most common tumour
• Occurs in surface epithelium
• In 2 forms
- Squamous papilloma
- Basal cell papilloma

Squamous papilloma Basal cell papilloma

• Derived from squamous cells • Derived from basal cell
• Seen mostly in adults • Middle age / older age
• Pedunculated lesion or raspberry like • Slightly pigmented
growth
TREATMENT: Simple excision.
2. XANTHELASMA:
• Creamy yellow plaque like lesion.
• Occurs on skin of upper and lower lids near the inner canthus.
• Common in middle age women
• associated with diabetics and those with high cholesterol level.
TREATMENT:
• Excision may be advised for cosmetic reasons.
• high rate of recurrence

3. HAEMANGIOMA:

• Common tumour
• In 3 forms.
- Capillary haemangioma
- Naevus flammeus
- Cavernous haemangioma

Capillary hemangioma Naevus flammeus Cavernous

hemangioma
• most common variety • Part of Sturge weber • Developmental
• occurs at birth syndrome. venous anomaly.
• Superficial, bright red in colour – • Dilated vascular • occurs in 1st decade
strawberry naevus channels present. of life
• Endothelial cells. they do not grow or • Endothelium lined
regress like capillary vascular channels.
TREATMENT: haemangioma
TREATMENT:
OBSERVATION: Left untouched until similar to capillary
7 years haemangiomas.

MEDICAL TREATMENT:
-Intralesional steroid
-High dose oral steroid
therapy
-oral prednisolone

SUPERFICIAL RADIOTHERAPY
- Given for large tumours

SURGERY: Rarely necessary

4. NEUROFIBROMA:
• Lids and orbit are commonly affected.
EYELID NEUROFIBROMA:
- Solitary neurofibroma
- Diffuse neurofibroma – “bag of worms” feel

5. KERATOCANTHOMA:
• Non pigmented protrusions.
• TREATMENT - Complete Excision and biopsy.

6. NAEVI:
Naevi are cutaneous lesions that arise from the arrested epidermal melanocytes.

PIGMENTED NAEVI

Acquired
Congenital
Junctional Intradermal Compound

• Small and uniform • Location: • Location: • Slightly

in colour. epidermis dermis elevated
• Split naevus • Brown in • Elevated
appearance lesions

PREMALIGNANT TUMOUR

SOLAR KERATOSIS XERODERMA PIGMENTOSA

- Common lesion of sun exposed skin
- Uncommon of eyelids. - Autosomal recessive disease
- Progressive cutaneous
CLINICAL FEATURES:
pigmentation
-Flat, scaly lesion
- Bird like facies
-Hyperkeratosis
- Predisposition to develop lid
tumours
HISTOLOGY:
- Characterized by parakeratosis
- Cellular atypia
MALIGNANT TUMOUR

malignant

basal cell squamous cell sebaceous gland malignant

carcinoma carcinoma carcinoma melanoma

BASAL CELL CARCINOMA

▪ Commonest malignant tumour seen in elder people
▪ involves most commonly lower lid
▪ Predisposing factors: sun exposure, old age, xeroderma pigmentosa, basal cell
naevus syndrome
▪ Clinical features: 4 forms
o Non ulcerated nodular form
o sclerosing type
o Pigmented basal cell
o Noduloulcerative basal cell (Rodent ulcer)
▪ Histology: commonest pattern: solid basal cell carcinoma with palisading appearance
▪ Treatment:
• Surgery: Moh’s microsurgical technique
• Radiotherapy and cryotherapy

SQUAMOUS CELL CARCINOMA

▪ Second commonest malignant tumour
▪ In elderly patient
▪ Pre-existing lesion such as Bowen’s disease, actinic keratosis.
▪ Risk factors: sun exposure, radiation, injury, fair skin.
▪ Clinical features:
o Ulcerated SCC – scaly, erythemous plaque like growth with elevated and
depressed margins
o Nodular SCC – rare presentation, polypoid verrucous lesion
o Cutaneous horns – with underlying invasive SCC
▪ Metastasis: metastasized in preauricular and sub mandibular lymph nodes.
▪ Histology: whorled arrangement forming epithelial pearls containing laminated
keratin material in the centre
▪ Treatment: similar to basal cell carcinoma.
SEBACEOUS GLAND CARCINOMA:
▪ Rare tumour arising from the meibomian glands
▪ Clinical features:
o Initially as a nodule.
o Rarely a diffuse tumour along the lid margin.
▪ Treatment:
o Surgical excision with reconstruction of lid margin.
o Recurrences are common

MALIGNANT MELANOMA:
▪ Rare tumour of the lid arises from the melanocytes in the skin.
▪ Clinical features: Present in 3 forms
o Lentigo maligna type:
▪ Flat, pigmented, well defined lesion, later on becomes elevated and
invades the dermis
o Superficial spreading type:
▪ mildly elevated, Pigmented lesion with irregular margins.
o Nodular type:
▪ rapidly growing lesion which ulcerates and bleeds frequently.

▪ Metastasis: Tumour spreads locally as well as to distant sites by lymphatics and

bloodstream.
▪ Treatment: It is a radio-resistant tumour. Therefore, Surgical excision and
Reconstruction of the lid.
 LACRIMAL APPARATUS

What will we learn here???

• Anatomy of lacrimal apparatus

Lacrimal gland
Lacrimal apparatus
• Tear film
• Dry eye disease
• Watering eye
• Dacryocystitis
Congenital
Adult
▪ Chronic
▪ Acute
• Dacryocystectomy
Conventional external approach DCR
Endonasal (surgical or laser) DCR
Endocanalicular laser DCR
• Swellings of lacrimal gland
Dacryoadenitis
▪ Acute
▪ Chronic
Mikulicz’s syndrome
Dacryops
Tumours of lacrimal gland
 ANATOMY OF LACRIMAL APPARATUS

Lacrimal apparatus = lacrimal glands + lacrimal passages

Lacrimal gland

ORBITAL PART
MAIN LACRIMAL
GLAND
PALPEBRAL PART
LACRIMAL
GLAND GLAND OF
ACCESSORY KRAUSSE
LACRIMAL
GLAND GLAND OF
WOLFRING

All lacrimal glands are structurally similar to salivary gland

Blood supply
• Lacrimal artery branch of ophthalmic artery

Nerve supply
• Sensory – lacrimal nerve, branch of ophthalmic division of trigeminal nerve
• Sympathetic – carotid plexus of cervical sympathetic chain
• Secretomotor fibres:

superior
greater pterygo
salivary zygomatic lacrimal lacrimal
petrosal palatine
nucleus in nerve nerve gland
nerve ganglion
pons
 Lacrimal passages:

LACRIMAL GLAND

DUCTS OF LACRIMAL
GLAND

LACRIMAL PUNCTA

LACRIMAL CANALICULI

LACRIMAL SAC

NASO LACRIMAL DUCT

INFERIOR MEATUS OF
THE NOSE

Lacrimal puncta: each punctum is situated in lacrimal papilla, tears drain in puncta
Lacrimal canaliculi: there are two canaliculi – superior and inferior, they together form a
common canaliculus which drain in lacrimal sac. Reflux of tears is prevented by valve of
Rosenmuller.
Lacrimal sac: the lacrimal which lies in lacrimal fossa has 3 parts – fundus, body and neck.
The neck is continuous with nasolacrimal duct
Nasolacrimal duct: located in bony canal formed by maxilla and the inferior turbinate. It
drains into the inferior meatus in nose. In the lower end of the duct, there is a valve – valve
of Hasner. This valve prevents reflux from nose
 TEAR FILM

TEAR FILM LAYERS

MUCOUS LIPID LAYER :
LAYER : AQUEOUS prevents the
LAYER : overflow of tears,
mucin secreted by retards their
conjunctival consists of tears evaporation, and
goblet cell and secreted by main lubricates the
gland of manz and accessory eyelids as they
cornea becomes lacrimal glands slide over the
hydrophilic surface of globe

Functions of tear film:

1. Keeps the cornea and conjunctiva moist
2. Provides oxygen to corneal epithelium
3. Washes away debris and noxious irritants
4. Presence of anti-bacterial substance that prevents infection
5. Facilitates movements of lids over globe

Tears are continuously secreted by

→ Main lacrimal glands (reflex secretion)
→ Accessory lacrimal glands (basal secretion)

Tears are drained by an active lacrimal pump mechanism

When eyelids close tears are drained by When eyelids open tears are drained by
→ Contraction of pretarsal orbicularis → Relaxation of pretarsal orbicularis
oculi oculi
→ Contraction of preseptal fibres of → Relaxation of preseptal fibres of
orbicularis orbicularis
 DRY EYE DISEASE

Definition:
Dry eye is a multifactorial disease of ocular surface characterised by loss of
homeostasis pf 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

Etiological classification:

lacrimal deficiency

sjogren' syndrome
aqueous deficiency dry lacrimal gland
eye obstruction
non - sjogren's
dry eye

keratoconjunctivitis sicca
hypersecretory state
disease related to
meibomian gland
others
evaporative
disorders of lid aperture
dry eye

disorders related to
ocular surface

Clinical features
Symptoms
• Irritation
• Foreign body sensation
• Feeling of dryness
• Itching
• Non-specific ocular discomfort
• Chronically sore eyes
 Signs

Tear film signs Conjunctival signs Corneal signs Signs of

causative disease
→ Stingy mucous → Lustreless → Punctate epithelial Such as
and particulate erosions, Filaments
matter → Mildly congested and Mucous → Posterior
presence plaques blepharitis

→ Marginal tear → Conjunctival → Cornea may lose → Conjunctival

strip xerosis lustre scarring diseases
reduced/absent
→ Keratinization → Vital stains, → Lagophthalmos
→ Froth in tears fluorescein, Rose maybe depicted
→ Rose Bengal / Lisamin
Bengal/Lisamin green staining (+ve)
green staining
(+ve)

Complications:

• Threatening vision loss

• Epithelial breakdown
• Corneal ulceration
• Melting
• Perforation
Tear film tests

tear film tests

tear film break rose bengal

schirmer - I test
up test staining

Tear film break up test (BUT)

→ It is the interval between a complete blink and appearance of first randomly
distributed dry spot of the cornea
→ It serves as an indicator of adequacy of mucin component of tears
→ Procedure: a drop of fluorescein is instilled. The cornea is then examined using a
cobalt blue light in slit lamp
→ Normal value: 15 – 35 seconds

Value <10 means unstable tear film

Schirmer I test
→ It measures total tear secretions

>15 mm Normal
5 – 10 mm Mild keratoconjunctivitis sicca
<5 mm Severe keratoconjunctivitis sicca

Rose Bengal staining

→ Very useful in detecting even mild cases of KCS

A Severe
B Moderate
C Mild or early cases
Grading
LEVEL - 1 - mild dry eye
LEVEL - 2 - moderate dry eye
LEVEL - 3 - severe dry eye
LEVEL - 4 - very severe dry eye

Treatment

• Supplementation of tear substitutes:

▪ Artificial tear drops – cellulose derivatives / polyvinyl alcohol
• Anti-inflammatory agents:
▪ Fluorometholone
▪ Topical cyclosporine
▪ Chloroquine eye drops
▪ Omega fatty acid supplements
• Mucolytics:
▪ 5% acetyl cysteine – QID
• Secretagogues:
▪ Pilocarpine and cevimeline
• Preservation of existing tears by reducing tears and decreasing drainage
• Treatment of causative disease of dry eye
• Additional measures
▪ Serum eye drops
▪ Contact lenses
▪ Submandibular gland transplantation
 WATERING EYE

→ Overflow of tears from the conjunctival sac.

Etiology

watering eye

hyperlacrimation epiphora

physiological mechanical
primary
cause obstruction

lacrimal sac nasolacrimal

reflex punctal causes canaliculi causes
causes duct causes

eversion of lower
central
punctum

punctal
obstruction

Clinical evaluation

→ Ocular examination with diffuse illumination using magnification.

▪ Done to rule out reflex hypersecretion, punctual causes of epiphora and
any swelling in the sac area

→ Regurgitation test
▪ A pressure with index finger is applied over the lacrimal sac.
▪ Reflex mucopurulent discharge indicates NLD blockage with chronic
dacryocystitis.

→ Fluorescein dye disappearance test

▪ A 2 ml of fluorescein dye is instilled in conjunctival sac.
▪ If it disappears in 2 minutes, it is normal.
▪ If it presents, it indicates partial blockage of NLD or atonia of lacrimal sac.
 → Lacrimal syringing test
▪ Normal saline is pushed into lacrimal sac from lower punctum with syringe
and cannula.
▪ In partial obstruction saline passes with considerable pressure on the
syringe. In complete obstruction it reflexes back through the same punctum
indicating common canaliculi obstruction and through the lower punctum
indicates lower sac or NLD obstruction.

→ Jones dye tests

▪ In the suspect of partial lacrimal sac block.

Jones test 1
➢ 2% fluorescein dye are instilled in the conjunctival sac and a cotton
bud dipped in 1% xylocaine is placed in the inferior meatus at the
opening of nasolacrimal duct.
➢ A dye-stained cotton bud indicates adequate drainage through the
lacrimal passages and the cause of watering is primary
hypersecretion.
➢ Unstained cotton bud indicates partial obstruction or failure of
lacrimal pump.
Jones test 2
➢ The cotton bud is again placed in the inferior meatus and lacrimal
syringing is performed.
➢ Positive: Partial obstruction
➢ Negative: lacrimal pump failure.

→ Dacryocystography
▪ In patients with mechanical obstruction.
▪ To perform it a radiopaque material such as lipiodol, pantopaque, dianosil
or condray-280 is pushed in the sac with the help of a lacrimal cannula and
X-rays are taken after 5 minutes and 30 minutes to visualize the entire
passage.

→ Radionucleate dacryocystography
▪ A non-invasive technique to assess the functional efficiency of lacrimal
drainage apparatus.
 DACRYOCYSTITIS

• Inflammation of lacrimal sac is referred to as dacryocystitis

• Two forms:
→ Congenital dacryocystitis
→ Adult dacryocystitis
▪ Chronic form
▪ Acute form

Congenital dacryocystitis
Also known as Dacryocystitis neonatorum or infantile dacryocystitis.

• Definition:
It is the chronic inflammation of the lacrimal sac occurring in newborn infants

• Etiology:
Follows stasis of secretions in the lacrimal sac due to Congenital blockage in
the nasolacrimal duct (NLD)
Causes of stasis:
➢ Membranous occlusion at lower end, near the valve of Hasner –
commonest cause
➢ Presence of epithelial debris and membranous occlusion at its upper end
near lacrimal sac, complete non-canalisation and rarely bony occlusion.
➢ Bacteria commonly associated- Staphylococcus, Streptococcus and
Pneumococcus species.

• Clinical features:
➢ Epiphora after 7 days
➢ mucopurulent discharge from eyes.
➢ Regurgitation test +ve.
➢ Swelling on the sac area.

• Differential diagnosis
➢ Ophthalmia neonatorum
➢ Congenital glaucoma.
 • Complications:
➢ Recurrent conjunctivitis
➢ Acute or chronic dacryocystitis
➢ Lacrimal abscess and fistulae formation

• Treatment:
➢ Massage over the lacrimal sac area (4 times a day) and topical antibiotics
for 6 to 9 months.
➢ Lacrimal syringing (irrigation) with normal saline and antibiotic solution.
(Started at the age of 3 months-once a week or once in 2 weeks)
➢ If not cured after 6 months – Probing of NLD with Bowman’s probe. (careful
probing should be done so that canaliculi are not damaged) In case of
failure, repeated after 3-4 weeks.
➢ Balloon catheter dilatation-Done when repeated probing is failed and
where obstruction is due to scarring or constriction.
➢ Intubation with silicone tube in NLD for six months if [Link] 5. Are a failure.
➢ If all the above are a failure, Dacryocystorhinostomy (DCR) can be done
after 4 yrs.

Adult dacryocystitis:

i. Chronic dacryocystitis
• More common
• Etiology:

factors responsible for

predisposing factors source of infection causative orgaism
statis of tears
• 40 - 60 years • anatomical factors like • infections from • Staphylococci
• female narrow bony canal conjunctiva, • Pneumococci
preponderance • foriegn bodies paranasal sinuses, • Streptococci
• heredity • excessive lacrimation etc.
• Pseudomonas
• poor personal • mild inflammation of pyocyanea
hygiene lacrimal sac
• poor socio • obstruction of lower
economic status end of nasolacrimal
duct
 • Clinical features:

Stages Clinical features

Stage of chronic ▪ Watering eye and mild redness.

catarrhal ▪ On syringing, clear fluid or few fibrinous mucous flakes
dacryocystitis regurgitate.
▪ Upon dacryocystography, block in NLD, a normal sized
lacrimal sac with healthy mucosa is revealed.
Stage of lacrimal ▪ Constant epiphora, associated swelling below inner
mucocele canthus.
▪ Regurgitation – Milk or gelatinous mucoid fluid from lower
punctum.
▪ Dacryocystography- distended sac with blockage in NLD.
▪ ENCYSTED MUCOCELE – Both canaliculi are blocked – large
fluctuations swelling with -ve regurgitation test.
Stage of chronic ▪ Epiphora, recurrent conjunctivitis and swelling in the inner
suppurative canthus and mild erythema of the skin.
dacryocystitis ▪ Regurgitation- purulent discharge in the lower punctum.
▪ Openings of canaliculi are blocked – ENCYSTED PYOCOELE.
Stage of chronic ▪ Persistent epiphora and discharge.
fibrotic sac ▪ Dacryocystography- small sac with irregular mucosal folds.

• Complications:
➢ Chronic intractable conjunctivitis
➢ Acute or chronic dacryocystitis
➢ Entropion of lower lid
➢ Maceration
➢ Eczema of lower lid skin
➢ Corneal ulceration
➢ Endophthalmitis when intraocular surgery is done in the presence of
dacryocystitis.

• Treatment:
➢ Conservative treatment – probing and lacrimal syringing
➢ Balloon catheter dilatation
 ➢ Dacryocystorhinostomy (DCR)
➢ Dacryocystectomy (DCT)
➢ Conjunctivodacryocystorhinostomy (CDCR)

ii) Acute dacryocystitis:

Acute suppurative inflammation of the lacrimal sac, characterised by presence
of painful swelling in the region of sac.

• Etiology:
➢ Acute exacerbation of chronic dacryocystitis.
➢ Acute peridacryocystitis
➢ Causative organisms- S. hemolyticus, Pneumococcus, Staph sp.

• Clinical features and treatment:

Stages Clinical features Treatment

Stage of ▪ Painful swelling ▪ Antibiotics – both systemic and

cellulitis ▪ Epiphora topical
▪ Malaise ▪ Systemic anti-inflammatory
▪ Redness and edema analgesics
▪ Hot fomentation

Stage of ▪ Occlusion of canaliculi ▪ 1st stage treatment (+)

lacrimal ▪ Pericystic swelling ▪ Pus drainage
abscess ▪ Later DCR / DCT

Stage of ▪ External fistula formed if ▪ Systemic antibiotics

fistula lacrimal abscess is ▪ Fistulectomy with DCT / DCR
formation unattended
▪ Rarely internal fistula

• Complications:
➢ Acute conjunctivitis
➢ Corneal abrasion
➢ Lid abscess
➢ Osteomyelitis of lacrimal bone
➢ Orbital cellulitis
➢ Cavernous sinus thrombosis
➢ Generalised septicaemia
 SURGICAL TREATMENT OF DACROCYSTORHINOSTOMY

3 types:
• Conventional external approach, DCR and
• Endonasal (surgical or laser) DCR
• Endocanalicular laser DCR.

Conventional external approach DCR

1. Anaesthesia. General anaesthesia is preferred

2. Skin incision. Either a curved incision along the anterior lacrimal crest or a straight
incision 8 mm medial to the medial canthus is made.
3. Exposure of medial palpebral ligament (MPL) and anterior lacrimal crest. MPL is
exposed by blunt dissection and cut with scissors to expose the anterior lacrimal crest.
4. Dissection of lacrimal sac. Periosteum is separated from the anterior lacrimal crest and
along with the lacrimal sac is reflected laterally with blunt dissection exposing the lacrimal
fossa.
5. Exposure of nasal mucosa. A 15 mm × 10 mm bony osteum is made by removing the
anterior lacrimal crest and the bones forming lacrimal fossa, exposing the thick pinkish
white nasal mucosa.
6. Preparation of flaps of sac. A probe is introduced into the sac through lower canaliculus
and the sac is incised vertically. To prepare anterior and posterior flaps, this incision is
converted into H shape.
7. Fashioning of nasal mucosal flaps is also done by vertical incision converted into H
shape.
8. Suturing of flaps. Posterior flap of the nasal mucosa is sutured with posterior flap of the
sac using 6–0 vicryl or chromic cat gut sutures. It is followed by suturing of the anterior
flaps.
9. Closure. MPL is sutured to periosteum, orbicularis muscle is sutured with 6–0 vicryl and
skin is closed with 6–0 silk sutures.

anaesthesia and skin incision

med palpebral ligament and anterior

lacrimal crest exposure

dissection of lacrimal sac

exposure of nasal mucosa

preparation of flaps of sac

fashioning and suturing of nasal flaps

closure

In simple words: post flap of sac and post flap of nasal mucosa are sutured together and
anterior flap of sac and mucosa are sutured together, so that tears from the eye drains
directly into the nasal mucosa
CAUSES OF FAILURE COMPLICATIONS
• Inadequate size and position of • Cutaneous scarring
ostium • Haemorrhage
• Unrecognized common canalicular • Cellulitis
obstruction • CSF rhinorrhoea
• Scarring
• Sump syndrome

Endoscopic DCR

1. Preparation and anaesthesia. Conjunctival sac is anaesthetised with topically

instilled 2% lignocaine. Then 3 ml of lignocaine 2% with 1 in 2 lac adrenalines is
injected into the medial parts of upper and lower eyelids and via subcaruncular
injection to the lacrimal fossa region.

2. Identification of sac area A 20-gauge light pipe is inserted via the upper canaliculi
into the sac. With the help of endoscope, the sac area which is trans illuminated by
the light pipe is identified and a further injection of lignocaine with adrenaline is
made below the nasal mucosa in this area.
 3. Creation of opening in the nasal mucosa, bones forming the lacrimal fossa and
posteromedial wall of sac can be accomplished by two techniques:
i. By cutting the tissues with appropriate instruments or
ii. By ablating with Holmium YAG laser (endoscopic
laser-assisted DCR).
Note. The size of opening is about 12 mm × 10 mm

4. Stenting of rhinostomy opening. The outflow system is then stinted using fine
silicone tubes passed via the superior and inferior canaliculi into the rhinostomy
and secured with a process of knotting. Nasal packing and dressing is done.

5. Postoperative care and removal of silastic lacrimal stents. After 24 hours of

operation nasal packs are removed and patient is advised to use decongestant,
antibiotic and steroid nasal drops for 3–4 weeks. The silastic lacrimal stents are
removed 8–12 weeks after surgery
CAUSES OF FAILURE COMPLICATIONS CONTRAINDICATIONS

• Inadequate bony • Orbital emphysema • Lacrimal sac tumours

opening • Trauma to canaliculi • Dacryoliths
• Anastomotic block by tubes • Large abscess of sac
• Iatrogenic • Infection
obstructions • Haemorrhage

ENDONASAL DCR EXTERNAL DCR

Advantages Disadvantages
No external scar Cutaneous scar
Relatively blood less surgery More blood loss
Less chance of injury to ethmoidal vessels Greater chance of damaging the
and cribriform plate surrounding structures
Less time consuming (15-30 mins) Time consuming (45-60 mins)
Time consuming (45-60 mins) Significant postoperative morbidity

Advantages Disadvantages
Less success rate (70-90%) More success rate (95%)
Requires more skilled ophthalmologists Easily performed
Expensive equipment Cheap
Requires reasonable access to middle Does not require familiarity with
meatus and familiarity with endoscopic endoscopic anatomy
anatomy

Endocanalicular laser DCR

→ A quick procedure carried under local anaesthesia

→ Useful in elderly
→ Success rate is 70%

laser probe passed an opening is created by

through a canaliculus ablation of structures

In Dacryocystectomy, the 1st four steps are similar to external DCR, after that we have
→ Removal of lacrimal sac
→ Curettage of bony NLD
→ Closure
 SWELLINGS OF LACRIMAL GLAND

1. DACRYOADENITIS
Inflammation of lacrimal gland

ACUTE CHRONIC
ETIOLOGY Primary infection or secondary → As sequel to acute form
to some local or systemic causes → In association with chronic
inflammation of conjunctiva
→ Due to systemic diseases
CLINICAL Painful swelling Painless swelling
FEATURES Red and swollen lid Proptosis, Diplopia
Proptosis A firm lobulated mobile mass is
Fistula as a complication present
TREATMENT Systemic antibiotics Treat the cause
Analgesics
Anti-inflammatory drugs

2. MIKULICZ’S SYNDROME

→ Bilateral symmetrical enlargement of lacrimal and salivary glands.

→ Associated with systemic diseases

3. DACRYOPS

→ Cystic swelling
→ Caused due to blockage of lacrimal glands causing retention of lacrimal secretion

4. TUMOURS OF LACRIMAL GLAND

tumours

epithelial non epithelial

benign malignant lymphoproliferative

pleomorphic lacrimal gland inflammatory

adenoma carcinoma conditions
Pleomorphic adenoma

→ Benign mixed tumour

→ It is a slowly progressive painless swelling of upper outer quadrant of orbit
→ Treatment consists of surgical removal with capsule

Lacrimal gland carcinoma

→ Occurs in 4th – 5th decade of life

→ They present as painful mass in supratemporal quadrant of orbit
→ On CT, there is an infiltrative tumor moulding the globe
→ Treatment includes complete macroscopic excision and high dose radiotherapy to
orbit
 ORBIT
What you learn here?

• Anatomy of Orbit
• Development anomalies of orbit
• Orbital mucormycosis
• Orbital infections
• Orbital cellulitis
• Cavernous sinus thrombosis
• Non infective orbital inflammation
• Orbital tumours

Anatomy of Orbit
Each orbit is a bony cavity containing an eye ball and extraocular appendages and muscles.
Bony orbit
• Quadrilateral pyramid shape
• Roof frontal and sphenoid
• Medial maxilla, lacrimal, ethmoid and sphenoid
• Lateral zygomatic, greater wing of sphenoid
• Base/inferior “roof of maxillary sinus” i.e Maxilla, Zygomatic, Palatine
Strongest wall lateral
Easily fractured floor and medial
Fracture of floor of orbit leads to maxillary sinusitis

• Apex of the bony orbit contains three openings.

a. Superior orbital fissure
i. Superior and inferior branch of oculomotor nerve (CN 3)
ii. Troclear nerve (CN 4)
iii. Ophthalmic branch of Trigeminal nerve (CN 5-1)
iv. Abducens nerve (CN 6)
v. Superior ophthalmic vein
b. Inferior orbital fissure
i. Inferior ophthalmic vein
ii. Maxillary branch of trigeminal nerve (CN 5-2)
c. Optic foramen
i. Optic nerve (CN 2)
 ii. Superior ophthalmic vein
Extraocular muscles

Extraocular appendages
1. Eyelids
2. Conjunctiva
3. Lacrimal apparatus
4. Orbital fat
 DEVELOPMENTAL ANOMALIES OF ORBIT

The orbit and its contents may be affected by a number of developmental abnormalities involving the
bones of the skull or face.
They are commonly hereditary (auto somal dominant)

The common abnormalities are :

1. Cranio-synostosis
● Due to premature closure of one or more cranial sutures.
● This closure causes a complete arrest of bone growth perpendicular to the closed suture, and
the compensatory growth of the cranium in other diameters, which causes the typical shape of
the skull.
Types :
1. Scaphocephaly (boat-shaped skull): Premature closure of sagittal suture.
2. Oxycephaly (tower-shaped skull): Premature closure of coronal suture
3. Trigonocephaly egg-shaped skull) : premature closure of frontal suture
4. Brachy-cephaly (clover-leaf skull) : Premature closure of all sutures.
The clinical features are :
1. Bilateral proptosis due to shallow orbit.
2. Esotropia or exotropia.
3. Papilloedema, due to increased CSF pressure
4. Optic atrophy primarily due to traction on the optic nerve, or secondary to papilloedema.
Treatment :
Craniotomy or orbital decompression to reduce CSF pressure and papilloedema.
2. Craniofacial dysostosis (Crouzon)
Brachycephaly is combined with hypoplasia of the maxilla
• Ophthalmic features:
● Widely separated eyeballs hypertelorism)
● Shallow orbits with proptosis.
● Corneal problems due to exposure.
● Divergent squint
● Optic atrophy.
• Non-ophthalmic features :
● High-arched palate.
● Irregular dentition
● Hooked (parrot-beak) nose.
● Mental retardation.
3. Mandibulo-facial dysostosis (Treacher Collins)
Hypoplasia of the zygoma and mandible
• Ophthalmic features
● Indistinct inferior orbital margin.
● Coloboma (notching) of the lower lid
● Anti-mongoloid slanting,
• Non-ophthalmic features :
● Bird-like face.
● Macrostomia with high-arched palate.
● External ear deformity.
4. Median facial cleft syndrome
● Hypertelorism with telecanthus
● Cleft nose, lip and palate.
● V-shaped frontal hairline (widows peak.
● Divergent squint.
5. Oxycephaly syndactyly (Apert)
● Tower skull with flat occiput.
● Mental retardation,
● Ventricular septal defect
● High-arched palate.
● Hypertelorism, shallow orbits and proptosis.
● Antimongoloid slanting with ptosis and exotropia.
● Syndactyly of the fingers and toes.
6. Hypertelorism
● Increased separation of eyes
● Widely separated orbits, and broad nasal bridge.
● The interpupillary distance (IPD) may be 85 mm or more.
● Divergent squint, telecanthus and mongoloid slanting.
● There may be optic atrophy due to associated narrowing of the optic canals.
● Hypertelorism also occurs in – median facial-cleft syndrome, Apert’s syndrome, Crouzon’s
syndrome etc.

ORBITAL MUCORMYCOSIS

● Other name: Phacomycosis

● Fungal infection ( mostly Mucor and Rhizopus)
● Begins in sinuses , erodes to orbital cavity.
● Can invade vessels and cause ischemic necrosis

Clinical features:
1. Pain
2. Proptosis
3. Necrotic areas with black eschar
Complications:
1. Meningitis
2. Brain abscess
3. Death
Diagnosis:
 1. Clinical
2. Biopsy ( finding nonseptate broad branching
hyphae) Treatment:
1. Correction of underlying disease (eg: diabetic ketoacidosis)
2. Surgical excision
3. IV Amphotericin B
4. Adjunctive hyperbaric oxygen
5. Exenteration

Orbital infection

ORBITAL INFECTIONS AND INFLAMMATIONS

CLASSIFICATION :

[Link] INFECTIONS:

• Acute orbital infections and related infections :

1. Preseptal cellulitis
2. Orbital cellulitis and intra orbital abcess
3. Orbital thrombophlebitis
4. Orbital osteo periostitis
5. Tenositis
6. Cavernous sinus thrombosis

[Link] ORBITAL INFECTION :

• Tberculosis
• Syphilis
• Actenomyosis
• Mycotic infections eg. Mucormycosis
• Parasitic infections

[Link]-INFECTIOUS ORBITAL INFLAMMATIONS:

• Isolated orbital inflammation

1. Idiopathic orbital inflammatory disease
2. Idiopathic sclerosis inflammation or orbit
3. Mysositis
• Systemic inflammation
1. Thyroid eye disease
2. Wogners granulomatosis
3. Sarcoidosis

[Link] INFECTION :

• Preseptal cellultis
Preseptal (or post septal) cellulitis refers to infection of the subcutaneous tissues anterior to
the orbital disease but is included here under because the facial veins are valves and
preseptal cellulitis .
ETIOLOGY :

• Causative organism : one usually staphylococcus aureus (or) streptococcus pyogenes and
occasionally haemophilly synthesis .

MODES OF INFECTION :

1. Enogenous infection may result following skin laceration insert and eyelid penetration .
2. Endotropin from local infections such as from an weak bordelum (or) areolar dacrocytosis .
3. Endogenous infection may occur by haematogenous spread drown remote infection or the
middle our (or) upper respiratory tract .

CLINICAL FEATURES :

Preseptal cellulitis presits as inflammatory ostoma of the eyelids and periorbital star with no
movement of the orbit .

CHARACTERISTIC FEATURES :

• Painful ocular periorbital swelling

• Erythema and hyporaemic or the lids
• Proptosis is absent
• occular movements are normal
• conjunctiva is usually not congested and unusual society is normal .

TREATEMENT :

• Systemic antibiotic , form the maintenance or treatment

• Mild to molecular cases may be treated by oral co-amoiodrone 500/125 mg tds (or)
fluconaccilin 500 mg for about 10 days.

Severe cases need hospitalization for infrastructure ceffticome 1-2 g/day in distilled doses .

[Link] analgesic and anti-inflammatory dress help in radius pain and swelling .

[Link] compress , 2-3 times a day , hours a 500 this effect

[Link] operation and debidecent is requires on the preforms or thickest mass (or) citra the
foreign bodies is suspected .

ORBITAL CELLULITIS

ORBITAL CELLULITIS :

• Acute inflammation of soft tissue of orbit behind the orbital septum .

• May or may not progress to a subperiostal abscess or orbital abcess .

CAUSATIVE AGENTS:

• Staph. Aureus , [Link]

• Strep. Pneumonia , haemophillus influenza

MODE OF INFECTION :
 • Exogenous – trachoma
• Contiguous – from adjacent structre
• Endogenous – blood spread

CLINICAL FEATURES :

SYMPTOMS :

• Swelling and severe pass increased by occular movement .

• Fever , prostration and defective vision .

SIGNS:

• Lid edema
• Chemosis of conjunctiva
• Axial proptosis
• Restriction of ocular movement
• Fundus : congestion of veins and disc edema

COMPLICATIONS :

Occular complications :

• Exposure keratitis , occlusion of central retinal artery or vein .

• Endophthal mitis , optic neuropathy .

Intra cranial complications :

• Meningitis , brain stem absecess

• Cavernous sinus thrombosis

Sub periostal abscess along medial orbital wall

Orbital abscess :

• Collection of pus within the orbital soft tissue

• Post traumatic or post operative complication

Temporal or parotid abcess

• Due to spread of infection

General septicimea or pyeremia

INVESTIGATION :

• Bacterial culture
• Complete haemmogram
• Xray pns
• Orbital ultrasonography
• CT scan and MRI scan

TREATMENT :

Orbital cellulitis is an emergency and so patient should be hospitalized

 a. Intensive antibiotic therapy
• Used to overcome the infection .
• Intravenous antibiotics should be administred
• For staphylococcus infection high doses of penicillinace – resistant antibiotic
([Link] ) combined with ampicillin shoul be given
• Cefotaxime , ciproflaxicin or vancomycin can be used as alternative for oxacillin
and penicillin combination .
• For [Link] especially In children chloramphenicol or clavulinic and should
also be added
• For anaerobes oral metronidazole 500 mg every behaviour should be added .

[Link] and anti-inflammatory drugs

• Helps to relieve pain and fever

[Link] antibiotic eye ointment

[Link] decongestant drops

[Link]

[Link] intervension:

• Suggested cause of unresponsiveness to antibiotics decrease in vision and pressure

of an orbital or subperiorbital abscess.
• Surgical intervention required are ad follows :
✓ Immediate conthotomy / cantholysis
✓ Free incision into the abscess
✓ Drowning of the thick abcess by a 2-3 cm curved incision .

CAVERNOUS SINUS THROMBOSIS

CAVERNOUS SINUS THROMBOSIS , refers to infected blood clot . it is described along with
infection of the orbit on it alos manifest an acute inflammatory type of proptosis.

CAVERNOUS SINUS ANATOMY :

Cavernous sinus is formed between the meningeal layer and industrial layer of duramater

The contents of cavernous sinus includes the 3rd cranial nerve , 4th cranial nerve ,

ophthalmus divisions and maxillary division of trigeminal nerve and 8th cranial nerve and
internal carotid artery

ETIOLOGY:

Septic thrombosis of the cavernous sinus is a disasterous regular , resulting from spread of
sepsis travelling along its tributaries from the infected sinuses , teeth , ears , nose and skin to
the face .

Very rarely cavernous sinus thrombosis may also occur after trauma .
Communications of cavernous sinuses and sources of infection anterior :

Anteriorly cavernous sinus is bounded by supraorbital fissure … so the superior and the
inferior ophthalmic veins drain into the sinuses and orbits

There fore , infection to cavernous sinuses may spread from infected facial wounds ,
erysipelas , squeezing of stye , furancles orbital cellulitis and sinusitis

POSTERIOR :

The posterior border of cavernous sinus includes the petrays part of the temporal bone . the
superior and inferior petrosal sinuses leave to join the lateral sinus . labyrinth veins opening
into the inferior petrosal sinuses bring infection from the mastoid air sinuses

SUPERIOR :

The cavernous sinus communicates with the veins of cerebrum and may be infected from
meningitis and cerebral abscesses

INFERIOR :

The sinus communicates with pterigoid venus plexus

MEDIALLY :

The two cavernous sinuses are connected to each other by transverse sinuses which
transfers infection from one side to the other .

The other sources of cavernous sinus thrombosis includes :

• Diabetes
• Cancer
• Trauma

SYMPTOMS :

• Unilateral visual loss

• Sudden headache
• Unilateral eye swelling
• Eyelid drooping
• High grade fever

[Link] to 3rd 4th 6th cranial nerve . the 3rd cranial nerve is involved in medial movement of the eye
ball and 6th cranial nerve involved in lateral movement of the eye ball and 4th cranial nerve supplying
the superior oblique muscle resulting in unable to move the eye ball inderiorly.

INVESTIGATIONS :

1. CT scan head and orbit may show involvement of cavernous sinuses and proptosis.
2. Mangentic resonance venography (angiography) in the investigation of choice which shows
an absence of flow void in thrombosed sinuses
3. Blood culture is recommended for sepsis.

COMPLICATIONS :

At any stage hyperpyrexia and signs of meningitis , pulmonary infarction may precude death
TREATMENT :

1. Antibiotics are the sheet anchor of treatment massive doses of modern potent broad
spectrum antibiotics should be injected intravenously
2. Analgesics and anti-inflammatory drugs control pain and fever
3. Anticoagulants role is controversial .

NON-INFECTIVE ORBITAL INFLAMMATION

1. Idiopathic Orbital Inflammatory Disease (Pseudotumor)

2. Tolosa-Hunt Syndrome

Idiopathic Orbital Inflammatory Disease (Pseudotumor)

➢ Pseudotumor – Condition of the orbit which,

o Clinically – present as tumours, but
o Histopathologically – proven as chronic inflammations.

➢ Recently called as Idiopathic Orbital Inflammatory Disease (IOID)

➢ IOID – Can occur throughout the orbit from lacrimal gland to orbital apex.

➢ Common Features:

o Age – Between 40 and 50 years

o Laterality – Unilateral (occasionally bilateral)
o Clinical Presentation – Swelling / puffiness of eyelids,
Congestive proptosis,
Orbital pain,
Restricted ocular movements,
 Diplopia, chemosis & redness
o Optic Nerve dysfunction – When posterior orbit involved
o Remission - Spontaneous after few weeks
o Recurrence - Common
o Frozen Orbit - In severe prolonged inflammation.

➢ Diagnosis:
o USG and CT – diffuse infiltrative lesion with irregular ill-defined margins and
variable density
(CT image of IOID)

o MRI:

▪ T1 MRI – Hypointense lesion c.f muscle.

 (T1 MRI)
▪ T2 MRI – Hyperintense lesion c.f muscle.

(T2 MRI)

o Incisional biopsy – confirm diagnosis in persistent cases.

➢ Treatment:
o NSAIDs
o Systemic Steroids (only after diagnostic biopsy)
o Radiotherapy
o Cytotoxic drugs
o TNF inhibitors.

Tolosa Hunt Syndrome (Non-specific granulomatous inflammation.)

➢ Involves – superior orbital fissure &/or orbital apex &/or cavernous sinus
 ➢ Clinical features:
o Manifestation – Painful ophthalmoplegia.
o Presentation
▪ Superior orbital fissure syndrome.
▪ Orbital apex syndrome.

➢ Superior orbital fissure syndrome:

o Involvement of structures passing through superior orbital fissure
o Features:
▪ Pain – Retro orbital ache.
▪ Sensory loss/Disturbance – along the course of 5th cranial nerve
▪ Ipsilateral ophthalmoplegia – due to involvement of 3rd,4th,6th CN
▪ Ptosis – due to 3rd CN palsy
➢ Orbital apex syndrome:
o Involvement of structures present at the apex of orbit (i.e., superior orbital fissure plus
optic canal)
o Features:
▪ Features of superior orbital fissure syndrome
+
▪ Features of optic nerve involvement (i.e., early visual loss + afferent pupillary
defect)
 ➢ Treatment:
o Systemic steroids.
o Radiotherapy.

ORBITAL TUMOURS

INCIDENCE: tumours of the eye and orbit are rare.

● Male to female incidence is similar.

● In adult melanoma is most common primary intraocular cancer followed by lymphoma.
● In Children retinoblastoma is the most common followed by medulloepithelioma.
● Metastases or secondary intraocular tumours are more common than primary tumours and
typically come from breast or ling cancer.
CLASSIFICATION:

BY ORIGIN-

● Primary- lesions originating from the orbital tissues.

● Secondary- lesions originating from the neighbouring cavities and tissues.
● Metastatic-lesions reach the orbit via hematogenous or lymphatic spread.
BENIGN ORBITAL TUMOURS-

● ptergium
● Chorodial hemangiomas
● Orbital pseudotumors
● Thyroid associates orbitopathy.
MALIGNANT ORBITAL TUMOURS-

● Metastatic carcinoma to the uvea

● Malignant 14frica of uvea
● Retinoblastoma
A)PRIMARY TUMOURS:

1)Developmental tumours

Dermoids- these are developmental tumors

● Arises from the embryonic displacement of the epidermis to a subcutaneous location.

● Lines with keratinizing epithelium and May contains one or more dermal adNeal structure.
● Two types- a)superficial dermoid
b)deep dermoids

● Superficial dermoid- seen in infancy

Firm ,round,localised lesions in the upper temporal or upper nasal aspect of orbit.
 Not extend deep into the orbit and are associated with bony defects.

Deep dermoid-present in adolescence with proptosis or a mass lesions having indistinct posterior
margins.

Associated with bony defects.

Treatment- surgical excision.

Epidermoid: composed of epidermis without any epidermal appendages in the wall of the cyst.

Almost always cyst.

Cyst wall contains keratin debris.

Treatment- surgical excision

Lipodermoid:solid tumours usually seen beneath the 15frica1515iva.

Located adjacent to the superior temporal quadrant of the globe.

Does not require any surgical intervention unless they enlarge significantly.

Teratomas: composed of ectoderm , mesoderm and endoderm.

May be solid , cystic or a mixture.

Bening but some solid tumours in Newborns are Malignant.

Treatment- exoneration is usually performed for solid tumours to effect a permanent cure.

Cystic tumours may be excused without removing the eyeball.

2)Vascular tumours:

Most common primary benign tumours of the orbit

These can be

● Haemangiomas
● Lymphangiomas
Capillary haemangiomas- seen at birth or during the first month.

Appears as periocular swelling in the anterior part of the orbit.

Increases in size on straining or crying.

Treatment- usually not required any treatment.

Indication for treatment are:optic nerve compression exposure keratitis ocular dysfunction or
cosmetic blemish.

Modes of therapy:

● Systemic or intralesional steroids

● Low dose superficial radiations
● Surgery and cryotherapy
● Systemic beta blocker.
CAVERNOUS HAEMANGIOMA:
 ● Commonest BENIGN ORBITAL tumours among adult with female preponderance.
● Locates in the retrobulbar muscle cone.
● Compress the optic nerve without causing proptosis.
Treatment- via lateral orbitotomy approach surgical tumour excision done.

3)LYMPHANGIOMA: uncommon tumour presenting with slowly progressive proptosis in a young

person.

Often enlarge because of spontaneous bleed within the vascular spaces leading to formation of
chocolate cysts which may regress spontaneously.

MESENCHYMAL TUMOUR:

● Highly MALIGNANT tumour of the orbit.

● Arises from the pluripotent mesenchymal cells which have potential to differentiate into
striated muscles.
● Primary orbital tumours among children.
Histopathology:rhabdomyosarcoma May be of three types.

● Embryonal sarcoma
● Alveolar sarcoma
● Pleomorphic sarcoma.
Clinical feature: present with rapidly progressive proptosis of sudden onset in a child of 7-8 yrs

It mimics an acute inflammatory process.

Commonly involved superonasal quadrant.

Ķdiagnosis:supported by x-rays showing bone destruction and CT/MRI scan.

Seen as well defined tumour with adjacent bone destruction.

Confirmed by biopsy.

Treatment:

● Surgical excision
● Chemotherapy regime
● Radiation therapy
● Exenteration.
NEURAL TUMOURS

Optic nerve glioma:

● Slow growing tumour arising from the astrocytes.

● Usually occur at the first decade of life
● Present as solitary or a part of von Recklinghausen’s neurofibromatosis
● Optic nerve alone is affected in cases with involve the optic chasms often mid brain and
hypothalamic involvement.
Clinical features:

● Gradual visual loss

● Painless unilateral axial proptosis occurring in a child between 4 and 8 yrs
 ● Funds EXAMINATION May may show optic atrophy.
Diagnosis:

● X-ray -show uniform regular enlargement of optic foramen.

● CT scan and ultrasonography -fusiform growth in relation to optic nerve.
Treatment:

● Surgical excision
● Radiotherapy
MENINGIOMA

Invasive tumour arising from arachnoid Villi

Two types

● Primary
● Secondary
Primary :also known as optic nerve sheath meningiomas.

● Tumour of meningothelial cells of meninges.

● Associated with neurofibromatosis
● Present with early visual loss associated with limitation of ocular movements optic disc
edema or atrophy and slowly progressive unilateral proptosis.
● Intramural stage-indistinguishable from optic nerve glioma.
Treatment:

● Observation is recommended if visual acuity is good.

● Surgical excision
● Prognosis for life is good.
Secondary orbital meningioma:

● Arises either from sphenoid bone or involve

It enroute to the orbit.

● Occur typically in the middle age.

Clinical feature:

● Greater proptosis and lesser visual impairment

● Biggy eyelid swelling and a ipsilateral swelling in the temporal region of the face.
● Observation is recommended
● Postoperative radiotherapy is advocated to reduce the risk of recurrence of the residual
tumour.
Lymphoprofliterature tumours

WHO classification of lymphoprofilative tumours is

● BENIGN reactive lymphoid hyperplasia

● MALIGNANT ORBITAL lymphoma
● Langerhans cell histocyctosis.
BENIGN reactive lymphoid hyperplasia (BHRL)

● Uncommon polyclonal proliferation of lymphoid tissue

 ● Occurring in the anterior part of superolateral orbit with a predilection for lacrimal gland
Clinical feature:

● Proptosis -painless progressive with medial displacement of the globe.

● Firm rubbery mass-palpable beneath superolateral orbital rim
● Pink subconjunctival infiltrate may also seen
Treatment

● Systemic steroid and loc radiotherapy

● May requires cytotoxic drugs
● Progression to systemic lymphoma.
Atypical lymphoid hyperplasia:

Atypical lymphoid hyperplasia (ALH) is an intermediate between BRLH and malignant lymphoma.

Feature are similar to BRLH except:

● May involve other systemic organs

● Usually does not respond to steroids.
MALIGNANT ORBITAL LYMPHOMA

● Involved by MALIGNANT non-Hodgkin B cell lymphoma.

● Hodgkin’s lymphoma seldom involve the orbit.
According to the REAL (Revised European American Lymphoma) classification

1)Mucosa associated lymphoid tissue (MALT)lymphoma:

● Accounts for 40-70% of all orbital lymphoma

● Usually unilateral but bilateral involvement May occur in 25%cases
● Present with gradual proptosis and palpable firm rubbery masses.
● Systemic involvement occurs in 50% of cases
Treatment includes radiotherapy or chemotherapy

Depending upon the grade and spread of tumours.

1. Chronic lymphocytic lymphoma:

● Low grade lesion of small mature appearing lymphocytes

2. Follicular center lymphoma:

● Low grade lesion with follicular Centers.

3. High grade lymphoma:

● Large cell lymphoma, lymphoblastic lymphoma and Burkitt’s lymphoma

La ngerhans cell histiocytosis:

● Formerly know as histiocytosis s is a group of diseases characterised by an idiopathic

abnormal profileration of histiocyctes with granuloma formation.
● Most commonly affects the children.
1)Hand Schuller Christian disease:

● Chronic disseminated from histiocytosis

 ● Involving both soft tissues and bones in older children of either sex.
● Characterised by triad of proptosis, Diabetes insipidus and bony defects in the skull.
4. letterer siwe disease:

● Diffuse soft tissue histiocytosis

● Characterised by widespread soft tissue and visceral involvement with or without bony
change.
● Slightly male preponderance and often occurs in the first three years of life.
3)unifocal or multifocal Eosinophilic granuloma:

● Solitary or multiple granulomas involving bones

● Occurs in elder children and frequently involves the orbital bones.
SECONDARY ORBITAL TUMOURS:

● Tumours of eyeball- retinoblastoma and malignant melanoma

● Tumours of eyelids-squamous cell carcinoma and basal cell carcinoma.
● Tumours of nose and paranasal sinuses-very commonly involve orbit.
*carcinoma

*sarcomas

*osteomas.

● Tumour of nasopharynx-nasopharynx is the commonest tumour involving the orbit.

*tumour show opthalmoneurological symptoms inClyde proptosis and involvement of fifth
and sixth cranial nerves.

● Tumours of cranial cavity invading orbit are glioma and meningioma.

C)metastatic orbital tumours:

● Hematogenous spread from distant primary focus .

Metastatic tumour in children

1. Neuroblastoma-fro. Adrenals and sympathetic chain.

2. Nephroblastoma-from kidney
3. Ewing’ s sarcoma-from the bones
4. Leukaemia infiltration
5. Testicular embryoral sarcoma and ovarian sarcoma.
Metastatic tumours in adults:

1. Carcinoma from lungs ( most common in male ) breast ( more common in female)prostate
thyroid and rectum.
2. Malignant melanoma from skin.
ORBITAL TUMOURS

TUMOUR CHILDREN ADULT

Primary Benign Dermoid cyst Cavernous haemangioma
Primary Malignant Rhabdomyosarcoma Lymphoma
Secondary Tumour Retinoblastoma Squamous cell carcinoma
Metastatic Tumour Neuroblastoma Carcinoma breast (females)
Carcinoma lungs (males)
 OCULAR INJURY
What you will learn here?

• Mechanical injuries
• Intra ocular foreign
bodies
• Sympathetic
ophthalmitis
• Extra global injuries
• Optic nerve injuries
• Orbit injuries
1) MECHANICAL INJURY
2) NON MECHANICAL INJURY
MECHANICAL INJURY

(1) CLOSED GLOBE INJURY

• Is the one in which eye wall (sclera & cornea) does not have full thickness wound but there is intraocular damage.
• It includes CONTUSION and LAMELLAR LACERATION
• CONTUSION - from blunt trauma
- damage may occur at the site of impact or at a distant site.
• LAMELLAR LACERATION - characterized by a partial thickness wound of the eye wall
- caused by sharp object or blunt trauma.

Causes and pathogenesis of damage

Modes of trauma
Blunt trauma may occur following

• Direct blow to the eyeball example - fist , tennis or other ball , blunt instrument like stick or big stone.
• Accidental blunt trauma to eyeball example – roadside accident , automobile accident , injury by agricultural and
industrial instruments etc,.

Mechanics of forces of blunt trauma

1. Direct impact on the globe
2. Compression wave force
3. Reflected compression wave force
4. Rebound compression wave force
5. Indirect force
Mechanism of damage
1. Mechanical tearing of the tissues of eyeball
2. Damage to the tissue cells sufficient to cause disruption of their physiological activity
3. Vascular damage leading to ischemia , edema and hemorrhage
4. Trophic change due to disturbance of nerve supply
5. Delayed complications of blunt trauma such as secondary glaucoma , hemophthalmitis , late rosette cataract and
retinal detachment.

Lesion of closed globe injury

a) Cornea
• simple corneal abrasion
• recurrent corneal abrasion
• partial corneal abrasion
• tears in descent’s membrane
• acute corneal edema
• blood staining of cornea
b) Sclera
partial thickness scleral wound may occur alone or in association with other lesion of closed globe injury.
c) Anterior chamber
• Traumatic hyphema
• Exudates ; may occur following traumatic uveitis
d) Iris, pupil & ciliary body
• Traumatic miosis
• Traumatic mydriasis
• Rupture of pupillary margin
• Radiating tears in the iris stroma
• Iridodialysis
• Antiflexion of the iris
• Retroflexion of the iris
• Traumatic aniridia or iridemia
• Angle recession
• Inflammatory change
e) Lens
• Vossius ring
• Concussion cataract
• Traumatic absorption of the lens
• Subluxtion of the lens
• Dislocation of the lens
f) Vitreous
• Liquefaction & appearance of cloud
• Detachment
• Vitreous hemorrhage
• Vitreous herniation
g) Choroid
• Rupture of the choroid
• Choroidal hemorrhage
• Choroidal detachment
• Traumatic choroiditis
h) Retina
• Commotio retinae
• Retinal hemorrhages
• Retinal tears
• Traumatic proliferative retinopathy
• Retinal detachment
• Concussion change at macula
i) Intraocular pressure change in closed globe injury
• Traumatic glaucoma
 • Traumatic hypotony
j) Traumatic change in the refraction
• Myopia
• Hypermetropia
OPEN GLOBE INJURY

• Refers to the full thickness wound of the sclera or cornea of both.

• Ti incudes RUPTURE & LACERATION of eye wall
• RUPTURE - refers to the full thickness wound of eye wall caused by the impact of blunt trauma.
• the wound occurs due to markedly raised intraocular pressure by an inside-out injury mechanism
• LACERATION - refers to the full thickness wound of eye wall caused by a sharp object.
- the wound occurs at the impact site by an outside-in mechanism.
- it include penetrating & perforating injuries.

Globe rupture
Type of globe rupture
1. DIRECT RUPTURE – may occur , though rarely , at the site of injury
2. INDIRECT RUPTURE - is more common
- occurs because of the compression force
- result in momentary increase in IOP
- result in an inside-out injury at the weakest part of eye wall

Clinical feature
Rupture of the globe may be associated with

• Prolapse of uveal tissue, vitreous loss, introcular hemorrhage & dislocation of the lens.
• IOP may be raised initially , but ultimately it is decreased.
• Accompanying signs include irregular pupil, hyphema, commotio retinae, choroidal rupture & retinal tears.

Treatment
• Repair of tear in the eye wall should be done meticulously under general anesthesia to save the eyeball whenever
possible.
• Postoperative treatment should include antibiotics, steroids and atropine.
• Enucleation may be required in a badly damaged eye where salvation is not possible.

Global laceration
Full thickness wound of eye wall caused by sharp object.

It include

• Penetrating injury
• Perforating injury
• Intraocular foreign bodies

(A) Penetrating and perforating injuries

Can cause severe damage to the eye and so should be treated as serious emergencies.

Modes of injury
a) Trauma by sharp and pointed instrument like needle,knives,nails,arrow,screw-driver,pens,pencil,compass,glass pieces etc,.
b) Trauma by foreign bodies travelling at very high speed such as bullet injury and iron foreign bodies in lathe worker

Mechanism of damage
a) Mechanical effect of the trauma or physical changes.
b) Introduction of infection
c) Post traumatic iridocyclitis

Traumatic lesions with management

a) Wound of the conjunctiva – wound more than 3mm should be sutured
b) Wound of the cornea
• Uncomplicated corneal wound - SMALL WOUND ; pad & bandage with atropine & antibiotic treatments. LARGE
WOUND; more than 2mm should always be sutured.
• Complicated corneal wound- 𝐶̅ iris prolapse should be sutured ; 𝐶̅ lens injury & vitreous loss,lensectomy & anterior
vitrectomy along with repair of corneal wound.
c) Wound of sclera- in corneo-scleral tear suture should be applied at limbus.
d) Wound of the lens-treated on general line
e) A badly (severely) wounded-such eye should be exercised.

INTRAOCULAR FOREGIN BODIES

Intraocular foreign bodies Penetrating injuries with foreign bodies are not infrequent. Seriousness of such injuries is
compounded by the retention of intraocular foreign bodies (IOFB).

• Common foreign bodies responsible for such injuries include: chips of iron and steel (90%), particles of glass, stone,
lead pellets, copper percussion caps, aluminium, plastic and wood.
For ex :
While chopping a stone with an iron chisel, it is commonly a chip of the chisel and not of the stone which enters the eye.

Modes of damage and Lesions

A penetrating/perforating injury with retained foreign body may damage the ocular structures by the following modes:
A. Mechanical effects
B. Introduction of infection
C. Reaction of foreign bodies
D. Post-traumatic Iridocyclitis
E. Sympathetic Ophthalmitis

Mechanical effects :
Common sites for retention of an intraocular foreign body
1. anterior chamber
2. iris
3. lens
4. vitreous
5. retina
6. choroid
7. sclera
8. orbital cavity

Mechanical effects depend upon the size, velocity and type of the foreign body.
Foreign bodies greater than 2 mm in size cause extensive damage.
The lesions caused also depend upon the route of entry and the site up to which a foreign body has travelled.

Traumatic lesions produced by intraocular foreign bodies include

• Corneal or/and scleral perforation, hyphema, iris hole
• Rupture of the lens and traumatic cataract,
• Vitreous hemorrhage and/or degeneration,
• Choroidal perforation, hemorrhage and inflammation
• Retinal hole, hemorrhages, edema and detachment.
1. Introduction of infection
• Introduction of infection Intraocular infection is the real danger to the eyeball.
• Fortunately, small flying metallic foreign bodies are usually sterile due to the heat generated on their commission.
However, pieces of the wood and stones carry a great chance of infection. Unfortunately, once intraocular infection is
established it usually ends in endophthalmitis or even panophthalmitis.
2. Reactions of the foreign body
Reactions of Inorganic foreign body depending upon its chemical nature following 4 types of reactions are noted in the
ocular tissues:
• No reaction is produced by the inert substances which include glass, plastic, porcelain, gold, silver and platinum
• Local irritative reaction leading to encapsulation of the foreign body occurs with lead and aluminium particles.
• Suppurative reaction is excited by pure copper, zinc, nickel and mercury particles.
• Specific reactions are produced by iron (Siderosis bulbi) and copper alloys (Chalcosis). Siderosis bulbi It refers to the
ocular degenerative changes produced by an iron foreign body. Siderosis bulbi usually occurs after 2 months to 2 years
of the injury. However, earliest changes have been reported after 9 days of trauma.
Mechanism:
• The iron particle undergoes electrolytic dissociation by current of rest and its ions are disseminated throughout the eye.
• These ions combine with the intracellular proteins and produce degenerative changes. In this process, the epithelial
structures of the eye are most affected.

Clinical manifestations include:

1. Anterior epithelium and capsule of the lens are involved first of all. Here, the rusty deposits are arranged radially in a
ring. Eventually, the lens becomes cataractous.
2. Iris. It is first stained greenish and later on turns reddish brown (heterochromia iridis).
3. Retina develops pigmentary degeneration which resembles retinitis pigmentosa. Electroretinography (ERG) shows
progressive attenuation of the b-wave over time.
4. Secondary open angle glaucoma may occur due to degenerative changes in the trabecular meshwork.
5. Chalcosis It refers to the specific changes produced by the alloy of copper in the eye.

Mechanism of chalcosis:
- Copper ions from the alloy are dissociated electrolytically and deposited under the membranous
structures of the eye.
- Unlike iron ions these do not enter into a chemical combination with the proteins of the cells and thus
produce no degenerative changes.

Clinical features include:

• Kayser-Fleischer ring.
• It is a golden brown ring which occurs due to deposition of copper under peripheral parts of the Descemet’s membrane
of the cornea.
• Sunflower cataract. It is produced by deposition of copper under the posterior capsule of the lens.
• It is brilliant golden green in colour and arranged like the petals of a sunflower.
• Retina- It may show deposition of golden plaques at the posterior pole which reflect the light with a metallic sheen.

3. Reaction of organic foreign bodies

• The organic foreign bodies such as wood and other vegetative materials produce a proliferative reaction by the
formation of giant cell
• Caterpillar hair produces ophthalmia nodosum, which is by a severe granulomatous iridocyclitis with nodule formation.

Management of Retained intraocular foreign Bodies (IOFB) diagnosis-

It is a matter of extreme importance particularly as the patient is often unaware that a particle has entered the eye. To come to
a correct diagnosis following steps should be taken
1) History - A careful history about the mode of injury may give a clue about the type of IOFB.
2) Ocular examination - A thorough ocular examination with slit-lamp including gonioscopy should be carried out.

The signs which may give some indication about IOFB are,

- subconjunctival hemorrhage, corneal scar, holes in the iris, and opaque track through the lens. With
clear media, sometimes IOFB may be seen on ophthalmoscopy in the vitreous or on the retina. IOFB
lodged in the angle of anterior chamber may be by gonioscopy.
3) Plain X-rays orbit - Anteroposterior and lateral views are still being recommended for the location of IOFB, as
most foreign bodies are radio opaque. However, many workers feel there is no use of plain film radiology (PFR), as
CT images are required for suspected IOFB, even if PFR is negative.
4) Localization of IOFB - Once IOFB is suspected clinically and later confirmed, on fundus examination and/or X-rays,
its exact localization is mandatory to plan the proper removal.

Following techniques may be used -

1) Radiological localization - Before the advent of ultrasonography and CT scan different specialized radiographic
techniques were used to localize IOFBs; which are now obsolete. However, a simple limbal ring method which is still
used (most centers have discarded it is described below:
- Limbal ring method. It is the most simple but nowadays, sparingly employed technique. A metallic ring
of the corneal diameter is stitched at the limbus and X-rays are taken
 - One exposure is taken in the anteroposterior view. In the lateral view three exposures are made one
each while the patient is looking straight, upwards and downwards, respectively.
- The position of the foreign body is estimated from its relationship with the metallic ring in different
positions. Ultrasonographic localization. It is being used increasingly these days. It can tell the position
of even non-radiopaque foreign bodies. CT scan. With axial and coronal cuts, CT scan is presently the
best method of IOFB localization.
- It provides cross-sectional images with a sensitivity and specificity that are superior to plain
radiography and ultrasonography
- Magnetic resonance imaging (MRI) is not recommended as a general screening tool, since it can cause
further damage by producing movement of a magnetic IO foreign body. However, after the CT has
excluded the presence of a metallic IO foreign body; MRI has a special role in localizing small plastic or
wooden IO foreign bodies
- Treatment IOFB should always be removed, except when it is inert and probably sterile or when little
damage has been done to the vision and the process of removal may be risky and destroy sight (e.g.,
minute FB in the retina
- Removal of magnetic IOFB is easier than the removal of non-magnetic FB. Usually a hand-held
electromagnet is used for the removal of magnetic foreign body. Method of removal depends upon the
site (location) of the IOFB as follows:
• Foreign body in the anterior chamber. It is removed through a corresponding corneal incision
directed straight towards the foreign body. It should be 3 mm internal to the limbus and in the
quadrant of the cornea lying over the foreign body.
• Magnetic foreign body is removed with a handheld magnet. It may come out with a gush of
aqueous.
• Non-magnetic foreign body is picked up with toothless forceps.
3. Sector iridectomy - foreign body entangled in the iris tissue (magnetic as well as non-magnetic) is removed by
performing sector iridectomy of the part containing foreign body
4. foreign body in the lens
- Magnet extraction is usually difficult for intralenticular foreign bodies. Therefore, magnetic foreign body
should also be treated as nonmagnetic foreign body. An extracapsular cataract extraction (ECCE) with
intraocular lens implantation should be performed.
- The foreign body may be evacuated itself along with the lens matter or may be removed with the help of
forceps.

Foreign body in the vitreous and the retina is removed by the posterior route as follows:
i. Magnetic removal- This technique is used to remove a magnetic foreign body that can be well localized and removed
safely with a powerful magnet without causing much damage to the intraocular structures.
ii. An intravitreal foreign body is preferably removed through a pars plana sclerotomy (5 mm from the limbus).
iii. A preplaced suture is passed and lips of the wound are retracted. A nick is given in the underlying pars plana part of the
ciliary body. And the foreign body is removed with the help of a powerful hand-held electromagnet. Preplaced suture is
tied to close the scleral wound. Conjunctiva is stitched with one or two interrupted sutures.
iv. For an intraretinal foreign body, the site of incision should be as close to the foreign body as possible. A trapdoor scleral
flap is created, the choroidal bed is treated with diathermy, choroid is incised and foreign body is removed with either
forceps or external magnet. Ii. Forceps removal with pars plana vitrectomy
v. This technique is used to remove all non-magnetic foreign bodies and those magnetic foreign bodies that cannot be
safely removed with a magnet. In this technique, the foreign body is removed with vitreous forceps after performing
three-pore pars plana vitrectomy under direct visualization using an operating microscope
 Sympathetic Ophthalmitis

- 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
- incidence Incidence of sympathetic ophthalmitis has markedly decreased in the recent years due to meticulous repair
of the injured eye utilizing microsurgical techniques and use of the potent steroids.
- Etiology of sympathetic ophthalmitis is still not known exactly
- However, the facts related with its occurrence are as follows:
Predisposing factors
a. It almost always follows a penetrating injury.
b. Wounds in the ciliary region (the so-called dangerous zone) are more prone to it.
c. Wounds with incarceration of the iris, ciliary body or lens capsule are more vulnerable.
d. It is more common in children than in adults.
e. It does not occur when actual suppuration develops in the injured eye.

Pathogenesis
Most accepted one is allergic theory, which postulates 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:

- Nodular aggregation of lymphocytes, plasma cells, epitheloid cells and giant cells scattered 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 epitheloid cells.
- Sympathetic perivasculitis. Retina shows perivascular cellular infiltration.

Clinical features
Exciting (injured) eye.
- It shows clinical features of persistent low grade plastic uveitis, which include ciliary congestion, lacrimation and
tenderness. Keratic precipitates may be present at the back of cornea (dangerous sign).
- Sympathizing (sound) eye. It is usually involved after 4–8 weeks of injury in the other eye. Earliest reported case is
after 9 days of injury.
- Most of the cases occur within the first year. However, delayed and very late cases are also reported.
- Sympathetic ophthalmitis, almost always, manifests as acute plastic iridocyclitis. Rarely it may manifest as
neuroretinitis or choroiditis. Clinical feature of the iridocyclitis in sympathizing eye can be divided into two stages:

Prodromal stage

Symptoms

- Sensitivity to light (photophobia) and transient indistinctness of near objects (due to weakening of
accommodation) are the earliest symptoms.
- Signs
• In this stage, the first sign may be presence of retrolental flare and cells or the presence of a few keratic
precipitates (KPs) on back of cornea.
• Other signs includes mild ciliary congestion, slight tenderness of the globe, fine vitreous haze and disc
oedema which is seen occasionally.
Fully-developed stage

- It is clinically by typical signs and symptoms consistent with acute plastic iridocyclitis

Treatment
a. Prophylaxis
i. Early excision of the injured eye. It is the best prophylaxis when there is no chance of saving useful vision.
 ii. When there is hope of saving useful vision, following steps should be taken:

- A meticulous repair of the wound using microsurgical technique should be carried out, taking great care that uveal
tissue is not incarcerated in the wound
- Immediate expectant treatment with topical as well as systemic steroids and antibiotics along with topical atropine
should be started.
- When the uveitis is not controlled after 2 weeks of expectant treatment, i.e., lacrimation, photophobia and ciliary
congestion persist and if KPs appear, this injured eye should be excised immediately

b. Treatment when sympathetic ophthalmitis has already supervened

I. Early excision (enucleation) should be done when the case is seen shortly after the onset of inflammation (i.e., during
prodromal stage) in the sympathizing eye, and the injured eye has no useful vision, this useless eye should be excised at
once.

II. Conservative treatment of sympathetic ophthalmitis on the lines of iridocyclitis should be started immediately, as follows:

1. Corticosteroids should be administered by all routes, i.e., systemic, periocular injections and frequent instillation of
topical drops.
2. Immunosuppressant drugs should be started in severe cases, without delay.
3. Atropine should be instilled three times a day in all cases.
Note : The treatment should be continued for a long time.
Prognosis
• If sympathetic ophthalmitis is diagnosed early (during prodromal stage) and immediate treatment with
steroids is started, a useful vision may be obtained. However, in advanced cases, prognosis is very poor,
even after the best treatment.
EXTRAOCULAR LESION
Extraocular lesions caused by blunt trauma are as follows:

Conjunctival lesions include:

• Subconjunctival haemorrhage occurs very commonly. It appears as a bright red spot.

• Chemosis and lacerating wounds of conjunctiva (tears) are also not uncommon.

Eyelid lesion include:

- Ecchymosis of eyelids is of frequent occurrence. Because of loose subcutaneous tissue, blood collects easily into the
lids and produces ‘black-eye.’
- Ecchymosis of the eyelids may characteristically appear as bilateral ring hematomas (panda eye) in patients with basal
skull fracture.
- Laceration and avulsion of the lids.
- Traumatic ptosis may follow damage to the levator muscle.

Lacrimal apparatus lesions include:

- Dislocation of lacrimal gland

- Lacerations of lacrimal passages especially the canaliculi.

Optic nerve injuries

• These are commonly associated with fractures of the base of skull. These may be in the form of traumatic papillitis,
lacerations of optic nerve, optic nerve sheath hemorrhage and avulsion of the optic nerve from back of the eye

Orbital injury
• There may occur fractures of the orbital walls; commonest being the ‘blow-out fracture’ of the orbital floor
• Orbital hemorrhage may produce sudden proptosis.
• Orbital emphysema may occur following ethmoidal sinus rupture