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
1.Ophthalmic 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
1.Type 1 and type 4 hypersensitivity reactions
Type 1: IgE mediated response
Type iv: cell mediated response
2.leads 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 limbus.it 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

A.ANATOMY:

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.

A.1.Dimensions of Cornea:

• Refractory index = 1.37

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

A.2.Histology:
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

A.3.Blood 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 anaerobic.Cells can survive only up to 6-7 hrs
Anaerobically

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

A.4.Nerve Supply:
• Long ciliary nerve – a branch of Naso-ciliary nerve from Ophthalmic branch of Trigeminal nerve
• Cornea is extremely sensitive (touch, pain, temperature)

A.5.Embryology:
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

B.PHYSIOLOGY:
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.

C.CONGENITAL 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

D.INFLAMMATIONS 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. C.Diptheria, N.gonorrhoeae, ,
N.meningitis, 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 ulcer.Where this causes increased hyperemia which can also affect the uveal tract,
etc, hence this futher causes Acute Anterior uveitis.The 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 E.COLI

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

A.Depending upon location:

1.Axial corneal degenerations
• Fatty degeneration
• Hyaline degeneration
• Amyloidosis
• Calcific degeneration (Band keratopathy)
• Salzmann’s modular degeneration
2.Peripheral 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)
B.Depending upon etiology:
1.Age related degenerations:
• Arcus senilis ,Vogt’s white limbal girdle,Hassall-Henle bodies,Moasaic degenerations
2.Pathological 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 women.and 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 e.g.after corneal perforation and in marked
corneal thinning.
4.Cosmetic -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:

1.ANTERIOR 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.
2.INTERCALARY 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.
3.CILIARY 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.
4.EQUITORIAL 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.
5.POSTERIOR 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 given.but 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 ~S.aureus
~Aspergillus
injuries, from affected orbital cellulitis, ~S.epidermidis
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:
I.Non infectious
Associated with: systemic diseases:
I.Chronic systemic
~Uveitis in sarcoidosis
bacterial infections:
~Behchet’s disease
~Tubecular
II.Arthritis:
~Leprotic
II.Spirochetal infections: ~Ankylosing spondylitis
~Syphilitic ~Reiter’s syndrome
III.Viral infections: ~Still’s disease
~HSV III.Lens-induced: I.Non-neoplastic
~Herpes Zoster ~Phacotoxic uveitis
II.Neoplastic
~Cytomegalo virus ~Phacoanaphylictic
IV.Parasitic: endophthamitis
~Toxoplasmosis IV.Traumatic uveitis
~Onchocercasis V.Idiopathic specific:
~Amoebiasis ~Fuch’s uveitis
V.Fungal
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.
iii.Choroidal 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

I.ASSOCIATED 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 s.lysozyme.
• 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).

II.ASSOCIATED 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.

III.LENS -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.

IV.TRAUMATIC 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.

V.IDIOPATHIC 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 acc.to 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: 1.endocrine disorders
2.biochemical 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 no.of 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

3.COMPLICATED 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

4.RADIATIONAL 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

1.control of diabetis mellitus
2.removal of cataractogenic drugs
3.removal of irradiation
4.adequate 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

A.Unifocal IOL :

➢ Most commonly used type

➢ Make patient emmetropic/hypermetropic/myopic

B.Multifocal IOL:

➢ Separate optics for near and distant vision

➢ Known as simultaneous vision lens
➢ 2 types-refractive and diffractive types
 ➢ Pseudoaccomadative lens

C.Accommodative 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