OPHTHALMOLOGY TICKETS

group 12

– Qs 1-5

1. Layers of the eyeball. Structure, functions.

The eye comprises of three layers namely; the outer fibrous layer, the middle
vascular/uveal layer and the inner nervous layer.

The outer layer is made up of the sclera and the cornea. The sclera is the outermost
transparent layer of the eye that maintains the shape of the eye as well as protects the
inner parts of the eye form harm by foreign particles and bacteria. By virtue of it being
transparent, it allows for the entry of light into the eye that ultimately allows sight. The
cornea has a curved structure that enables the focus of light waves.

The middle layer is also referred to as uvea or vascular tunic because it contains blood
vessels that transmit blood throughout the eye. This layer is made up of the choroid,
ciliary body and iris. The choroid has a brown pigment that facilitates the absorption of
light where as the ciliary body is responsible for controlling the shape of the lens. The iris
, which is the colored part of the eye, regulates the amount of light entering the eye by
increasing or decreasing depending on the light intensity.

The inner layer is also known as the retina or the sensory tunic. The purpose of this layer
is to receive the light from an object and convert it into electrical impulses that are then
transmitted via the optic nerve to the brain. It consists of photorecetors (rods and cons),
macula lutea, fovea centralis and optic disc.
(Also divided into 1. anterior segment which includes lens,iris,cornea and anterior and
posterior aqueous humour filled sacs. 2. Posterior segment which includes structures
posterior to lens – vitreous humour,retina,choroid and optic disc.)

2. Apparatus of eye movement. Functions and innervations.

The eyes are the visual organs of the human body, and move using a system of six
muscles. The retina, a specialised type of tissue containing photoreceptors, senses light.
These specialised cells convert light into electrochemical signals. These signals travel
along the optic nerve fibers to the brain, where they are interpreted as vision in the visual
cortex.

Six extraocular muscles facilitate eye movement. These muscles arise from the common
tendinous ring in the orbit, the eye cavity, and attach to the eyeball. The six muscles are
the lateral, medial, inferior and superior rectus muscles, and the inferior and superior
oblique muscles. The muscles, when contracting, cause movement of the eyeball, by
pulling the eyeball towards the muscle. For example, the lateral rectus is on the lateral
side of the eyeball. When it contracts, the eyeball moves so that the pupil looks outwards.
The medial rectus causes the eyeball to look inwards; the inferior rectus downwards and
the superior rectus upwards. The superior oblique muscle and inferior oblique muscle
attach at angles to the eyeball.
Eye movements are controlled by muscles innervated by cranial nerves III, IV and VI.
Oculomotor function can be divided into two categories: (1) extraocular muscle function
and (2) intrinsic ocular muscles (controlling the lens and pupil). The extraocular muscles
include: the medial, inferior, and superior recti, the inferior oblique, and levator palpebrae
muscles, all innervated by the oculomotor nerve (III); the superior oblique muscle,
innervated by the trochlear nerve (IV); and the lateral rectus muscle, innervated by the
abducens nerve (VI). The intrinsic eye muscles are innervated by the autonomic systems
and include the iris sphincter and the ciliary muscle (innervated by the parasympathetic
component of cranial nerve III), and the radial pupillodilator muscles (innervated by the
ascending cervical sympathetic system with its long course from spinal segments T1
through T3).

3. The fibrous coat of the eyeball. Function, structure and innervations.

The tough outermost layer of the eye is known as the fibrous layer and is composed of
two fused but physically quite different structures:
• Sclera – "white of the eye"
• Cornea – "window of the eye"
The sclera is opaque, and constitutes the posterior five-sixths of the eyeball; the cornea is
transparent, and forms the anterior sixth.

The sclera is rigid to give the eye its shape, and opaque to exclude light. The cornea is
transparent, smooth, and admits light into the eye. Also, the cornea has a curved surface
that refracts light to help the lens focus images on the retina. Limbus is the junction
between cornea and sclera where conjunctiva is attached firmly.

Sclera is richly supplied with nerves. The posterior ciliary nerves enters the sclera near
the optic nerve. The anterior part of sclera is mainly innervated by the two long posterior
ciliary nerves and posterior part receives nerve supply from numerous short posterior
ciliary nerves.

The cornea is one of the most sensitive tissues of the body, as it is densely innervated
with sensory nerve fibres via the ophthalmic division of the trigeminal nerve by way of
70–80 long ciliary nerves and short ciliary nerves.
The ciliary nerves run under the endothelium and exit the eye through holes in the sclera
apart from the optic nerve (which transmits only optic signals). The nerves enter the
cornea via three levels; scleral, episcleral and conjunctival.

4.The vascular layer of the eyeball. Structure, parts, function and blood supply.

The vascular coat (or uvea ) consists of the choroid, ciliary body and iris in continuation
structurally.
Choroid:
•sandwiched between the outer sclera and the inner retina.
•opaque and deeply pigmented with melanin to absorb excessive light, else internal
reflection would form multiple images on the retina.
•contains a blood vessels network to supply oxygen and food to other parts of the eye,
especially to the retina. It is less vascular where the retina is thin.

Ciliary body:
The ciliary body is made up of ciliary muscles and ciliary processes.
•Ciliary muscles are the thickenings around the edge of the choroid. The antagonistic
action of the circular and radial ciliary muscles is responsible for eye accommodation. It
holds the lens in place by suspensory ligaments calledZonular ligaments.
•Ciliary processes are short, black tissues arranged radially. They secrete aqueous
humour.

Iris:
•the opague ring of tissue visible through the cornea, in front of the lens
•made up of connective tissues and muscles with a circular opening, called the pupil.
•Similar to the ciliary body, the muscles are of two types ---- radial and circular. They
change the pupil size to control the amount of light entering the eye (i.e. pupillary
response). This can be compared to the diaphragm controlling the aperture size in a
camera.

The iris and ciliary body are supplied by the anterior ciliary arteries, the long posterior
ciliary arteries and anatosmotic connections from the anterior choroid . The anterior
ciliary arteries travel with the extraocular muscles and pierce the sclera near the limbus to
join the major arterial circle of the iris. The long posterior ciliary arteries (usually two)
pierce the sclera near the posterior pole, then travel anteriorly between the sclera and
choroid to also join the major arterial circle of the iris. The major arterial circle of the iris
gives off branches to the iris and ciliary body. Most of the venous drainage from the
anterior segment is directed posteriorly into the choroid and thence into the vortex veins.

5. Retina. Structure, blood supply and function.

The inner layer of the eye consists of the retina, the light detecting part of the eye. The
retina itself is comprised of two cellular layers:
• Neural layer – Consists of photoreceptors; the light detecting cells of the retina. It
is located posteriorly and laterally in the eye.
• Pigmented layer – Lies underneath the neural layer and is attached to the choroid
layer. It acts to support the neural layer, and continues around the whole inner surface of
the eye.

Anteriorly, the pigmented layer continues but the neural layer does not – this is part is
known as the non visual retina. Posteriorly and laterally, both layers of the retina are
present. This is the optic part of the retina.
The optic part of the retina can be viewed during ophthalmoscopy. The center of the
retina is marked by an area known as the macula. It is yellowish in colour, and highly
pigmented. The macula contains a depression called the fovea, which has a high
concentration of light detecting cells. It is the area responsible for high acuity vision. The
area that the optic nerve enters the retina is known as the optic disc – it contains no light
detecting cells.

The retina is supplied by the central retinal artery and the short posterior ciliary arteries.
The central retinal artery travels in or beside the optic nerve as it pierces the sclera then
branches to supply the layers of the inner retina (i.e., the layers closest to the vitreous
compartment). Retinal venules and veins coalesce into the central retinal vein, which
exits the eye with the optic nerve parallel and counter-current to the central retinal artery.
1. Optic nerve, visual pathway and visual centers.
2. The transparent structures of the eyeball – the cornea, the lens and the vitreous body.
Structure and function.
3. Innervations of the eye apparatus and the eyeball.
4. Blood supply of the eye.
5. The orbit. Structure.

optic nerve :
The optic nerve, also known as cranial nerve II, is a paired nerve that transmits visual
information from the retina to the brain. The optic nerve is derived from optic stalks
during the seventh week of development and is composed of retinal ganglion cell axons
and glial cells. In humans, the optic nerve extends from the optic disc to the optic chiasm
and continues as the optic tract to the lateral geniculate nucleus, pretectal nuclei, and
superior colliculus
The optic nerve is located in the back of the eye. It is also called the second cranial nerve
or cranial nerve II.
The job of the optic nerve is to transfer visual information from the retina to the vision
centers of the brain via electrical impulses.
The optic nerve is made of ganglionic cells or nerve cells.
It consists of over one million nerve fibers.
Our blind spot is caused by the absence of specialized photosensitive (light-sensitive)
cells, or photoreceptors, in the part of the retina where the optic nerve exits the eye.
Glaucoma is one of the most common illnesses affecting the optic nerve. Glaucoma is
caused by high intraocular pressure, or high pressure in the fluid that is inside the eye (
vitreous fluid).

Cornea
The cornea is the transparent part of the eye that covers the front portion of the eye.
It covers the pupil (the opening at the center of the eye), iris (the colored part of the eye),
and anterior chamber (the fluid-filled inside of the eye). The cornea's main function is to
refract, or bend, light. The cornea is responsible for focusing most of the light that enters
the eye.
The cornea is composed of proteins and cells. It does not contain blood vessels, unlike
most of the tissues in the human body.
Since there are no nutrient-supplying blood vessels in the cornea, tears and the aqueous
humor (a watery fluid) in the anterior chamber provide the cornea with nutrients.
The cornea is comprised of five layers: the epithelium, Bowman's layer, the stroma,
Descemet's membrane, and the endothelium.
The first layer, the epithelium, is a layer of cells covering the cornea. It absorbs nutrients
and oxygen from tears and conveys it to the rest of the cornea. It contains free nerve
endings. It also prevents foreign matter from entering the eye.
The cornea tends to repair itself quickly from minor abrasions. However, deeper
abrasions may cause scars to form on the cornea, which causes the cornea to lose its
transparency, leading to visual impairment. Infection,keratitis,keratoconus,pterygium,dry
eye are some of the dieseaes.

Lens
The lens is located in the eye. By changing its shape, the lens changes the focal distance
of the eye. In other words, it focuses the light rays that pass through it (and onto the
retina) in order to create clear images of objects that are positioned at various distances. It
also works together with the cornea to refract, or bend, light.
The lens is of ellipsoid, biconvex shape
The lens consists of the lens capsule, the lens epithelium, and the lens fibers.
The lens capsule is the smooth, transparent outermost layer of the lens, while the lens
fibers are long, thin, transparent cells that form the bulk of the lens. The lens epithelium
lies between these two and is responsible for the stable functioning of the lens. It also
creates lens fibers for the lifelong growth of the lens.
Common diseases of the lens include cataracts, which cause opacity, or cloudiness, in the
lens. Other common ailments are presbyopia, ectopia lentis, aphakia, and nuclear
sclerosis.

Vitreous humor
he vitreous humorcomprises a large portion of the eyeball. It is a clear gel-like substance
that occupies the space behind the lens and in front of the retina at the back of the eye.
Because the eye must process visual data, this liquid must be clear enough for light to
easily pass through it. Most of this humor consists of water, as well as a lower amount of
collagen, salt, and sugar.
This humor is a stagnant (immobile) fluid that is not served by any blood vessels and is
not actively regenerated or replenished. (This is in contrast to the aqueous humor, which
fills the anterior chamber in front of the lens.)
If a substance enters the vitreous humor, it will remain suspended in the gel until it can be
surgically removed. These substances, which can include blood or clumps of cells, are
collectively referred to as floaters.
If left alone, floaters can affect a person's field of vision. As people age, vitreous thins.
This can result in a condition called posterior vitreous detachment, where the vitreous
separates from the retina.
Posterior vitreous detachment occurs in most people by age 70. It can cause floaters but
generally resolves on its own over time.
Problems with the vitreous humor may ultimately lead to detachment of the retina from
the back wall of the eye, which may require surgery. Retinal detachment can result in
permanent loss of vision.
Innervtion of eye :
1 Motor
• 1.1 Sensory
• 1.2 Anatomical Course of the Nerves
• 1.3 CN III
• 1.4 CN V
• 1.5 CN VII
• 1.6 Sympathetic
• Muscles enable you to move your eyes. Ocular nerves allow you to interpret what
you see and blood vessels keep your eyes oxygenated. Six muscles, collectively called
the extraocular muscles, move the eyeball. A seventh muscle moves the eyelid and is also
found in the orbit.
• The muscles of the human eye
• The following muscles help your eyes move around.
• Levator palpebrae superioris: Originates on the sphenoid bone above the optic
canal. It inserts into the superior tarsis and skin of the eyelid. It’s innervated by the
oculomotor nerve and elevates the superior eyelid.
• Superior oblique: Originates on the sphenoid bone and inserts into the sclera deep
to the superior rectus muscle. It’s innervated by the trochlear nerve and abducts,
depresses, and medially rotates the eyeball.
• Inferior oblique: Originates on the anterior part of the orbital floor and inserts onto
the sclera deep to the lateral rectus muscle. It’s innervated by the oculomotor nerve and
abducts, elevates, and laterally rotates the eyeball.
• Superior rectus: Originates on the common tendinous ring and inserts into the
sclera behind the corneoscleral junction. It’s innervated by the oculomotor nerve, and it
elevates, adducts, and medially rotates the eyeball.
• Inferior rectus: Originates on the common tendinous ring and inserts into the
sclera behind the corneoscleral junction. It’s innervated by the oculomotor nerve and
depresses, adducts, and laterally rotates the eyeball.
• Medial rectus: Originates on the common tendinous ring and inserts into the sclera
behind the corneoscleral junction, this muscle is innervated by the oculomotor nerve and
adducts the eyeball.
• Lateral rectus: Originates on the common tendinous ring and inserts into the sclera
behind the corneoscleral junction. It’s innervated by the abducent nerve and abducts the
eyeball.

The nerves of the eye

The eyes are served by the following cranial nerves and their branches:
• Optic nerve (CN II): Sensory nerve that transmits impulses from the retina to the
brain
• Oculomotor nerve (CN III), trochlear nerve (CN IV), and abducent nerve (CN VI)
: Enter the orbital space through the superior orbital fissure to innervate the extraocular
muscles.
• Ophthalmic nerve (part of the trigeminal nerve, CN V): This nerve has three
branches:
• The lacrimal nerve runs to the lacrimal gland and gives off branches to the
conjunctiva and skin of the superior eyelid.
• The frontal nerve enters through the superior orbital fissure and provides sensory
innervation to the superior eyelid, scalp, and forehead.
• The nasociliary nerve is the sensory nerve to the eyeball. It also has branches that
serve the orbit and other parts of the face. One of its branches, the infratrochlear nerve,
supplies the eyelids, conjunctiva, and lacrimal sac.
• Ciliary ganglion: This group of postsynaptic parasympathetic nerve cell bodies is
associated with the oculomotor nerve and ophthalmic nerve (CN V1). Presynaptic
parasympathetic fibers from the oculomotor nerve synapse on the cell bodies of
postsynaptic parasympathetic neurons in the ciliary ganglion.
Short ciliary nerves emerge from the ciliary ganglion and enter the eye. The short ciliary
nerves contain postsynaptic parasympathetic fibers from the ciliary ganglion, afferent
fibers of the nasociliary nerve, and postsynaptic sympathetic fibers from the internal
carotid plexus. Postsynaptic parasympathetic fibers innervate the ciliary muscle and
sphincter pupillae muscle. Afferent fibers convey sensory impulses from the iris and
cornea. Postsynaptic sympathetic fibers innervate the dilator pupillae muscle.
The long ciliary nerves contain afferent and postsynaptic sympathetic fibers from the
nasociliary nerve. Long ciliary nerves bypass the ciliary ganglion and run to the iris,
cornea, and dilator pupillae muscle.

blood supply of eyeball:

lood flow to the orbit (and beyond) comes from branches of the internal carotid artery,
chiefly via the ophthalmic artery and its branches:
• Ophthalmic artery: Branches from the internal carotid artery and passes through
the optic canal into the orbital cavity
• Central artery of the retina: Runs from the ophthalmic artery to the eyeball
alongside the optic nerve; it branches at the optic disc and supplies the retina
• Supraorbital artery: Starts at the ophthalmic artery and exits the orbit at the
supraorbital notch to supply the forehead and scalp
• Supratrochlear artery: Runs from the ophthalmic artery to the forehead and scalp
• Lacrimal artery: Runs from the ophthalmic artery along the lateral rectus muscle
to supply the lacrimal gland, conjunctiva, and the eyelids
• Dorsal nasal artery: Branches from the ophthalmic artery and runs along the nose
to supply it with blood
• Short posterior ciliary arteries: Branch from the ophthalmic artery and pierce the
sclera at the edge of the optic nerve; they supply the choroid and the rods and cones of
the retina
• Long posterior ciliary arteries: Branch from the ophthalmic artery and pierce the
sclera to supply the ciliary body and iris
• Posterior ethmoidal artery: Leaves the ophthalmic artery to supply blood to
ethmoidal cells
• Anterior ethmoidal artery: Runs from the ophthalmic artery to supply ethmoidal
cells, frontal sinus, nasal cavity, and skin over the nose
• Anterior ciliary artery: Runs from the muscular branches of the ophthalmic artery
through the sclera near the rectus muscles and forms an arterial network in the iris and
ciliary body
• Infraorbital artery: Runs from the maxillary artery along the infraorbital groove
and out to the face
Blood is returned from the orbits via the superior and inferior ophthalmic veins, which
pass through the superior orbital fissure into the cavernous sinus. The central vein of the
retina may join an ophthalmic vein or enter the cavernous sinus directly. Vorticose veins
drain the vascular layer of the eyeball, and the scleral venous sinus encircles the anterior
chamber of the eyeball.

The orbit
The orbits (figs. 45-1 and 45-2) are two bony cavities occupied by the eyes and
associated muscles, nerves, blood vessels, fat, and much of the lacrimal apparatus. Each
 orbit is shaped like a pear or a four-sided pyramid, with its apex situated posteriorly and
its base anteriorly. The orbit is related (1) on its superior side to the anterior cranial fossa
and usually to the frontal sinus, (2) laterally to the temporal fossa in (anterior) and to the
middle cranial fossa (posterior), (3) on its inferior side to the maxillary sinus, and (4)
medially to the ethmoidal and the anterior extent of the sphenoidal sinuses.
he margin of the orbit, readily palpable, is formed by the frontal, zygomatic, and
maxillary bones (fig. 45-1A). It may be considered in four parts: superior, lateral, inferior
, and medial.
The superior margin, formed by the frontal bone, presents near its medial end either a
supraorbital notch or a supraorbital foramen, which transmits the nerve and vessels of the
same name.
The lateral margin is formed by the zygomatic process of the frontal bone and the frontal
process of the zygomatic bone.
The inferior margin is formed by the zygomatic and maxillary bones. The infraorbital
foramen, for the nerve and artery of the same name, is less than 1 cm inferior to the
inferior margin.
The medial margin, formed by the maxilla as well as by the lacrimal and frontal bones, is
expanded as the fossa for the lacrimal sac. The fossa passes inferiorly through the floor of
the orbit as the nasolacrimal canal, which transmits the nasolacrimal duct from the
lacrimal sac to the inferior meatus of the nose

Walls of the orbit.

he orbit possesses four walls (fig. 45-1A and C): a roof, lateral wall, floor, and medial
wall.
The roof (frontal and sphenoid bones) presents the fossa for the lacrimal gland
anterolaterally and the trochlear pit for the cartilaginous or bony pulley of the superior
oblique muscle anteromedially. The optic canal lies in the posterior part of the roof,
between the roots of the lesser wing of the sphenoid bone. It transmits the optic nerve and
ophthalmic artery from the middle cranial fossa.
The posterior aspect of the lateral wall (zygomatic and sphenoid bones) is demarcated by
the superior and inferior orbital fissures. The superior orbital fissure lies between the
greater and lesser wings of the sphenoid bone. It communicates with the middle cranial
fossa and transmits cranial nerves III, IV, and VI, the three branches of the ophthalmic
nerve, and the ophthalmic veins (fig. 45-5). The inferior orbital fissure communicates
with the infratemporal and pterygopalatine fossae and transmits the zygomatic nerve. The
lateral walls of the two orbits are set at approximately a right angle from one another,
whereas the medial walls are nearly parallel to each other (fig. 45-3).
The floor (maxilla, zygomatic, and palatine bones) presents the infraorbital groove and
canal for the nerve and artery of the same name. The inferior oblique muscle arises
anteromedially, immediately lateral to the nasolacrimal canal.
The medial wall (ethmoid, lacrimal, and frontal bones) is very thin. Its main component (
the orbital plate of the ethmoid) is papyraceous (paper-thin). At the junction of the medial
wall with the roof, the anterior and posterior ethmoidal foramina transmit the nerves and
arteries of the same name.
In summary, the orbit communicates with the middle cranial fossa (via the optic canal
and superior orbital fissure), the infratemporal and pterygopalatine fossae ( via the
inferior orbital fissure), the inferior meatus of the nose (via the nasolacrimal canal), the
nasal cavity (via the anterior ethmoidal foramen), and the face ( via supraorbital and
infraorbital foramina).
Question N-11
Fissures of the orbit, nerves and blood vessels.
Fissures:
1. Optic fissure
2. Superior orbital fissure
3. Inferior orbital fissure
4. Supraorbital foramen
5. Infraorbital foramen
6. Infraorbital groove

Nerves:
1. Lacrimal nerve
2. Frontal nerve
3. Trochlear nerve
4. Abducens nerve
5. Superior and inferior division of occulomotor nerve
6. Nasociliary nerve

Blood supplay:
1. Ophthalmic artery
2. Central artery of the retina
3. Ciliary artery
4. Lacrimal artery

12. Lacrimal organs and tracts.

The lacrimal tract is the physiological system containing the orbital structures for tear
production and drainage.[1]
It consists of:
• The lacrimal gland, which secretes the tears, and its excretory ducts, which
convey the fluid to the surface of the human eye;
• The lacrimal canaliculi, the lacrimal sac, and the nasolacrimal duct, by which the
fluid is conveyed into the cavity of the nose, emptying anterioinferiorly to the inferior
nasal conchae from the nasolacrimal duct;
• The innervation of the lacrimal apparatus involves both the a sympathetic supply
through the carotid plexus of nerves around the internal carotid artery, and
parasympathetically from the lacrimal nucleus of the facial nerve.

13. Intraocular muscles. Function and innervations.

1. superior rectus muscle- innervated by occulomotor nerve, function: look laterally and
upward
2. inferior rectus muscle- innervated by occulomotor nerve, function: look laterally and
downward
3. Lateral rectus muscle- innervated by abducens nerve , function: look laterally
4. medial rectus muscle- innervated by occulomotor nerve, function: look medially
5. superior oblique muscle- innervated by trochlear nerve, function: looks medially and
downward
6. Inferior oblique muscle- innervated by occulomotor nerve, function: look medially and
upward
7. levator palpebral superior- innervated by occulomotor nerve, function: retract and
elevate the eyelid

Question 14: Conjunctiva. Structure.

The conjunctiva lines the inside of the eyelids and covers the sclera (white part of the eye
). It is composed of non-keratinized,stratified columnar epithelium with goblet cells, and
also stratified columnar epithelium
Function:The conjunctiva helps lubricate the eye by producing mucus and tears, although
a smaller volume of tears than the lacrimal gland.[1]It also contributes to immune
surveillance and helps to prevent the entrance of microbes into the eye
The conjunctiva is a thin, semitransparent mucous membrane that covers the posterior
surface of the eyelids and is then reflected onto the eyeball, where it extends to the
limbus of the cornea. The conjunctiva takes its name from the fact that it conjoins the
eyelids with the eyeball. This junction is indirect, with the conjunctiva forming a fornix
on three sides of the globe and an extendible plica on the fourth side. Such an
arrangement allows the globe and the eyelids to move independently of each other. When
viewed by light microscopy, the conjunctiva is revealed as a nonkeratinizing squamous
epithelium containing mucin-secreting goblet cells. This epithelium overlies a loose
connective tissue, the substantia propria, which is highly vascularized, contains afferent,
sensory, and efferent (sympathetic and parasympathetic) innervation, and is well
endowed with lymphoid tissue. Not only does the conjunctiva function to enable
independent motion of the globe and eyelids, it also protects the cornea and hence the
interior of the eye from the external environment by secreting mucins, antibacterial
proteins, electrolytes, and water to form the inner mucous layer of the tear film and
perhaps a portion of the aqueous layer. Without these normal quantitative and qualitative
conjunctival secretions, a variety of mucous-deficiency diseases develop that in the worse
possible case lead to extensive damage to the cornea and a sight-threatening condition

15. Chambers of the eyeball. Iridocorneal angle.

The anterior chamber (AC) is the fluid-filled space inside the eye between the iris and the
cornea's innermost surface, theendothelium.[1] Aqueous humor is the fluid that fills the
anterior chamber. Hyphema and glaucoma are two main pathologies in this area. In
hyphema, blood fills the anterior chamber. In glaucoma, blockage of the canal of
Schlemm prevents the normal outflow of aqueous humor, resulting in accumulation of
fluid, increased intraocular pressure, and eventually blindness. The normal depth of
anterior chamber of eye is 3.5mm to 2.5mm; less than 2.5mm depth can be risk for angle
closure glaucoma.
• Pathology: Glaucoma
• Hyphema
• Hypopyon
• Intraocular pressure
• Ocular hypertension
The posterior chamber is a narrow space behind the peripheral part of the iris, and in
front of the suspensory ligament of the lensand the ciliary processes. The Posterior
Chamber consists of small space directly posterior to the iris but anterior to the lens. The
posterior chamber should not be confused with the vitreous chamber.
Iridocorneal angle: the acute angle between the iris and the cornea at the periphery of the
anterior chamber of the eye in this angle are occur the open/close angle glaucoma
 16. Anterior chamber. Drainage system of the eye, structure of the iridocorneal angle.

The anterior chamber angle and the trabecular meshwork are located where the cornea
meets the iris. The trabecular meshwork is important because it is the area where the
aqueous humor drains out of the eye. If the aqueous humor cannot properly drain out of
the eye, the pressure can build up inside the eye, causing opticnerve damage and
eventually vision loss, a condition known asglaucoma.

Drainage system: Anatomy:

The tear drain consists of two small openings called the puncta, one in your upper and the
other in your lower eyelid. Each of these openings lead into a small tube called a
canaliculus which, in turn, empties into the tear sac at the inside corner of your eye along
your nose. An opening into the lacrimal sac leads into a canal called the nasolacrimal
duct which passes through the bony structures surrounding your nose and empties tears
into your nasal cavity How
does the tear drain work?
The tears pass through the lacrimal drainage system by blinking and the principle of
capillary action. When blinking, your lids push tears evenly across your eyes to keep
your eyes moist and healthy. Blinking also pumps tears into the puncta and by capillary
action they are drawn into the lacrimal sac which travels through the tear duct and drains
into your nose. If the tear duct is blocked or the capillary action of the tears is not
working, your tears back up and spill over your eyelids as if you are crying. Tears
trapped in the tear sac also become stagnant and infected like a pond in the forest when
the water has sat there for a period of time.
Structure of iridocorneal angle: the acute angle between the iris and the cornea at the
periphery of the anterior chamber of the eye, it have shape of triangle and between them
are locate the trabecular mashwork from were the aqueous humor are going out.

17. The LENS:

• The lens is a transparent, biconvex, crystalline structure placed between iris and
the vitreous in a saucer shaped depression the patellar fossa.
• Its diameter is 9-10 mm and thickness varies with
• age.
• It has got two surfaces: the anterior surface is
• less convex than the posterior. These two surfaces meet at the equator.
• Its refractive index is 1.39 and total power is 20 D.
FUNCTION
Focusing mechanism and accomodation, part of optical system

STRUCTURE
1. Lens capsule. It is a thin, transparent, hyaline membrane surrounding the lens.
2. Anterior epithelium. It is a single layer of cuboidal cells which lies deep to the anterior
capsule. In the equatorial region these cells become columnar, are actively dividing and
elongating to form new lens fibres throughout the life.
3. Lens fibres. The epithelial cells elongate to form lens fibres.
i. Nucleus. It is the central part containing the oldest fibres.
Embryonic,Fetal,Infantile,Adult nucleus
ii.Cortex. It is the peripheral part which comprises the youngest lens fibres.
Suspensory ligaments of lens (Zonules of Zinn).Also called as ciliary zonules. These hold
the lens in position and enable the ciliary muscle to act on it.
18. The EYELIDS – structure, function, innervation and blood supply
FUNCTION
• protect the anterior surface of the globe from local injury.
• aid in regulation of light reaching the eye
• in tear film maintenance, by distributing the protective and optically important
tear film over the cornea during blinking;
• and in tear flow, by their pumping action on the conjunctival sac and lacrimal sac.
STRUCTURE
• the skin and subcutaneous tissue;
• the orbicularis oculi muscle
• the submuscular areolar tissue
• the fibrous layer, consisting of the tarsi and the orbital septum;
• the lid retractors of the upper and lower eyelids
• the retroseptal fat pads
• the conjunctiva.

INNERVATION
• Sensory innervation of the eyelids is subserved by terminal branches of the
ophthalmic and maxillary divisions of the trigeminal nerve (CN V).
• Opthalmic nerve divides into a larger supraorbital nerve and a smaller
supratrochlear nerve. Terminal branches of these nerves supply sensation to the upper
eyelid and forehead.
• Infratrochlear nerve, a terminal branch of the nasociliary nerve (CN V1), supplies
the skin and conjunctiva of the medial canthus, the most medial aspect of the eyelids, and
the nasolacrimal sac.
• The sensory supply of the remaining lower eyelid is provided by the infraorbital
nerve (CN V2) and the zygomaticofacial nerve (CN V2).
• The zygomaticofacial nerve supplies skin to the lateral lower eyelid, while the
palpebral branch of the infraorbital nerve supplies the central lower eyelid skin and
conjunctiva.
• Facial nerve-Orbicularis oculi
• The levator palpebra superioris is innervated by the superior branch of the
oculomotor nerve, entering the muscle from its inferior surface in its posterior third.
BLOOD SUPPLY
• The internal and external carotid arteries contribute to lid arterial supply.
• The internal carotid arterial supply is from the terminal branches of the
ophthalmic artery medially (giving supraorbital, supratrochlear, and dorsal nasal branches
) and the lacrimal artery laterally.
• The external carotid artery contributes via branches of the facial artery, the
superficial temporal artery, and the infraorbital artery.

19. VISUAL ACUITY-ITS EXAMINATION

Visual acuity or Central Vision, is the main function of the macula.
It is tested by Reading Snellen charts, distance of 5m or more, since this distance helps in
giving parallel rays.
VOD visual ocular Dextra VOS visual ocular sinistra.

Other tests which are based on the same principle

as Snellen’s test types are as follows:
(a) Simple picture chart: used for children
(b) Landolt’s C-chart: used for illiterate patients
(c) E-chart: used for illiterate patients

Near vision is tested by asking the patient to read the near vision chart, kept at a distance
of 35 cm in good illumination, with each eye separately.

If patient cant see from this distance, we try bringing him closer to the board, or use
fingers or hand motion and calculate power accordingly.
Also Light perception is checked, asking the patient about the direction of light on each
eye, procectio certa or incerta.

20. COLOUR VISION & ITS TESTING

• Normal color vision requires healthy function of the macula and optic nerve (
mainly cones are responsible).
• The most common abnormality is red-green “color blindness,”. Depressed color
vision may also be a sensitive indicator of certain kinds of acquired macular or optic
nerve disease.

• The most common testing technique utilizes a series of polychromatic plates, such
as those of Ishihara or Hardy-Rand-Rittler.
• The plates are made up of dots of the primary colors printed on a background
mosaic of similar dots in a confusing variety of secondary colors.
• The primary dots are arranged in simple patterns (numbers or
• geometric shapes) that cannot be recognized by patients with deficient color
perception.

21. PERIPHERAL VISION. Its outer aspects. Methods of examination. Pathology of

visual fields:
The visual field can be divided into central, and peripheral field :
• _ Central field includes an area from the fixation point to a circle 30° away. The
central zonecontains physiologic blind spot on the temporal side.
• _ Peripheral field of vision refers to the rest of thearea beyond 30° to outer extent
of the field of vision.

Perimetry.: Usually performed separately for each eye, it assesses the combined function
of the retina, the optic nerve,and the intracranial visual pathway.
• It is used clinically to detect or monitor field loss due to disease at any of these
locations. It is the procedure for estimating extent of the visual fields.
• It can be classified as below:
Kinetic perimetry.
In this the stimulus of known luminance is moved from periphery towards the centre to
establish isopters. Various methods of kinetic perimetry are: confrontation method,
Lister’s perimetery, tangent screen scotometry and Goldmann’s perimetry.

Static perimetry.
This involves presenting a stimulus at a predetermined position for a preset duration with
varying luminance. Various methods of static perimetry adopted are Goldmann perimetry
, Friedmann perimetry, automated perimetry.

Confrontation method:
The patient is seated facing the examiner at a distance of 1metre. While testing the left
eye, the patient covers his right eye and looks into the examiner’s right eye. The
examiner occludes his left eye and moves his hands in from the periphery keeping it
midway between the patient and himself.The patient and the examiner ought to see the
hand simultaneously, for the patient’s field to be considered normal. The hand is moved
similarly from above,below and from right and left.

Lister’s perimetry:
It has a metallic semicircular arc, graded in degrees, with a white dot for fixation in the
centre. The arc can be rotated in different meridians.The patient is seated facing the arc
with his chin firmly in the chin-rest. With one eye occluded, he
fixates the white dot in the centre. A test object (usually white and of size 3 to 5 mm) is
moved along the arc from extreme periphery towards the centre,and the point at which
the patient first sees the object is registered on a chart. The arc is moved through
30degrees each time and 12 such readings are taken. The details of the object regarding
its colour and size are noted.With the help of this perimeter extent of peripheral field is
charted.

22.BINOCULAR VISION & ITS EXAMINATION

• When a normal individual fixes his visual attention on an object of regard, the
image is formed on the fovea of both the eyes separately; but the individual perceives a
single image. This state is called binocular single vision.
• Binocular single vision is a conditioned reflex which is not present since birth but
is acquired during first 6 months and is completed during first few years.
Grades of binocular single vision
There are three grades of binocular single vision,which are best tested with the help of a
synoptophore.
Grade I — Simultaneous perception.
It is the power to see two dissimilar objects simultaneously. It is tested by projecting two
dissimilar objects (which can be joined or superimposed to form a complete picture) in
front of the two eyes. For example, when a picture of a bird is projected onto the right
eye and that of a cage onto the left eye, an individual with presence of simultaneous
perception will see the bird
in the cage .
Grade II—Fusion.
It consists of the power to superimpose two incomplete but similar images to form one
complete image.The ability of the subject to continue to see one
complete picture when his eyes are made to converge or diverge a few degrees, gives the
positive and negative fusion range, respectively.
Grade III— Stereopsis
. It consists of the ability to perceive the third dimension (depth perception). It can be
tested with stereopsis slides in synoptophore

Suppression Testing
The presence of suppression is readily demonstrated with the Worth four-dot test. Glasses
containing a red lens over one eye and a green lens over the other are worn by the patient.
A flashlight containing red, green, and white spots is viewed.The color spots are markers
for perception through each eye,and the white dot, potentially visible to each eye, can
indicate the presence of diplopia. The separation of the spots and the distance at which
the light is held determine the size of theretinal area tested. Foveal and peripheral areas
may be testedat distance and near, respectively.

Fusion Potential
 In individuals with a manifest deviation, the status of binocular fusion potential can be
determined by the red filter test. A red filter is placed over one eye. The patient is
directed to look at a distance or near fixation light target. A red light and a white light are
seen. Prisms are placed over one or both eyes in an attempt to bring the two images
together. If fusion potential exists, the two images come together and are seen as a single
pink light. If no fusion potential exists, the patient will continue to see one red and one
white light.

Ophth tickets 23-29

23. Accommodation. Its mechanism. Pathologic and physiologic alterations (spasm and palsy).

Accommodation is the process by which the vertebrate eye changes optical power to maintain

a clear image or focus on an object as its distance varies.

Accommodation acts like a reflex, but can also be controlled.

Occurs by optical power changing the form of the elastic lens using the ciliary body (in humans
up to 15 dioptres).
When humans accommodate to a near object, they also converge their eyes and, as a result,
constrict their pupils. However, the constriction of the pupils is not part of the process called
lens accommodation. The combination of these three movements (accommodation,
convergence and miosis) is under the control of the Edinger-Westphal nucleus and is referred to
as the near triad, or accommodation reflex.
-Accommodative spasm is a condition in which the ciliary muscle of the eye remains in a
constant state of contraction. Normal accommodation allows the eye to "accommodate" for near
-vision. However in a state of perpetual contraction, the ciliary muscle cannot relax when
viewing distant objects. This causes vision to blur when attempting to view objects from a
distance.
-Palsy is vice versa - paralysis of the ciliary muscles of the eye so as to prevent accommodation.

24. Age-related accommodation – correction (Presbyopia)

25. Refraction. Its clinical types.

Refraction is the phenomenon which makes image formation possible by the eye.

It includes 2 main types :
1. Emmetropia (optically normal eye) can be defined as a state of refraction, where in the
parallel rays of light coming from infinity are focused at the sensitive layer of retina with
the accommodation being at rest
2. Ametropia (a condition of refractive error), is defined as a state of refraction, when the
parallel rays of light coming from infinity (with accommodation at rest), are focused
either in front or behind the sensitive layer of retina, in one or both the meridians.
The ametropia includes myopia, hypermetropia and astigmatism.
26. Subjective and objective methods of examination of refraction.

27. Myopia. Its development, types, degrees and complications.

Myopia or short-sightedness is a type of refractive error in which optical power of the eye is too
high (usually due to an elongated globe) and parallel rays of light are brought to a focus in front
of the retina. It results from normal biological variation in the development of eye which may or
may not be genetically determined.

28. Hyperopia. Diagnostics, degrees and correction.

Far-sightedness - It is that dioptric condition of the eye in which with the
accommodation at rest the incident parallel rays of light come to a focus posterior
to the light sensitive layer of the retina.
29. Near point and far point of vision

30. Astigmatism - In an eye with astigmatism, light fails to come to a single focus on the
retina to produce clear vision. Instead, multiple focus points occur, either in front of the
retina or behind it
Types :
Myopic astigmatism - One or both principal meridians of the eye are nearsighted.
Hyperopic astigmatism - One or both principal meridians are farsighted.
Mixed astigmatism - One principle meridian is nearsighted, and the other is farsighted.

Astigmatism also is classified as regular or irregular

Regular astigmatism - the principal meridians are 90 degrees apart (perpendicular to each
other). Irregular astigmatism - the principal meridians are not perpendicular.

Astigmatism Correction Options

Usually can be corrected with eyeglasses, contact lenses or refractive surgery.

In addition to the spherical lens power used to correct nearsightedness or farsightedness,

astigmatism requires an additional "cylinder" lens power to correct the difference
between the powers of the two principal meridians of the eye.
So an eyeglasses prescription for the correction of myopic astigmatism, for example,
could look like this: -2.50 -1.00 x 90.

1) The first number (-2.50) is the sphere power (in diopters) for the correction of myopia
in the flatter (less nearsighted) principal meridian of the eye.
2) The second number (-1.00) is the cylinder power for the additional myopia correction
required for the more curved principal meridian. In this case, the total correction required
for this meridian is -3.50 D (-2.50 + -1.00 = -3.50 D).
3) The third number (90) is called the axis of astigmatism. This is the location (in degrees
) of the flatter principal meridian, on a 180-degree rotary scale where 90 degrees
designates the vertical meridian of the eye, and 180 degrees designates the horizontal
meridian.

31. Anisometropia The two eyes have unequal refractive power. One eye may be myopic
and the other hyperopic or one eye may be markedly stronger than the other.
Anisometropia is a serious concern in newborns and young children because it can lead
to amblyopia (impaired vision in one eye). With a major degree of anisometropia, the
brain cannot reconcile the difference in images coming from the two eyes. It develops a
preference for the image coming from one eye and suppresses the image from the other
eye and, in time, the brain loses the ability to "see" the image from the suppressed eye.

32. Diseases with red eye syndrome - common problem that can affect one or both eyes.
The redness associated with red eye comes from blood vessels on the surface of your eye
that are expanded (dilated) due to some form of irritation or infection.

Conjunctivitis (Pinkeye) is redness and swelling of the conjunctiva, the mucous

membrane that lines the eyelid and eye surface. The lining of the eye is usually clear. If
irritation or infection occurs, the lining becomes red and swollen
Most cases of pinkeye are caused by:
1) Infections caused by viruses or bacteria.
2) Dry eyes from lack of tears or exposure to wind and sun.
3) Chemicals, fumes, or smoke (chemical conjunctivitis)
4) Allergies.

Pterygium
Refers to a benign growth of the conjunctiva. Commonly grows from the nasal side of the
conjunctiva. It is usually present in the palpebral fissure. It is associated with and thought
to be caused by ultraviolet-light exposure, low humidity, and dust. The predominance of
pterygia on the nasal side is possibly a result of the sun's rays passing laterally through
the cornea, where it undergoes refraction and becomes focused on the limbic area.
Sunlight passes unobstructed from the lateral side of the eye, focusing on the medial
limbus after passing through the cornea. On the contralateral(medial) side, however, the
shadow of the nose medially reduces the intensity of sunlight focused on the
lateral/temporal limbus.

Subconjunctival Hemmorhage
Many tiny blood vessels are located in the conjunctiva and in the space between the
conjunctiva and the underlying sclera. In addition to covering the sclera, the conjunctiva
also lines the insides of your eyelids. It contains many tiny glands that secrete fluid to
protect and lubricate your eye.
One of of the small vessels can burst occasionally. Even a tiny amount of blood can
spread out a lot in the narrow space. As the conjunctiva only covers the cornea is
unaffected. Your cornea is responsible for your sight, so any bleeding under the
conjunctiva shouldn’t affect your vision.
~ Bleeding under the conjunctiva is not a dangerous condition. It doesn’t usually require
treatment, and it often goes away on its own within two weeks.

The dry eye syndrome

You need tears to moisten the eyes and to wash away particles that have gotten in.
A healthy tear film on the eye is necessary for good vision.
Dry eyes develop when the eye is unable to maintain a healthy coating of tears
Treatment
1) The first step in treatment is artificial tears. These come as preserved (screw cap bottle
) and unpreserved (twist open vial).
2) Start using the drops at least 2 to 4 times per day.
If your symptoms are not better after a couple of weeks of regular use:
* Fish oil 2 to 3 times per day
* Glasses, goggles or contact lenses that keep moisture in the eyes
* Medicines such as Restasis, topical corticosteroids, and oral tetracycline and
doxycycline
* Tiny plugs placed in the tear drainage ducts to help moisture stay on the surface of the
eye longer

Keratitis
Keratitis is an inflammation of the cornea. Keratitis is sometimes caused by an infection
involving bacteria, viruses, fungi or parasites. Noninfectious keratitis can be caused by a
minor injury, wearing your contact lenses too long
Treatment
Depends on the cause of the keratitis. Infectious keratitis can progress rapidly, and
generally requires urgent antibacterial, antifungal, or antiviral therapy to eliminate the
pathogen. Antibacterial solutions include levofloxacin, gatifloxacin, moxifloxacin,
ofloxacin.

In addition, contact lens wearers are typically advised to discontinue contact lens wear
and replace contaminated contact lenses and contact lens cases.
Acyclovir is the mainstay of treatment for HSV keratitis and steroids should be avoided
at all costs in this condition. Application of steroids to a dendritic ulcer caused by HSV
will result in rapid and significant worsening of the ulcer to form an 'amoeboid' or '
geographic' ulcer, so named because of the ulcer's map like shape

Diseases of the sclera

Episcleritis - Can be either Simple or Nodular
Common inflammatory condition seen in younger patients. The majority of etiologies
remain elusive. Associated generalized conditions include allergy, collagen-vascular
disease and infection, but these probably comprise less than thirty percent of cases. The
pathology of episcleritis demonstrates non-specific inflammatory cells with
lymphocytes. Most patients have an acute onset with redness, aching, and a sense of
warmth. Pain can be significant and usually is localized to the inflamed section of the eye
, either nasal or temporal.

Scleritis - More severe and chronic disease. Its onset can be quite rapid and startling,
leading to severe pain, loss of vision and even globe perforation. It is usually seen in the
older patient, over the age of forty. Early diagnosis and treatment are important to the
successful management of the disease. Unlike episcleritis, which usually does not affect
the underlying sclera, in scleritis, the episclera is always involved in the inflammatory
process. Thus the patient presents with a red eye that can rapidly progress to a more
fulminant course. Often, both eyes are involved. Almost half of the patients in our
practice with a diagnosis of scleritis had a underlying connective tissue disease. The most
common diagnosis is rheumatoid arthritis in the severe necrotizing form, which is less
often associated with diffuse anterior or nodular scleritis.
Ectasia - Occur when the sclera distorts outward. When uvea is involved it is referred to
as staphyloma. Staphylomas can occur in response to inflammation. The location of the
staphyloma predisposes it to pathologic risk. Anterior and intercalary staphylomas are
frequently associated with retinal detachment and glaucoma.

Acute Glaucoma Attack

Unlike Primary Open-Angle Glaucoma, where the IOP increases slowly, in acute angle-
closure, it increases suddenly. This sudden rise in pressure can occur within a matter of
hours and become very painful. If the pressure rises high enough, the pain may become
so intense that it can cause nausea and vomiting.
The eye becomes red, the cornea swells and clouds, and the patient may see haloes
around lights and experience blurred vision.
An acute attack is an emergency condition. If treatment is delayed, eyesight can be
permanently destroyed. Scarring of the trabecular meshwork may occur and result in
chronic glaucoma, which is much more difficult to control. Cataracts may also develop.
Damage to the optic nerve may occur quickly and cause permanently impaired vision.
An acute attack may be stopped with a combination of drops which constrict the pupil,
and drugs that help reduce the eye´s fluid production. As soon as the IOP has dropped to
a safe level, your ophthalmologist will perform a laser iridotomy. A laser iridotomy is an
outpatient procedure in which a laser beam is used to make a small opening in the iris

Acute Iridocyclitis
Acute Iridocyclitis are sub-types of a condition called uveitis.
Uveitis is a condition causing inflammation of the middle eye or uvea.
The uvea itself consists of three parts: Iris, Ciliary body, Choroid
Iridocyclitis is a type of anterior uveitis that involves the iris and ciliary body. It is a
leading cause of visual impairment in many people. Symptoms include pain and redness
in the eye, increased sensitivity to light, and blurry vision.
Types of iridocyclitis
Acute iridocyclitis: Sudden onset of inflammation of the iris and ciliary body. It may last
for less than 3 months with the usual duration around 6 weeks.
Chronic iridocyclitis: Persistent inflammation of the iris and ciliary body. The condition
lasts more than 3 months then recurs within 3 months of finishing treatment.
Recurrent iridocyclitis: Characterized by relapse and remission of the disease.
33. The eyelid margin diseases
Blepharitis
Eyelid margin disease is a common and persistent inflammation of the eyelids
Symptoms include: eye and eyelid irritation, itchiness redness and burning of the eye
Occurs in people who have a tendency toward oily skin, dandruff or dry eyes.
With blepharitis, both the upper and lower eyelids become coated with oily particles and
bacteria near the base of the eyelashes. It may cause irritation, itchiness, redness, and
stinging or burning of the eye.
What causes blepharitis?
Everyone has bacteria on the surface of their skin, but in some people, bacteria thrive in
the skin at the base of the eyelashes. Large amounts of bacteria around the eyelashes can
cause dandruff-like scales and particles to form along the lashes and eyelid margins.
Blepharitis also is associated with meibomianitis - a dysfunction and inflammation of the
nearby oil glands of the eyelids (called meibomian glands).
Treatment
Warm compresses, Eyelid scrubs, Antibiotic ointment

Hordeolum
 A hordeolum is a common disorder of the eyelid. It is an acute focal infection (usually
staphylococcal) involving either the glands of Zeis (external hordeola, or styes) or, less
frequently, the meibomian glands (internal hordeola)

Chalazion
A chalazion is a small bump that appears on your eyelid because of a blocked oil gland. It
can develop on the lower or upper eyelid, and it often disappears without treatment in
about one month. In rare cases, chalazia are caused by skin cancer.
A chalazion is similar to a stye, but is usually smaller and less painful.

Parasitic Blepharitis
high incidence of Blepharitis is caused by Demodex Parasite infestation. These little
mites are found at the roots of the eyelashes and can cause a whole spectrum of eye
conditions from slight irritation and dandruff-like material on the eyelashes, to more
serious scarring and eye inflammation , even turning in of the eyelashes which constantly
rub and irritate the eye.
There are 2 main species of this parasite - 1) Demodex folliculorum, tends to be clustered
to the root of the lashes, while 2) demodex brevis, tends to present individually in the oil
glands of the eyelid margin.
Demodex mites are present on most humans in small quantities, and on pets. People that
allow pets to sleep in their beds often acquire these bugs from them. They can also be
spread on towels and linens from person to person. As they are on a nocturnal cycle, they
will come out of the lash roots while you are sleeping to mate and reproduce on your skin
, then burrow into the hair follicles by morning.

34. Abscess, Phlegmona, Treatment

Phlegmona - Spreading diffuse inflammatory process with formation of
suppurative/purulent exudate or pus. This is the result of acute purulent inflammation
which may be related to bacterial infection.
Treatment: The main goal of treatment is to remove the cause of the phlegmonous
process in order to achieve effective treatment and prevention of recidives.
~ If the patient's condition is severe, however, immediate operation is usually necessary
with application of drainage system. All of these are done under general anaesthesia.
During operation, the cavity or place of phlegmonous process are washed with antiseptic,
antibiotic solutions and proteolyic ferments.
~ In post-operative period, patients are treated with intravenous antibiotics,
haemosorbtion, vitaminotherapy. Additionally, the use of i/v or i/m antistaphylococci γ-
globulin or anatoxin can be taken as immunotherapy.
During operation of phlegmon dissection at any location, it is important:
1) to avoid spreading of pus during operation;
2) to take into account the cosmetic value of the operating site, especially when treating
phlegmmonous process of the face; and
3) to avoid damaging nerves.

35 – conjunctivitis-

Conjunctivitis is an inflammation or infection of the conjunctiva, the thin transparent layer of tissue that
lines the inner surface of the eyelid and covers the white part of the eye. Conjunctivitis, often called “pink
eye,” is a common eye disease, especially in children. It may affect one or both eyes. Some forms of
conjunctivitis can be highly contagious and easily spread in schools and at home. While conjunctivitis is
usually a minor eye infection, sometimes it can develop into a more serious problem.
Conjunctivitis may be caused by a viral or bacterial infection. It can also occur due to an allergic reaction
to irritants in the air like pollen and smoke, chlorine in swimming pools, and ingredients in cosmetics or
other products that come in contact with the eyes. Sexually transmitted diseases like Chlamydia and
gonorrhea are less common causes of conjunctivitis.

People with conjunctivitis may experience the following symptoms:

 A gritty feeling in one or both eyes

 Itching or burning sensation in one or both eyes

 Excessive tearing

 Discharge coming from one or both eyes

 Swollen eyelids

 Pink discoloration to the whites of one or both eyes

 Increased sensitivity to light

What causes conjunctivitis?

The cause of conjunctivitis varies depending on the offending agent. There are three main categories of
conjunctivitis: allergic, infectious and chemical:

Allergic Conjunctivitis

 Allergic Conjunctivitis occurs more commonly among people who already have seasonal allergies
. At some point they come into contact with a substance that triggers an allergic reaction in their
eyes. 

 Giant Papillary Conjunctivitis is a type of allergic conjunctivitis caused by the chronic presence of
a foreign body in the eye. This condition occurs predominantly with people who wear hard or rigid 
contact lenses, wear soft contact lenses that are not replaced frequently, have an exposed suture
on the surface or the eye, or have a glass eye.

Infectious Conjunctivitis
  Bacterial Conjunctivitis is an infection most often caused by staphylococcal or streptococcal
bacteria from your own skin or respiratory system. Infection can also occur by transmittal from
insects, physical contact with other people, poor hygiene (touching the eye with unclean hands), or
by use of contaminated eye makeup and facial lotions. 

 Viral Conjunctivitis is most commonly caused by contagious viruses associated with the common
cold. The primary means of contracting this is through exposure to coughing or sneezing by persons
with upper respiratory tract infections. It can also occur as the virus spreads along the body’s own
mucous membranes connecting lungs, throat, nose, tear ducts, and conjunctiva.

 Ophthalmia Neonatorum is a severe form of bacterial conjunctivitis that occurs in newborn babies.
This is a serious condition that could lead to permanent eye damage unless it is treated immediately
. Ophthalmia neonatorum occurs when an infant is exposed to Chlamydia or gonorrhea while
passing through the birth canal.

Chemical Conjunctivitis

Chemical Conjunctivitis can be caused by irritants like air pollution, chlorine in swimming pools, and
exposure to noxious chemicals.

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How is conjunctivitis diagnosed?

Conjunctivitis can be diagnosed through a comprehensive eye examination. Testing, with special
emphasis on evaluation of the conjunctiva and surrounding tissues, may include:

 Patient history to determine the symptoms the patient is experiencing, when the symptoms began,
and the presence of any general  health or environmental conditions that may be contributing to the
problem.

 Visual acuity measurements to determine the extent to which vision may be affected.

 Evaluation of the conjunctiva and external eye tissue using bright light and magnification.

 Evaluation of the inner structures of the eye to ensure that no other tissues are affected by the
condition.

 Supplemental testing may include taking cultures or smears of conjunctival tissue, particularly in

cases of chronic conjunctivitis or when the condition is not responding to treatment.
Using the information obtained from these tests, your optometrist can determine if you have conjunctivitis
and advise you on treatment options.

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How is conjunctivitis treated?

Treatment of conjunctivitis is directed at three main goals:

1. To increase patient comfort.

2. To reduce or lessen the course of the infection or inflammation.

3. To prevent the spread of the infection in contagious forms of conjunctivitis.

The appropriate treatment for conjunctivitis depends on its cause:

 Allergic conjunctivitis—The first step should be to remove or avoid the irritant, if possible. Cool
compresses and artificial tears sometimes relieve discomfort in mild cases. In more severe cases,
non-steroidal anti-inflammatory medications and antihistamines may be prescribed. Cases of
persistent allergic conjunctivitis may also require topical steroid eye drops.

 Bacterial conjunctivitis—This type of conjunctivitis is usually treated with antibiotic eye drops or
ointments. Improvement can occur after three or four days of treatment, but the entire course of
antibiotics needs to be used to prevent recurrence.

 Viral Conjunctivitis—There are no available drops or ointments to eradicate the virus for this type
of conjunctivitis. Antibiotics will not cure a viral infection. Like a common cold, the virus just has to
run its course, which may take up to two or three weeks in some cases. The symptoms can often be
relieved with cool compresses and artificial tear solutions. For the worst cases, topical steroid drops
may be prescribed to reduce the discomfort from inflammation, but do not shorten the course of the
infection. Some doctors may perform an ophthalmic iodine eye wash in the office in hopes of
shortening the course of the infection. This newer treatment has not been well studied yet, therefore
no conclusive evidence of the success exists. 

ANSWER NO. 37 : Viral etiology conjunctivitis (herpes, adenoviral). Clinic, treatment and prevention.

Viral conjunctivitis, or pinkeye, is a common, self-limiting condition that is typically caused by adenovirus.
Other viruses that can be responsible for conjunctival infection include herpes simplex virus (HSV),
varicella-zoster virus (VZV), picornavirus (enterovirus 70, Coxsackie A24), poxvirus (molluscum
contagiosum, vaccinia), and human immunodeficiency virus (HIV).

Viral conjunctivitis is highly contagious, usually for 10-12 days from onset as long as the eyes are red.
Patients should avoid touching their eyes, shaking hands, and sharing towels, among other activities.
Transmission may occur through accidental inoculation of viral particles from the patient's hands or by
contact with infected upper respiratory droplets, fomites, or contaminated swimming pools. The infection
usually resolves spontaneously within 2-4 weeks.
Signs and symptoms

Signs and symptoms of viral conjunctivitis may include the following:

• Itchy eyes

• Tearing

• Redness

• Discharge

• Light sensitivity (with corneal involvement)

Diagnosis

Generally, a diagnosis of viral conjunctivitis is made on the clinical features alone. Lab tests are typically
not necessary, but they may be helpful in some cases. Specimens can be obtained by culture and smear
if inflammation is severe, in chronic or recurrent infections, with atypical conjunctival reactions, and in
patients who fail to respond to treatment. Giemsa staining of conjunctival scrapings may aid in
characterizing the inflammatory response.

Management

Treatment of adenoviral conjunctivitis is supportive. Patients should be instructed to use cold compresses
and lubricants, such as artificial tears, for comfort. Topical vasoconstrictors and antihistamines may be
used for severe itching but generally are not indicated. For patients who may be susceptible, a topical
astringent or antibiotic may be used to prevent bacterial superinfection.

Virus-specific treatments

Patients with conjunctivitis caused by HSV usually are treated with topical antiviral agents.

Treatment of VZV eye disease includes oral acyclovir to terminate viral replication.

For conjunctivitis associated with molluscum contagiosum, disease will persist until the skin lesion is
treated. Removal of the central core of the lesion or inducement of bleeding within the lesion usually is
enough to cure the infection.

Prevention

Preventing transmission of viral conjunctivitis is important. Both patient and provider should wash hands
thoroughly and often, keep hands away from the infected eye, and avoid sharing towels, linens, and
cosmetics. Infected patients should be advised to stay home from school and work. Those who wear
contact lenses should be instructed to discontinue lens wear until signs and symptoms have resolved.

ANSWER NO.38 Pterigium.

Pterygium (Surfer's Eye) most often refers to a benign growth of the conjunctiva. A pterygium commonly
grows from the nasal side of the conjunctiva. It is usually present in the palpebral fissure. It is associated
with and thought to be caused by ultraviolet-light exposure (e.g., sunlight), low humidity, and dust. The
predominance of pterygia on the nasal side is possibly a result of the sun's rays passing laterally through
the cornea, where it undergoes refraction and becomes focused on the limbic area.

Presentation:

Persistent redness from smoke, inflammation, foreign body sensation, tearing, dry and itchy eyes.

In advanced cases the pterygium can affect vision as it invades the cornea with the potential of obscuring
the optical center of the cornea and inducing astigmatism and corneal scarring.

Diagnosis is straightforward. Physical examination using a slit lamp. Additional tests might include:

• a visual acuity test, which involves reading letters on an eye chart

• corneal topography, which is used to measure curvature changes in your cornea

• photo documentation, which involves taking pictures to track the growth rate of the pterygium

Treatment:

A variety of options are available for the management of pterygium, from irradiation, to conjunctival auto-
grafting or amniotic membrane transplantation, along with glue and suture application. As it is a benign
growth, pterygium typically does not require surgery until it grows to such an extent that it causes visual
loss or presents with acute symptoms, or pulls on the cornea, distorting vision.

Prevention:

As it is associated with excessive sun or wind exposure, wearing protective sunglasses with side shields
and/or wide brimmed hats and using artificial tears throughout the day may help prevent their formation or
stop further growth. Surfers and other water-sport athletes should wear eye protection that blocks 100%
of the UV rays from the water, as is often used by snow-sport athletes.

39. Dry eye syndrome

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Tears are needed to lubricate the eyes and to wash away particles and foreign objects. A healthy tear film on the eye
is necessary for good vision.

Dry eyes develop when the eye is unable to maintain a healthy coating of tears
Causes

Dry eye usually occurs in people who are otherwise healthy. It becomes more common with age. This can occur due
to hormonal changes that make your eyes produce fewer tears.

Other common causes of dry eyes include:

 Dry environment or workplace (wind, air conditioning)

 Sun exposure

 Smoking or second-hand smoke exposure

 Cold or allergy medicines

Dry eye can also be caused by:

 Heat or chemical burns

 Previous eye surgery

 A rare autoimmune disorder in which the glands that produce tears are destroyed (Sjogren syndrome)

Symptoms

Symptoms may include:

 Blurred vision

 Burning, itching, or redness in the eye

 Gritty or scratchy feeling in the eye

 Sensitivity to light

Exams and Tests

Tests may include:

 Visual acuity measurement

 Slit lamp exam

 Diagnostic staining of the cornea and tear film

 Measurement of tear film break-up time (TBUT)

 Measurement of rate of tear production (Schirmer's test)

 Measurement of concentration of tears (osmolalilty)

Treatment

The first step in treatment is artificial tears. These come as preserved (screw cap bottle) and unpreserved (twist open
vial). Preserved tears are more bottle) convenient, but some people are sensitive to preservatives. There are many
brands available without a prescription.

Start using the drops at least 2-4 times per day. If your symptoms are not better after a couple of weeks of regular
use:

 Increase use (up to every 2 hours)

 Try a different brand

 Talk to your health care provider .

6. Classification of conjunctivitis. Exogenous infectious conjunctivitis (acute epidemical,
pneumococcus, gonorrhoeae, diphtheriae, alergic). Diagnosis, clinic, treatment and
prevention.
7. Classification of conjunctivitis, clinic and treatment.
8. Viral etiology conjunctivitis (herpes, adenoviral). Clinic, treatment and prevention.
9. Pterigium.
10. The dry eye syndrome, diagnostic, clinic and treatment.

40. Pathology of lacrimal pathway, diagnosis, clinic and treatment.

(sjogrens syndrome, watering eye, dry eye- look 39 question, darcocystitis- look 41
quesion)
SJOGREN’S SYNDROME
autoimmune chronic inflammatory disease with multi-system involvement. It typically
occurs in women between 40 and 50 years of age. Its main feature is an aqueous
deficiency dry eye — the keratoconjunctivitis sicca (KCS).
primary Sjogren’s syndrome- patients present with sicca complex– a combination of
KCS and xerostomia (dryness of mouth).
In secondary Sjogren’s syndrome dry eye and/or dry mouth are associated with an
autoimmune disease, commonly rheumatoid arthritis.
pathological features - focal accumulation and infiltration by lymphocytes and plasma
cells with destruction of lacrimal and salivary glandular tissue.

Watering eye
overflow of tears from the conjunctival sac due to excessive secretion of tears (
hyperlacrimation) or may result from obstruction to the outflow of normally secreted
tears (epiphora).

Causes of hyperlacrimation
1.Primary hyperlacrimation- direct stimulation of the lacrimal gland. It may occur in
early stages of lacrimal gland tumours and cysts and due to the effect of strong
parasympathomimetic drugs.
2. Reflex hyperlacrimation. It results from stimulation of sensory branches of fifth nerve
due to irritation of cornea or conjunctiva.
3. Central lacrimation - seen in emotional states, voluntary lacrimation and hysterical
lacrimation.

Causes of epiphora- Lacrimal pump failure, mechanival obstruction.

Clinical evaluation- Ocular examination, Regurgitation test, Fluorescein dye
disappearance test, Lacrimal syringing test, Jones dye tests, Dacryocystography.

41. Dacryocystitis (acute, chronic and infants) Phlegmona of the lacrimal sac
–diagnostic and treatment.
Inflammation of the lacrimal sac.
two forms: congenital and adult dacryocystitis.

CONGENITAL DACRYOCYSTITIS (dacryocystitis neonatorum)

inflammation of the lacrimal sac occurring in newborn infants
etiology- congenital blockage in the nasolacrimal duct by- membranous occlusion’ at its
lower end (mostly) , presence of epithelial debris, membranous occlusion at its upper end
near lacrimal sac, complete noncanalisation and rarely bony occlusion.
Common bacteria associated with congenital dacryocystitis are staphylococci,
pneumococci and streptococci.
Clinical picture-
1) Epiphora, develops after seven days of birth. followed by copious mucopurulent
discharge from the eyes.
2. Regurgitation test is usually positive, i.e., when pressure is applied over the lacrimal
sac area, purulent discharge regurgitates from the lower punctum.
3. Swelling on the sac area
Differential diagnosis- disease causes watering in childhood- ophthalmia neonatorum and
congenital glaucoma.
Complications - recurrent conjunctivitis, acute on chronic dacryocystitis, lacrimal abscess
and fistulae formation.
Treatment- 1. Massage over the lacrimal sac area and topical antibiotics
2. Lacrimal syringing (irrigation) with normal saline and antibiotic solution
3. Probing obstruction with Bowman’s probe
4. Intubations with silicone tube
5. Dacryocystorhinostomy (DCR) operations

ACUTE DACRYOCYSTITIS
Etiology- develops from neighbouring infected structures, Causative organisms -
Streptococcus haemolyticus, Pneumococcus and Staphylococcus
Clinical picture- 3 stages:
1. Stage of cellulitis- painful Swelling, epiphora , fever and malaise.
2. Stage of lacrimal abscess- pus forms
3. Stage of fistula formation- external fistula below the medial palpebral ligament . rarely,
the abscess
may open up into the nasal cavity forming an internal fistula.
Complications - Acute conjunctivitis, Corneal abraision which may be converted to
corneal ulceration, Lid abscess, Osteomyelitis of lacrimal bone, Orbital cellulitis, Facial
cellulitis and acute ethmoiditis.
Treatment- antibiotics, Dacryocystorhinostomy, Dacryocystectomy.

CHRONIC DACRYOCYSTITIS
More common than acute.
Etiology-
A. Predisposing factors- A. Predisposing factors
1. Age- between 40 and 60 years of age.
2. Sex- (80%) in females
3. Race - Negroes than in Whites
4. Heredity.
5.Poor personal hygiene
B. Factors responsible for stasis of tears in lacrimal sac- Anatomical factors, Foreign
bodies, Excessive lacrimation, inflammation.
C. Causative organisms. These include: staphylococci, pneumococci, streptococci and
Pseudomonas pyocyanea.
Clinical picture-four stages
1. Stage of chronic catarrhal dacryocystitis- inflammation, watering eye, mild redness in
the inner canthus.
2. Stage of lacrimal mucocoele- epiphora , swelling just below the inner canthus, Milky
or gelatinous mucoid fluid regurgitates from the lower punctum on pressing the swelling
3. Stage of chronic suppurative dacryocystitis- purulent discharge, epiphora, swelling at
the inner canthus with mild erythema of the overlying skin.
4. Stage of chronic fibrotic sac- fibrosis due to thickening of mucosa, epiphora and
discharge
Treatment- Conservative treatment by repeated lacrimal syringing,
Dacryocystorhinostomy, Dacryocystectomy, Conjunctivodacryocystorhinostomyif
canaliculi is blocked.
Phlegmon is a spreading diffuse inflammatory process with formation of
suppurative/purulent exudate or pus. This is the result of acute purulent inflammation
which may be related to bacterial infection, however the term 'phlegmon' mostly refers to
a walled-off inflammatory mass without bacterial infection, one that may be palpable on
physical examination.
An example would be phlegmon of diverticulitis. In this case a patient would present to
the emergency department with left lower-quadrant abdominal tenderness, and the
diagnosis of sigmoid diverticulitis would be high on the differential diagnosis, yet the
best test to confirm it would be CT scan

42. Keratitis. Classification of keratitis, symptoms, treatment and outcome.

Inflammation of cornea.
Etiology- exogenous- bacterial, viral, fungal, allergic.
Endogenous- autoimmune
Risk factors- contact lens, trauma, epithelial damage, systemic diseases.
Clinical- pain, watery eyes, decreased vision, photophobia, blepherospasm.
Bacterial is most common- staphylococcus- purulent discharge.
Viral : adenoviral – infectious, so hygiene should be maintained.
white spots occur, no steroids should be used.
Herpes- dendritic ulcer, vesicles.
Complication- ulcer which leads to severs infection
Diagnosis- slit lamb test, fluorescent dye test
Treatment- depends on symptoms.
Anti microbial, artificial tears, corneal transplant.

43. Diseases of the sclera (episcleritis, scleritis) clinic and treatment. Staphyloma of
the sclera.

Episcleritis- benign recurrent inflammation of the episclera

typically affects young adults, being twice as common in women than men.
Etiology
_ Exact etiology is not known.
_ It is found in association with gout, rosacea and psoriasis.
_ It has also been considered a hypersensitivity reaction to endogenous tubercular or
streptococcal toxins.

Two clinical types- diffuse episcleritis,- whole eye may be involved

nodular episcleritis, a pink or purple flat nodule form.
Symptoms- redness, mild ocular discomfort described as gritty, burning or foreign body
sensation.
Rarely, mild photophobia and lacrimation may occur.
Clinical course. Episcleritis runs a limited course of 10 days to 3 weeks and resolves
spontaneously
Treatment- Topical corticosteroid eyedrops, Cold compresses, Systemic non-steroidal
anti-inflammatory drugs.

SCLERITIS
chronic inflammation of the sclera
Etiology- Autoimmune collagen disorders, Metabolic disorders like gout and
thyrotoxicosis, infections.
Clinical features- moderate to severe pain , localised or diffuse redness, mild to severe
photophobia and lacrimation.
Types- anterior and posterior scleritis.
necrotizing and non necrotizing.
Treatment- NSAID’s, topical steroids.

Staphyloma
localised bulging of weak and thin outer layer of the eyeball (cornea or sclera).
Anatomical types :-
1. Anterior staphyloma.
2. Intercalary staphyloma- bulge in limbal area lined by root of iris
3. Ciliary staphyloma- bulge of weak sclera lined by ciliary body.
4. Equatorial staphyloma- bulge of sclera lined by the choroid in the equatorial region
5. Posterior staphyloma- bulge of weaksclera lined by the choroid behind the equator

44. Diseases of the uveal tracts, clinic, treatment and complications. Behchet disease’s
.

Uveitis- Inflammation of the uveal tract

0 iritis or anterior uveitis-- Inflammation of the iris
cyclitis or intermediate uveitis- inflammation of cilliary boby
posterior uveitis - Inflammation of the posterior segment .

etiology- infections, allergic, toxins, trauma, non infective systemic disease.

complains - ocular pain (less frequent with posterior uveitis or choroiditis), photophobia,
blurring of vision,redness of the eye
clinical
reduced visual acuity, eye will be inflamed in acute anterior disease, mostly around the
limbus (ciliary injection).
•00Inflammatory cells may be visible clumped together on the endothelium of the cornea
particularly inferiorly (keratitic precipitates or KPs).
•00Slit lamp examination will reveal aqueous cells and flare.
•00The vessels on the iris may be dilated.
•00The iris may adhere to the lens (posterior synechiae or PS).
•00The intraocular pressure may be elevated.
•00There may be cells in the vitreous.
•00There may be retinal or choroidal foci of inflammation.
•00Macular oedema may be present
Treatment- corticosteroids, Broad spectrum antibiotic drops, Non-steroidal anti-
inflammatory drugs, Immunosuppressive drugs.

BEHCET’S DISEASE
an idiopathic multisystem disease characterized by recurrent, non-granulomatous uveitis,
aphthous ulceration, genital ulcerations and erythema multiforme.
Etiology. It is still unknown; the basic lesion is an obliterative vasculitis probably caused
by circulating immune complexes. The disease typically affects the young men who are
positive for HLA-B51.
Clinical features. Uveitis seen in Behcet’s disease is typically bilateral, acute recurrent
iridocyclitis associated with hypopyon. It may also be associated with posterior uveitis,
vitritis, periphlebitis retinae and retinitis in the form of white necrotic infiltrates.
Treatment. No satisfactory treatment is available, so poor visual prognosis.
Corticosteroids may by helpful initially but ultimate response is poor. In some cases the
disease may be controlled by chlorambucil.

QUESTIONS 45-49

45. Gradual vision loss

A)KERATOCONUS
 Keratoconus (KC) is a progressive, noninflammatory, bilateral ectatic corneal
disease, characterized by paraxial stromal thinning and weakening that leads to corneal
surface distortion.
 Visual loss occurs primarily from irregular astigmatism and myopia, and
secondarily from corneal scarring.
 Corneal thickness changes from 600 microns to about 400 microns.
 More common among people from hot,humid places. Condition of younger
people-late teenage years to 40 years.Some association with dry eye syndrome.
 Stromal changes occur-collagen layer alignment changes from longitudinal to
wavy,making it weak because of which it is pushed forward by the normal IOP.
 Signs and symptoms:
• Distortions
• Glare/flare
• Monocular diplopia or ghost images
• Multiple unsatisfactory attempts to obtain optimum spectacle correction
• Itchy eye
 Signs according to stages:
1)Mild:
• Absent or minimal external and corneal signs
• Oblique astigmatism on refraction; moderate-to-high myopia
• Irregular astigmatic keratometry values
• Typical nipple pattern with the application of a diagnostic rigid contact lens
2)Moderate:
• Presence of one or more corneal signs of keratoconus (eg, enhanced appearance of
corneal nerves, Vogt striae, Fleischer ring, corneal scarring)
• Superficial corneal scarring (fibular, nebular, or nodular)
• Deep stromal scarring
• Scarring at the level of the Descemet membrane resembling posterior
polymorphous corneal dystrophy
• Paraxial stromal thinning as seen on corneal optical coherence tomography (OCT)
pachymetry with biomicroscope slit-lamp examination
• Keratometry values of 45-52 diopters (D)
• “Scissoring” or the oil drop sign
• Munson sign-bulging of lower eyelid upon downward gaze.
3)Advanced:
• Keratometry values greater than 52 D
• Enhancement of all corneal signs, symptoms, and visual loss/distortion
• Vogt striae; Fleischer ring and/or scarring
• Acute corneal hydrops
 Diagnostic procedures:
• Refraction
• Slit-lamp biomicroscopy
• Rigid gas-permeable (GP) contact lens application
• Keratometry
• Videokeratography
• OCT pachymetry
• Orbscan-reveals topography of cornea
 Treatment:
• Scleral lenses
• Collagen cross-linking by artificially aging the cornea using riboflavin and UV
radiation.
• Implantation of intrastromal corneal ring segments
• Corneal transplantation
• Keratoplasty

B)Cataract-see answer for Q.50

C)Primary Open-angle glaucoma
 Occurs when trabecular network is blocked by pigment deposits or debris.This
blocks outflow of aqueous humour from the eye.
 Such loss develops in the presence of open anterior chamber angles, characteristic
visual field abnormalities, and intraocular pressure that is too high for the continued
health of the eye. It manifests with optic disc cupping and optic neuropathy.
 It is asymptomatic for most of its course and only becomes apparent in later stages
when the patient begins to note deterioration in their peripheral vision.
 Diagnosis:
• Patient history is important- ocular history,family history
• Screening of population,especially those at risk is crucial- compare size of optic
disc excavation in both eyes by fundoscopy, check visual acuity, tonometry, gonioscopy,
slit lamp exam of AC.
• Lab tests: fluorescein angiography, ocular blood flow analysis using Doppler
flowmetry, colour vision measurements,etc.
 Treatment:
• Pharmacotherapy- beta blockers,diuretics,miotic agents.
• Surgery: shunt implants, Laser trabeculoplasty,trabeculectomy, deep sclerotomy
with/without collagen implant.

D)Age-related macular degeneration

 Mostly affects people older than 50 years. Condition which results in blurry or no
vision at the center of the visual field.
 No symptoms at first.on progression, patients find it difficult to recognize faces,
drive,read,etc.
 Occurs due to deposition of metabolites(drusen) in sub-retinal space. Incidence
increases with risk factors such as advanced age, positive family history,obesity,smoking,
hypertension,sedentary lifestyle,exposure to sunlight.
 Dry AMD- drusen accumulation
Wet AMD-neovasculature from choroid through Bruch’s membrane. These vessels are
fragile and vulnerable to rupture and leakage thus causing exudation and haemorrhage.
Worse prognosis.
 Signs and symptoms:
Metamorphopsia
Photostress
Blurred vision
Trouble telling colours apart
Loss in contrast sensitivity
 Diagnosis:
From symptoms
Perimetry
Amsler grid test-lines appear wavy instead of straight and some blank patches too
Fundus photography-dry AMD
Fluorescein angiography-wet AMD
 Treatment:
Dry AMD-no treatment,but must control it and not allow progression to wet type.
Vitamin supplements, stop smoking, improve diet,etc.
Wet AMD- anti-angiogenic(anti-VGEF) agents-Bevacizumab, thermal laser
photocoagulation,verteporfin therapy,photodynamic therapy.

46.KERATOCONUS-see Q.45 A
47.CATARACT
A)Congenital cataract:
 Opacification of the lens that is usually diagnosed at birth and can progress to
blindness if not treated promptly.
 Two types:
1) Unilateral-most cases are sporadic and arise due to intrauterine infection,
especially Rubella.Other causes may be pcular abnormalities or trauma.Surgery at 6
months-1year to prevent development of amblyopia.
2) Bilateral-most cases are inherited.Better prognosis than unilateral type and
syrgery can be done at 3 years.Mostly associated with hypoglycaemia, trisomies,
prematurity and TORCH infections
 Diagnosis:
Physical exam:
1)must include location,density,colour and shape of opacity.
2)Sciascopy-leukocoria (white reflex) is seen.
3)Slit lamp exam
4)Dilated pupil fundoscopy
 Treatment:
Surgery involves cataract extraction and phacoemulsification followed by implantation of
two lenses-+10D (temporary) and +20D (permanent). At 7 years, +10D lens is removed.
Main goal of treatment is to prevent amblyopia and strabismus.

B)Senile cataract
Senile cataract is an age-related, vision-impairing disease characterized by gradual
progressive thickening of the lens of the eye.
 Signs and symptoms
Decreased visual acuity
Glare
Myopic shift
Monocular diplopia
Clinical staging:
1)Hypermature cataract - Patient generally sees worse than count fingers (CF) or hand
motion (HM) owing to a dense white, deeply dark opaque brunescent, or Morgagnian
cataract
2)Mature cataract - Patient cannot read better than 20/200 on the visual acuity chart
3)Immature cataract - Patient can distinguish letters at lines better than 20/200
4)Incipient cataract or dysfunctional lens syndrome - Patient reports visual complaints
but can still read at 20/20 despite lens opacity confirmed via slit lamp examination
 Diagnosis:
1.Examination of adnexa and intraocular structures
2.swinging flashlight test
3.Slit lamp exam
4.Direct and indirect ophthalmoscopy
5.examination of nuclear size and brunescence (brown opacity)
 Treatment:
1.intracapsular cataract excision-not in use anymore
2.extracapsular cataract excision-removal of lens nucleus through an opening in the
anterior capsule but posterior capsule is left intact.
3.Phacoemulsification-a needle is ultrasonically guided through anterior capsule to
fragment and aspirate the lens nucleus.
All these are followed by intraocular lens implantation- a foldable lens is implanted using
a small 4mm incision in limbus.

48.Circulation of intraocular fluid,etc.

• Aqueous humour is produced continually by the ciliary body.
• Aqueous humor is secreted into the posterior chamber by the ciliary body,
specifically the non-pigmented epithelium of the ciliary body (pars plicata).
• It flows through the narrow cleft between the front of the lens and the back of the
iris, to escape through the pupil into the anterior chamber, and then to drain out of the eye
via the trabecular meshwork.
• From here, it drains into Schlemm's canal by one of two ways: directly, via
aqueous vein to the episcleral vein, or indirectly, through collector channels to the
episcleral vein by intrascleral plexus and eventually into the veins of the orbit.
• IOP = F / C + PV
Where F = aqueous fluid formation rate, C = outflow rate, PV = episcleral venous
pressure. Normal IOP=12-22 mmHg.
• The anterior chamber angle is the actual anatomical angle created by the root of
the iris and the peripheral corneal vault.
• The depth of the angle in a healthy eye is approximately 30°, with the superior
part usually less deep than the inferior half. However the depth is influenced by gender,
age and refractive error.
• Assesing AC angle:
1.Van Herick test-slit lamp used.
2.Smith method
3.Gonioscopy-gold standard.
Direct-using a contact lens and a binocular microscope or just penlight.
Indirect-relies on mirrors or prisms to reflect light from the angle to the viewer.More
preferable.
• Intraocular hypertension causes:
Excessive aqueous production-very rare cause
Inadequate aqueous drainage-as in glaucoma
Certain medications-asthma drugs
Ocular trauma
Anatomical variations of intraocular structures
• Causes of intraocular hypotension:
Chronic inflammation
Certain exercises

49)GLAUCOMA
 In infants,glaucoma can be primary-due to developmental abnormalities in the
eye’s aqueous outflow system or secondary to trauma,inflammation and tumors.
 Its manifestations may not be recognized until infancy or early childhood.It is
relatively rare but its impact on vision can be extreme.
 The classic triad of manifestations, any one of which should arouse suspicion of
glaucoma in an infant or young child, includes epiphora, photophobia, and
blepharospasm.
 Signs:
Corneal edema with Haab striae indicate globe distension.
Deep anterior chamber
On fundoscopy-fundus is pale and optic disc is irregular.
 Diagnosis:
Tonometry
Pachymetry
Gene analysis to detect mutations in CYP1B1 gene
 Treatment:
• Primary congenital glaucoma almost always is managed surgically. Medical
therapy is used only as a temporizing measure prior to surgery and to maximize pressure
control after surgery.
• Goniotomy
• Trabeculectomy
B)Primary glaucoma-see Q.45
C)secondary glaucoma(angle-closure type)
 Secondary glaucoma develops as part of another disease of the body- ocular or
systemic.
 Aqueous humour’s access to trabecular meshwork is blocked in one of three
ways:
• Pupillary block-iris is bowed forward by aqueous humour which is unable to get
through the pupil due to posterior synechiae between lens and iris.
• Obstruction of trabecular network directly as a reault of posterior pressure from
ciliary bod,lens or vitreous.
• Peripheral anterior synechiae between peripheral iris and angle structures.
 Causes:
• Inflammation-with uveitis and iridocyclitis
• Phacogenic glaucoma-eg.with cataract
• Due to intraocular haemorrhage-hyphema
• Traumatic
• Neovascular-diabetics
• Drug-induced
 Signs and symptoms:
Painful red eye-trigeminal pain
Decrease in visual acuity
Nausea and vomiting
Diaphoresis
Pupillary dilation
Corneal haze
 Diagnosis:
On palpation,eye is very rigid
Tonometry
Gonioscopy
Ophthalmoscopy with dilated pupils to inspect optic nerve damage
Pachymetry
Perimetry
Nerve fibre analysis
 Treatment:
Pharmacotherapy: beta-blockers, diuretics, sedatives.
Iridotomy-to relieve high IOP
Treat underlying condition

50. Acute closed-angle glaucoma attack, clinic, diagnosis and treatment.

 Intraocular pressure occurs due to blockage of the aqueous humour outflow by
closure of a narrower
angle of the anterior chamber.
Etiology:- Anatomical factors
i)Hypermetropic eyes with shallow anterior chamber.
ii) Eyes in which iris-lens diaphragm is placed anteriorly.
iii)Eyes with narrow angle of anterior chamber, which may be due to: small eyeball,
relatively large size of the lens and smaller diameter of the cornea or bigger size of the
ciliary body.
iv)Plateau iris configuration.
Pathogenesis:-
1.Effect of precipitating factors there occurs mid dilatation of the pupil which increases
the amount of apposition between iris and anteriorly placed lens with a considerable
pressure resulting in relative pupil block.(in other cases it depends on what is the etiology
)
2.The aqueous collects in the posterior chamber and pushes the peripheral flaccid iris
anteriorly , resulting in appositional angle closure due to iridocorneal contact .
3.Eventually there occurs rise in IOP which is transient to begin with. But slowly the
appositional angle closure is converted into synechial angle closure (due to formation of
peripheral anterior synechiae) and an attack of rise in IOP may last long.
4.Glaucomatous damage to the optic nerve also may occur due to the increased IOP,
either in a sudden attack or in intermittent episodes over a long period of time.

Clinical picture:-
1. ocular pain, nausea and vomiting, headache, and blurred vision is sudden.
2. Patients may complain of seeing haloes around lights. Haloes and blurry vision
are the result of corneal edema.

Diagnosis:-
• Gonioscopic visualization of an occluded anterior chamber angle.
• Tonometry demonstrates an elevated IOP, which may be as high as 40-80 mm Hg.
• Biomicroscopy may reveal a fixed or sluggish and middilated pupil, a shallow
anterior chamber, corneal epithelial edema and bullae, ciliary injection, and cells and
flare.
• Ophthalmoscopy may reveal a swollen optic disc in an acute attack

Treatment:-
Beta-blockers
Surgical iridectomy
51. Acute glaucoma attack, acute iridocyclitis. Differential diagnosis and treatment.
Acute glaucoma Iridocyclitis
Pain in trigeminal sites Pain only in the eyeball
Dilated pupil and no light reaction Irregular pupil(synchiasis)
Blurred and edematous cornea Clear cornea
Ciliary flush Ciliary flush( around the borders)
On palpation,stone like eyelids Painful on palpation
Treatment: beta-blockers
iridectomy Treatment: Mydriatic-cycloplegic drugs
Corticosteroids
Antibiotics

52. Ophthalmoplegia associated with common diseases. (Hypertension and diabetic

retinopathy). Clinic, stages, ophthalmoscopic picture, and new methods of treatment.
1. Hypertensive retinopathy
 Fundus changes occurring in patients suffering from systemic hypertension.
Pathogenesis:-
i)Vasoconstriction
ii)Arteriosclerotic changes
iii)Increased vascular permeability
Stages:-
Grade I :- mild generalized arteriolar attenuation, broadening of the arteriolar light reflex
and vein concealment.
Grade II:- narrowing and focal attenuation of arterioles associated with deflection of
veins at arteriovenous crossings (Salus’ sign).
Grade III:-copper-wiring of arterioles, banking of veins distal to arteriovenous crossings (
Bonnet sign), tapering of veins on either side of the crossings (Gunn sign) and right-angle
deflection of veins (Salu’s sign). Flame-shaped haemorrhages, cotton-wool spots and
hard exudates are also present.
Grade IV:- silver wiring of arteries and papilloedema

Keith Wagener Barker (KWB) Grades

Grade 1
Arteriolar constriction/attenuation/sclerosis -`silver wiring` and vascular tortuosities
Grade 2
As grade 1 + Irregularly located, tight constrictions - Known as `AV nicking` or `AV
nipping`
Grade 3
As grade 2 + Retinal edema, cotton wool spots and flame-hemorrhages
Grade 4
 As grade 3 + optic disc edema + macular star
Treatment :- Mangement of hypertension

2.Diabetic Retinopathy
Retinal changes seen in patients with diabetes mellitus

i)Non- Proliferative:-
 Microaneurysms and retinal hemorrhages
 Hard exudative
 Retinal edema
 Cotton wool spots
 Venous abnormalities

ii)Proliferative:- 25 years of onset of diabetes(juvenile onset diabetes)

 Neovascularistaion

iii)Diabetic maculopathy

 Increased permeability of the retinal capillaries.

 clinically significant macular edema and other changes.

iv)Advanced diabetic eye disease

It is marked by complications such as:
 Persistent vitreous haemorrhage,
 Tractional retinal detachment and
 Neovascular glaucoma.

Diagnosis:-
 Visual acuity test
 Opthalmoscopy
 Fundus florescein angiography
 Slit lamp biomicroscopy

Treatment:-
 Drugs : -Protein kinase C (PKC) inhbitors,
Vascular endothelial growth factors (VEGF) inhibitors,
Aldose reductase and ACE inhibitors, and
Antioxidants such as vitamin E
 Photocoagulation
 Surgery:-laser

53. Retinal degenerations - dystrophies, diagnostic and treatment.

 Retinitis pigmentosa
 This primary pigmentary retinal dystrophy is a hereditary disorder predominantly
affecting the rods more than the cones.
 Clinical picture:- Night blindness,Dark adaptation,Tubular vision
Retinal pigmental changes
Optic disc-pale and waxy

 Diagnosis:-Electroretinography
  Treatment:- There is no cure for retinitis pigmentosa; however, the efficacy and
safety of various prospective treatments are currently being evaluated. The efficiency
of various supplements, such as Vitamin A, DHA, and Lutein, in delaying disease
progression remains an unresolved, yet prospective treatment option.
54. Acute visual loss. Causes, clinic, diagnostic and treatment. Emergency care.
Prognosis.
Refer to the diseases : Diabetic Retinopathy(52)
Central retinal artery occlusion(55)
Central retinal venous occlusion(56)
Retinal detachment(58)
Acute angled glaucoma (50)

55) central retinal artery occlusion :

Occurs due to the obstruction at the level of lamina cribrosa .

Causes: atherosclerotic – related thrombosis (75% of CRAO).

Emboli from carotid artery (20% of CRAO).

Increased intraocular pressure.

Symptoms: sudden painless loss of vision.

Signs: direct papillary light reflex absent.

Opthalmoscopy, retinal arteries- narrowed, retinal veins- normal.

Retina appears opaque & cherry red spot in the central part.

Complication: neovascular glaucoma.

Treatment: immediate lowering of IOP. (by iv mannitol & ocular massage for 10-15 secs).
Vasodilators & inhalation of 5% co2 95% o2 (by asking patient to breathe in polythene bag).

Prognosis: Patients with visualized retinal artery emboli, whether or not obstruction is present,
have a 56% mortality rate over 9 years, compared to 27% for an age-matched population without retinal
artery emboli. • Life expectancy of patients with CRAO is 5.5 years compared to 15.4 years for an age-
matched population without CRAO

56) central retinal vein occlusion :

2nd common cause of blindness after diabetic retinopathy.

Causes: increased IOP, hyperviscosity of blood.

 Classification: i) ischaemic CRVO (hemorrhagic) ii) non ischaemic (venous stasis retinopathy).

Ischaemic CRVO:

Refers to acute complete occlusion of crv.

Fundus examination →massive engorgement, congestion & tortuosity of retinal veins are seen. Massive
retinal hemorrhage (splashed tomato appearance).

Macula → pigmentary changes & chronic cystoids edema.

Also neovascularisation → disc or periphery.

Complications: rubeosis iridis & nvg, vitreous hemorrhage & proliferative retinopathy in few cases.

Treatment : PRP ( panretinal photocoagulation) or cryoapplication.

Prognosis : The primary concern is vision loss; the prognosis of RVO depends on the location of the
occlusion and the degree of ischaemia.

83 57) Retinitis & central serous chorioretinitis :

Retinitis is a disease that threatens vision by damaging the retina (inflammation)

Types of Retinitis
Retinitis pigmentosa (RP). This is a group of genetic eye diseases you inherit from one or both
parents.

Some examples of RP and related diseases:

 Usher syndrome

 Leber's congenital amaurosis (LCA)

 Rod-cone disease

 Bardet-Biedl syndrome

CMV retinitis. This is a type of retinitis that develops from a viral infection of the retina.

CMV (cytomegalovirus) is a herpes virus. Most people have been exposed to the virus, but it
usually causes no harm. When a herpesvirus is reactivated in people with weaker immune
systems, it can cause retinitis.

Symptoms of CMV retinitis. In early stages, CMV retinitis causes no symptoms.

 You may develop symptoms, first in one eye, over a few days.

Symptoms may include:

 Floaters (specks or clouds in your field of vision)

 Blurred vision

 Loss of side vision

Treatment for CMV retinitis antiviral medication such as ganciclovir.

Chorioretinitis :

Chorioretinitis (CR) is an inflammatory process that involves the uveal tract of the eye.

Inflammation is usually caused by congenital viral, bacterial, or protozoal infections in neonates.

Diagnosis :

o Ophthalmologic examination can reveal exudative "cotton balls" (ie, focal atrophic and pigmented
scars of the retina). Vitreous inflammations can manifest as transient floating opacities. However,
these findings are common in all patients with chorioretinitis regardless of the etiology.

 Other abnormal physical findings should be documented; these include intrauterine growth
retardation, microcephaly, microphthalmia, cataract, uveitis, hearing defect, osteomyelitis,
hepatosplenomegaly, lymphadenopathy, dermal erythropoiesis, carditis, and congenital heart disease.

Treatment :

Based on etiology.

Eye symptoms can be treated as follows:

o Steroids may have a role in the acute management of many vasculitides, collagen vascular diseases, or
sarcoidosis; in some infectious processes (eg, MTB); or in some cases infections caused byToxoplasma
 species.

o Laser treatment of retinal lesions is used in certain conditions with good results.

85 58) Retinal detachment :

Retinal detachment refers to separation of the inner layers of the retina from the underlying retinal
pigment epithelium 

Signs and symptoms

Symptoms of retinal detachment may include the following:

 Photopsia (common initially)

 Visual field defect (developing over time; may help localize detachment)

 Floaters

The history should include inquiries into the following:

 History of trauma

 Previous ophthalmologic surgery

 Previous eye conditions (eg, uveitis and vitreous hemorrhage)

 Duration of visual symptoms and visual loss

Physical examination should include the following:

 Checking of visual acuity

 External examination for signs of trauma and checking of the visual field

 Assessment of pupil reaction

 Measurement of intraocular pressure in both eyes

 Slit-lamp biomicroscopy

 Examination of the vitreous for signs of pigment or tobacco dust

 Examination of the dilated fundus with ophthalmoscopy (preferably indirect)..

Diagnosis

Retinal detachment occurs by 3 basic mechanisms and thus is classified into the following 3 main types:

 Rhegmatogenous retinal detachment (the most common type) – This results when a hole, tear, or break in the
neuronal layer allows fluid from the vitreous to seep between and separate sensory and RPE layers

 Traction retinal detachment – This results from adhesions between the vitreous gel/fibrovascular proliferation
and the retina

 Exudative (serous) retinal detachment – This results from exudation of material into the subretinal space from
retinal vessels (as in hypertension, central retinal venous occlusion, vasculitis, or papilledema)

Treatment

 Scleral buckling

 Pars plana vitrectomy

 Pneumatic retinopexy.

86 59) Retinoblastoma :
Retinoblastoma is the most common intraocular tumor .
 Arises from a multipotential precursor cell (mutation in the long arm of chromosome 13 band 13q14)
that could develop into almost any type of inner or outer retinal cell.
2 causes: hereditary & non hereditary retinoblastoma.
3 stages:
Endophytic growth occurs when the tumor breaks through the internal limiting membrane and has an
ophthalmic appearance of a white-to-cream mass showing either no surface vessels or small irregular
tumor vessels. This growth pattern is typically associated with vitreous seeding,
Exophytic growth occurs in the subretinal space. This growth pattern is often associated with subretinal
fluid accumulation and retinal detachment. The tumor cells may infiltrate through the Bruch membrane
into the choroid and then invade either blood vessels or ciliary nerves or vessels.
Diffuse filtrating growth :
This is a rare subtype comprising 1.5% of all retinoblastomas. It is characterized by a relatively flat
infiltration of the retina by tumor cells but without a discrete tumor mass.

Retinoblastoma can cause secondary changes in the eye, including glaucoma, retinal detachment, and
inflammation secondary to tumor necrosis.
Differential Diagnoses
 Congenital Cataract

 Exudative Retinal Detachment

 Pediatric Tuberculosis

 Retinopathy of Prematurity

 Uveitis, Anterior, Childhood

 Vitreous Hemorrhage

Diagnosis :
Patients noted to have presenting signs of retinoblastoma should undergo prompt examination.
o Complete eye examination should be performed including an estimation of the patient's visual acuity for
both eyes.
 o A dilated fundus examination with indirect ophthalmoscopy should be completed since ancillary
diagnostic studies play only a secondary role when the fundus can be visualized clearly.

Treatment :
Chemotherapy
Radiation therapy
Surgical procedure :
Enucleation
o Enucleation is performed when there is no chance of preserving useful vision in an eye.

o Patients generally requiring enucleation are those who present with total retinal detachments and/or the
posterior segment is full of the tumor, in which case it is clear the patient cannot retain any form of
useful vision.

Cryotherapy (freezing)
Photocoagulation.

91 Strabismus: Misalignment of the visual axis of the tow eyes affecting

the ability to attain stereopsis.
Causes: Refractive errors
Orbital size discrepancy
Issues of extraocular muscles: Weakness, improper insertion and
abnormal tonic innervation.
Lesions on neurogenic, myogenic or at the level of neuromuscular
junction.
Causes can also be classified as Paretic and non-paretic.
Types: Pseudostabismus: the visual axes are in fact parallel, but the eyes
seem to have a squint
Latent squint (Heterophoria): persistent symptoms.
Manifest squint (Heterotropia): Symptoms appear when eye is
tired.
Directions: Horizontal: Eso-toward midline;more common in
young people.
Exo-away from midline; more common in elderly.
Vertical: Hypo-upward deviation.
 Hyper-downward deviation.
According to pattern
Concomitant : amount of deviation in the squinting eye remains
constant (unaltered) in all the directions of gaze.
Non Concomtant: the amount of deviation varies in different directions
of gaze.
Primary deviation: deviation of affected eye while doing the cover test.
Secondary deviation :deviation of normal eye while doing the cover test.
Primary and secondary deviation are equal in concomitant gaze.
Secondary.
Secondary deviation is more than primary deviation in case of paralytic
strabismus.

Symptoms: Diplopia, blurry vision, headache, poor depth of perception.

Diagnosis: Check cardinal eye movements.
Cover-uncover test: To reveal manifest deviation.
Cross-Cover test: To reveal latent deviation.
Prism and cover test: reveals amount of deviation.
Treatment: Spectacles with full correction of refractive.
Occlusion therapy: occlusion of normal eye.
Orthoptic exercises.
Surgery.

95Inflammatory diseases of Optic nerve.

Optic Neuritis(ON): Optic neuritis includes inflammatory and
demyelinating disorders of the optic nerve.
Causes: Idiopathic, Heriditary ON, Demyelinating disorders(
eg:Multiple Sclerosis), Viral infections, Toxic, acute ethmoiditis,
syphilis, cryptococcal meningitis in people with AIDS.
Anatomical types:
Papillitis. It refers to involvement of the optic disc in inflammatory and
demyelinating disorders.
This condition is usually unilateral but sometimes may be bilateral.
Neuroretinitis refers to combined involvement of optic disc and
surrounding retina in the macular area.
Retrobulbar neuritis is characterized by involvement of optic nerve
behind the eyeball.
Clinical features of acute retrobulbar neuritis are essentially similar to
that of acute papillitis except for funduschanges and ocular changes.
Symptoms: Eye pain, decreased VA, dyschromatopsia, Uhtoff’s
phenomenon(worsening of vision with increased temperature), Pulfrich
effect(difficulty in jugging movement).
Diagnosis:Full eye exam.
Marcus Gunn pupil indicates RAPD
Papillitis: hyperaemia of the disc and blurring of the margins, disc
edema,physiological cup is obliterated retinal veins are congested and
tortuous. Splinter haemorrhages and fine exudates may be seen on the
disc.
macular star formation is seen in neuroretinitis.
In retrobulbar neuritis fundus appears normal
Most common fielddefect in optic neuritis is a relative central or
centrocaecal scotoma
Visually evoked response (VER) shows reduced amplitude and delay in
the transmission time.
MRI of brain to check for white matter lesions.
Treatment: depends on underlying cause. Methylprednisolone for
patient with acute ON and with brain lesions supportive of multiple
sclerosis on MRI.

Retinitis pigmentosa.
Primary pigmentary retinal dystrophy is a hereditary disorder
predominantly affecting the rods more than the cones.
Most common mode of inheritance is autosomal recessive, followed by
autosomal dominant. X-linked recessive is the least common.
It appears in the childhood and progresses slowly, often resulting in
blindness in advanced middle age.Affects both eyes equally.
Visual symptoms:Night blindness, Dark adaptation, Tubular vision
occurs in advanced cases.
Fundus changes : Retinal pigmentary changes. These are typically
perivascular and resemble bone corpuscles in
shape.These changes are found in theequatorial region initially.
Retinal arterioles are narrowed
Optic disc becomes pale and waxy in later stages and ultimately optic
atrophy occurs
 Other associated changes which may be seen are colloid bodies,
choroidal sclerosis, cystoid macular
oedema, atrophic or cellophane maculopathy.
Visual field changes: Annular or ring-shaped scotoma progressing to
central vision only to blindness.
Ocular associations. These include myopia, primary open angle
glaucoma, microphthalmos, conical cornea
and posterior subcapsular cataract.
Diagnosis: Electroretinography.
Visual field and visual acuity tests.
Optical coherence Tomography.
Treatment: there is no effective treatment for the disease.
1. Measures to stop progression:: vasodilators, placental extracts,
transplantation of rectus muscles into
suprachoroidal space, light exclusion therapy, ultrasonic therapy and
acupuncture therapy.
Vitamin A and E have been recommended to check its progression.
2. Low vision aids (LVA) in the form of ‘magnifying glasses’ and ‘night
vision device’ may be of some help.
3. Rehabilitation.
4. Prophylaxis. Genetic counselling for consanguinous marriages may
help to reduce the incidence of disease. Further, affected individuals
should be advised not to produce children.

Optic Atrophy.
Degeneration of the optic nerve, which occurs as an end result of any
pathologic process that damages axons in the anterior visual system, i.e.
from retinal ganglion cells to the lateral geniculate body.
Types
Primary optic atrophy refers to the simple degeneration of the nerve
fibres without any complicating process within the eye e.g., syphilitic
optic atrophy of tabes dorsalis.
Secondary optic atrophy occurs following any pathologic process which
produces optic neuritis or papilloedema.
Ophthalmoscopic classification
1.Primary optic atrophy : Colour of the disc is chalky white or white
with bluish hue. Its edges (margins) are sharply outlined.
Slight recession of the entire optic disc occurs in total atrophy. Lamina
cribrosa is clearly seen at the bottom of the physiological cup. Major
retinal vessels and surrounding retina
are normal.
2. Consecutive optic atrophy Disc appears yellow waxy, edges are not so
sharply defined as in primary optic atrophy,Retinal vessels are
attenuated.
3. Post-neuritic optic atrophy Optic disc looks dirty white in colour.
Due to gliosis
its edges are blurred, physiological cup is obliterated and lamina
cribrosa is not visible.
Retinal vessels are attenuated and perivascular sheathing is often present
.
4. Glaucomatous optic atrophy. It is characterised by deep and wide
cupping of the optic disc and nasal shift of the blood vessels
5.Ischaemic optic atrophy. Ophthalmoscopic features are pallor of the
optic disc associated
with marked attenuation of the vessels.
Ascending versus descending optic atrophy.
Ascending optic atrophy: In it the nerve fibre degeneration progresses (
ascends) from the
eyeball towards the geniculate body.
Descending or retrograde optic atrophy proceeds from the region of the
optic tract, chiasma or posterior portion of the optic nerve towards the
optic disc.

Pathological features:
The ophthalmoscopic appearance of the atrophic optic disc depends
upon the balance
between loss of nerve tissue and gliosis. Following three situations may
occur:
1. Degeneration of the nerve fibres may be associated with excessive
gliosis.
2. Degeneration and gliosis may be orderly and the proliferating
astrocytes arrange themselves in
longitudinal columns replacing the nerve fibres (columnar gliosis). Such
pathological features are seen in primary optic atrophy.
3. Degenration of the nerve fibres may be associated with negligible
gliosis. It occurs due to progressive decrease in blood supply. Such
pathological changes are labelled as cavernous optic atrophy and are
features of glaucomatous
and ischaemic (vascular) optic atrophy.
Causes: Primary: lesions proximal to the optic disc without
papilloedema; multiple sclerosis, retrobulbar neuritis (idiopathic),
Leber’s and other hereditary optic atrophies, intracranial tumours
pressing directly on the anterior visual pathway traumatic severance or
avulsion of the optic nerve,toxic amblyopias and tabes dorsalis.
Degenerative or inflammatory lesions of thechoroid and/or retina.
Postneuritic optic atrophy. It develops as asequelae to long-standing
papilloedema or papillitis.
Glaucoma.
Vascular conditions causing disc ischemia.
Clinical features: Loss of vision severity and onset depends on
underlyng cause.
RAPD
Visual field loss: central-in focal ON; peripheral-in systemic infections;
eccentric-nerve or tract compression.
General opthalmoscopic findings are pallor of the disc and decrease in
the number of small blood vessels
Treatment depends on underlying cause. Vision cannot be recovered
once complete atrophy has set in.

Papilloedema
The passive disc swelling associated with increased intracranial pressure
which is almost always bilateral although it may be asymmetrical.
Causes:
Congenital anomalous elevation (Pseudopapilloedema)
2. Inflammations: Papillitis, Neuroretinitis
3. Ocular diseases: Uveitis, Hypotony,Vein occlusion
4. Orbital causes :Tumours ,Graves’orbitopathy,Orbital cellulitis
5. Vascular causes: Anaemia, Uremia, Anterior ischaemic optic
neuropathy
6. Increased intracranial pressure

Clinical features:
General features: headache, nausea, projectile vomiting and diplopia.
Focal neurological deficit may be associated.
Ocular features:history of
recurrent attacks of transient blackout of vision
 (amaurosis fugax). Visual acuity and papillary reactions usually remains
normal until the late stages of diseases when optic atrophy sets in.
Diagnosis:  ophthalmoscopy or fundus photography and possibly slit
lamp examination.
Clinical features can be described in four stages: Early: Obscuration of
the disc margins
Fully developed: optic disc oedema and its forward elevation above the
plane of retina; usually up to
1-2 mm; Physiological cup of the optic disc is obliterated; Disc becomes
markedly hyperaemic and blurring of the margin is present all-around. (
iv) Multiple soft exudates and superficial haemorrhages may be seen
near the
Chronic: acute haemorrhages and exudates resolve,and peripapillary
oedema is resorbed; optic disc has champagne cork appearance.
Atrophic: appears after 6-9 months and is characterized by severely
impaired visual acuity; greyish white discoloration and pallor of the disc
due to atrophy of the neurons and associated gliosis.
Pupillary light reactions are usually normal in all four stages.
Treatment: Depends on underlying cause.
92 1) PARALYTIC STRABISMUS
It refers to ocular deviation resulting from complete
or incomplete paralysis of one or more extraocular
muscles.
Etiology
The lesions may be neurogenic, myogenic or at the
level of neuromuscular junction.
I. Neurogenic lesions
1. Congenital. Hypoplasia or absence of nucleus is
a known cause of third and sixth cranial nerve
palsies. Birth injuries may mimic congenital
lesions.
2. Inflammatory lesions. These may be in the form
of encephalitis, meningitis, neurosyphilis or
peripheral neuritis (commonly viral). Nerve trunks
may also be involved in the infectious lesions of
cavernous sinus and orbit.
3. Neoplastic lesions. These include brain tumours
involving nuclei, nerve roots or intracranial part
of the nerves; and intraorbital tumours involving
peripheral parts of the nerves.

4. Vascular lesions. These are known in patients

with hypertension, diabetes mellitus and
atherosclerosis. These may be in the form of
haemorrhage, thrombosis, embolism, aneurysms
or vascular occlusions. Cerebrovascular accidents
are more common in elderly people.
5. Traumatic lesions. These include head injury
and direct or indirect trauma to the nerve trunks.
6. Toxic lesions. These include carbon monoxide
poisoning, effects of diphtheria toxins (rarely),
alcoholic and lead neuropathy.
7. Demyelinating lesions. Ocular palsy may occur
in multiple sclerosis and diffuse sclerosis.
II. Myogenic lesions
1. Congenital lesions. These include absence,
hypoplasia, malinsertion, weakness and musculofacial
anomalies.
2. Traumatic lesions. These may be in the form of
laceration, disinsertion, haemorrhage into the
muscle substance or sheath and incarceration of
muscles in fractures of the orbital walls.
3. Inflammatory lesions. Myositis is usually viral in
origin and may occur in influenza, measles and
other viral fevers.
4. Myopathies. These include thyroid myopathy,
carcinomatous myopathy and that associated with
certain drugs. Progressive external ophthalmoplegia
is a bilateral myopathy of extraocular
muscles; which may be sporadic or inherited as
an autosomal dominant disorder.

Investigations of a case of paralytic squint

A. Evaluation for squint
Every case of squint should be evaluated utilising
the tests described on page 327-329. Additional tests
Fig. 13.26. Diplopia chart of a patient with
right lateral rectus palsy. Fig. 13.27. Hees screen.
required for a case of paralytic squint are :
1. Diplopia charting. It is indicated in patients
complaining of confusion or double vision. In it
patient is asked to wear red and green diplopia
charting glasses. Red glass being in front of the
right eye and green in front of the left. Then in
a semi-dark room, he is shown a fine linear light
from a distance of 4 ft. and asked to comment on
the images in primary position and in other
positions of gaze. Patient tells about the position
and the separation of the two images in different
fields. Fig. 13.26 shows diplopia charting in a
patient with right lateral rectus palsy.
2. Hess screen test. Hess screen/Lees screen (Fig.
13.27) test tells about the paralysed muscles and
the pathological sequelae of the paralysis, viz.,
 overaction, contracture and secondary inhibitional
palsy.
The two charts are compared. The smaller chart
belongs to the eye with paretic muscle and the
larger to the eye with overacting muscle (Fig.
13.28).
3. Field of binocular fixation. It should be tested
in patients with paralytic squint where applicable,
i.e., if patient has some field of single vision. This
test is performed on the perimeter using a central
chin rest.

Management
1. Treatment of the cause. An exhaustive
investigative work-up should be done to find out
the cause and, if possible, treat it.
2. Conservative measures. These include: wait and
watch for self-improvement to occur for a period
of 6 months, vitamin B-complex as neurotonic;
and systemic steroids for non-specific
inflammations.
3. Treatment of annoying diplopia. It includes use
of occluder on the affected eye, with intermittent
use of both eyes with changed headposture to
avoid suppression amblyopia.
4. Surgical treatment. It should be carried out in
case the recovery does not occur in 6 months.
Aim of treatment is to provide a comfortable field
of binocular fixation, i.e., in central field and lower
quadrants. The principles of surgical treatment
involve strengthening of the paralysed muscle
by resection; and weakening of the overacting
muscle by recession.

93 2) Amblyopia

, also called lazy eye, is a disorder of sight.[1] It results in decreased vision in an eye that
otherwise appears normal, or out of proportion to associated structural problems of the eye.
Whenever the brain does not receive visual signals from an eye for a long period of time, there is
a risk of amblyopia. It also can occur when the brain "turns off" the visual processing of one eye
to prevent double-vision, for example in strabismus (crossed eyes). The cause of amblyopia is
within the brain.[2]
Detecting the condition in early childhood increases the chance of successful treatment,
especially if detected before the age of five. The earlier it is detected, and the underlying cause
corrected with glasses or surgery, the better the long term outcomes.[3]
This disorder has been estimated to affect 1–5% of the population.[4] It often occurs during early
childhood.
Amblyopia
Definition. Amblyopia, by definition, refers to a partial
loss of vision in one or both eyes, in the absence of
any organic disease of ocular media, retina and visual
pathway.
Pathogenesis. Amblyopia is produced by certain
amblyogeneic factors operating during the critical
period of visual development (birth to 6 years of age).
The most sensitive period for development of
amblyopia is first six months of life and it usually
does not develop after the age of 6 years.
Amblyogenic factors include :
Visual (form sense) deprivation as occurs in
anisometropia,
Light deprivation e.g., due to congenital cataract,
and
Abnormal binocular interaction e.g., in strabismus.
Types. Depending upon the cause, amblyopia is of
following types:
1. Strabismic amblyopia results from prolonged
uniocular suppression in children with unilateral
constant squint who fixate with normal eye.
2. Stimulus deprivation amblyopia (old term:
amblyopia ex anopsia) develops when one eye is
totally excluded from seeing early in life as, in
congenital or traumatic cataract, complete ptosis
and dense central corneal opacity.
3. Anisometropic amblyopia occurs in an eye
having higher degree of refractive error than the
fellow eye. It is more common in anisohypermetropic
than the anisomyopic children.
Even 1-2D hypermetropic anisometropia may
cause amblyopia while upto 3D myopic
anisometropia usually does not cause amblyopia.
4. Isoametropic amblyopia is bilateral amblyopia
occurring in children with bilateral uncorrected
high refractive error.
5. Meridional amblyopia occurs in children with
uncorrected astigmatic refractive error. It is a
selective amblyopia for a specific visual meridian.
Clinical characteristics of an amblyopic eye are:
1. Visual acuity is reduced. Recognition acuity is
more affected than resolution acuity.
2. Effect of neutral density filter. Visual acuity when
tested through neutral density filter improves by
one or two lines in amblyopia and decreases in
patients with organic lesions.
3. Crowding phenomenon is present in amblyopics
i.e., visual acuity is less when tested with multiple
letter charts (e.g., Snellen’s chart) than when
tested with single charts (optotype).
4. Fixation pattern may be central or eccentric.
Degree of amblyopia in eccentric fixation is
proportionate to the distance of the eccentric
point from the fovea.
5. Colour vision is usually normal, may be affected
in deep amblyopia with vision below 6/36.
Treatment of amblyopia should be started as early
as possible (younger the child, better the prognosis).
Occlusion therapy i.e., occlusion of the sound eye,
to force use of amblyopic eye is the main stay in the
treatment of amblyopia. However, before the

3) RETINOPATHY OF PREMATURITY
Retinopathy of prematurity (ROP) is a bilateral
proliferative retinopathy, occurring in premature
infants with low birth weight who often have been
exposed to high concentration of oxygen. Earlier this
disease was known as retrolental fibroplasia.
Etiopathogenesis
Low birth weight and decreased gestational age are
now considered the primary causative factors.
Supplemental oxygen administration which was for a
long time considered as the important causative factor
is now considered only a risk factor. Based on the
above facts, two important hypothesis are postulated
to describe pathogenesis of disease:
1. Classical theory postulates that owing to
exposure to high concentration of oxygen, there
occurs obliteration of premature retinal vessels.
This is followed by neovascularisation and fibrous
tissue proliferatiion which ultimately forms a
retrolental mass.
2. Spindle cell theory proposed recently postulates
the induction of retinal and vitreal
neovascularization by spindle cell insult in a
premature retina.

Differential diagnosis
Advanced retrolental fibroplasia needs to be
differentiated from other causes of leukocoria (see
page 282).
Screening and management
Treatment of well-established disease is
unsatisfactory. Prophylaxis is thus very important.
To prevent ROP, the premature newborns should not
be placed in incubator with an O2 concentration of
more than 30 percent and efforts should be made to
avoid infection and attacks of apnoea. Further, a
regular screening is very important.
 Treatment

Photocoagulation or cryotherapy may check

progression of the disease if applied in the early stage.
However, once the retina is detached the treatment
becomes increasingly difficult and success rate
declines to 33 percent.

984) Superior orbital fissure syndrome[edit]

Superior orbital fissure syndrome, also known as Rochon-Duvigneaud's syndrome,[3][4] is a
neurological disorder that results if the superior orbital fissure is fractured. Involvement of the
cranial nerves that pass through the superior orbital fissure may lead to diplopia, paralysis of
extraocular muscles, exophthalmos, and ptosis. Blindness or loss of vision indicates involvement
of the orbital apex, which is more serious, requiring urgent surgical intervention. Typically, if
blindness is present with superior orbital syndrome, it is called orbital apex syndrome.
Superior orbital fissure syndrome: A neurological condition that can result from a fracture of the
orbital fissure which is a cleft that lies behind the nose. The disorder that can also result from
facial fractures, cavernous sinus infections or retrobulbar tumors or infections. Damage to the
nerves that pass through the orbital fissure causes the symptoms.

95
5) Traumas of the eye. (From wikipedia.. Am not sure wether this is the exact answer that the
teacher need)
Physical or chemical injuries of the eye can be a serious threat to vision if not treated
appropriately and in a timely fashion. The most obvious presentation of ocular (eye) injuries is
redness and pain of the affected eyes. This is not, however, universally true, as tiny
metallicprojectiles may cause neither symptom. Tiny metallic projectiles should be suspected
when a patient reports metal on metal contact, such as with hammering a metal surface.
Intraocular foreign bodies do not cause pain because of the lack of nerve endings in the vitreous
humour and retina that can transmit pain sensations. As such, general or emergency room
doctors should refer cases involving theposterior segment of the eye or intraocular foreign bodies
to an ophthalmologist. Ideally, ointment would not be used when referring to an ophthalmologist,
since it diminishes the ability to carry out a thorough eye examination.

Effects[edit]
Closed globe injury or Non-penetrating trauma: The eye globe is intact, but the seven rings of the
eye have been classically described as affected by blunt trauma.
Penetrating trauma: The globe integrity is disrupted by a full-thickness entry wound and may be
associated with prolapse of the internal contents of the eye. Such injuries are often referred to as
a Globe fracture or a Globe rupture, although these can be incurred by blunt trauma as well.
Perforating trauma: The globe integrity is disrupted in two places due to an entrance and exit
wound (through and through injury). This is a quite severe type of eye injury.
Blowout fracture of the orbit is caused by blunt trauma, classically described for fist or ball
injury, leading to fracture of the floor or medial wall of the orbit due to sudden increased
pressure on the orbital contents.
Muscular Entrapment Fracture of the orbital bones can lead to muscular entrapment limiting
gaze in one direction.
Diagnosis[edit]
 The goal of investigation is the assessment of the severity of the ocular injury with an eye to
implementing a management plan as soon as is required. The usual eye examinationshould be
attempted, and may require a topical anesthetic in order to be tolerable. Many topical agents
cause burning upon instillation. Proxymetacaine has been found to have the best tolerance.[3]
The first step is to assess the external condition of the eye and orbit, and check for perforations,
hyphema, uveal prolapse, or globe penetration. If the pupil is teardrop-shaped, and the anterior
chamber is flat, this is almost always a perforating injury of the cornea or limbal area.
Depending on the medical history and preliminary examination, the primary care physician
should designate the eye injury as a true emergency, urgent or semi-urgent.

Management[edit]
Irrigation[edit]
The first line of management for chemical injuries is usually copious irrigation of the eye with an
isotonic saline or sterile water. In the cases of chemical burns, one should not try to buffer the
solution, but instead dilute it with copious flushing.
Patching[edit]
Depending on the type of ocular injury, either a pressure patch or shield patch should be applied.
Up until circa 1987, pressure patches were the preferred method of treatment for corneal
abrasions in non-contact lens wearers; Multiple controlled studies conducted by accredited
organizations such as the American Academy of Ophthalmology have shown that pressure
patching is of little or no value in healing corneal abrasions and is actually detrimental to healing
in some cases. Pressure patching should never be used on an individual presenting with a corneal
abrasion who has a history of contact lens wear. In this circumstance, a virulent infection caused
by the bacterium Pseudomonas aeruginosa is at a clearly delineated increased risk for occurrence
. These infections can cause blindness within 24 – 48 hours and there is a possibility that the
infection can move into the peri-orbital socket, resulting in the need for evisceration of the
eyeball. In rare cases, the infection can enter the brain and cause death to the patient.
In cases of globe penetration, pressure patches should never be applied, and instead a shield
patch should be applied that protects the eye without applying any pressure. If a shield patch is
applied to one eye, the other eye should also be patched due to eye movement. If the uninjured
eye moves, the injured eye will also move involuntarily possibly causing more damage.
Suturing[edit]
In cases of eyelid laceration, sutures may be a part of appropriate management by the primary
care physician so long as the laceration does not threaten the canaliculi, is not deep, and does not
affect the lid margins.

11. Paralytic strabismus. Diagnosis and treatment.

12. Amblyopia. Causes.Tratment.
13. Retinopathy of prematurity. Etiology, diagnostic, treatment, prognosis.
14. Syndrome of the superior orbital fissure.
15. Traumas of the eye (erosion, hemorrhage, traumatic cataract, retinal holes and retinal
detachment). Diagnosis and treatment.
100 1. (A)Penetrate injury of the eye. Diagnostic, treatment, complications.
(B) Diagnostic and localization methods of intraocular foreign body.

(A)
Penetrating injury is defined as a single full-thickness wound of the eyewall caused by a sharp
object.
Perforating injury refers to two full-thickness wounds (one entry and one exit) of the eyewall
caused by a sharp object or missile.
Effects of penetrating/perforating injury
• Mechanical effects of the trauma or physical changes
• Introduction of infection.
• Sympathetic ophthalmitis
(Sympathetic ophthalmia is a rare bilateral granulomatous panuveitis following perforating eye
injury that results in chronic ocular inflammation and possibly loss of vision.)
Management depending upon injury site:
Wounds of the cornea-
Small central wound does not need stitching, only pad and bandage with atropine and antibiotic
ointments.
Large corneal wound (more than 2 mm) should always be sutured.
Corneal wounds with iris prolapse should be sutured meticulously after excising the iris (the
prolapsed iris should never be reposited; since it may cause infection.)
When associated with lens injury and vitreous loss, lensectomy and anterior vitrectomy may be
performed along with repair of the corneal wound
Wounds of the sclera
(Managed as above)
In corneo-scleral tear, first suture should be applied at the limbus.
Wounds of the lens
(Extensive lens ruptures with vitreous loss should be managed as above)
Small wounds in the anterior capsule may seal and lead on to traumatic cataract, These should be
treated as for cataract.
A badly (severely) wounded eye. It refers to extensive corneo-scleral tears associated with
prolapse of the uveal tissue, lens rupture, vitreous loss and injury to the retina and choroid.
Usually there seems to be no chance of getting useful vision in such cases. So, preferably such
eyes should be excised.
(B)
Diagnosis
1. History. A careful history about the mode of injury may give a clue about the type of foreign
body (IOFB) present etc.

2. Ocular examination. A thorough ocular examination with slit-lamp including gonioscopy
should be carried out.
Subconjunctival haemorrhage, corneal scar, holes in the iris, and opaque track through the lens
are seen; With clear media, sometimes IOFB may be seen on ophthalmoscopy in the vitreous or
on the retina.
3. Plain X-rays orbit. Antero-posterior and lateral views are indispensable for the location of
IOFB, as most foreign bodies are radio opaque.
Localization of IOFB
Once IOFB is suspected clinically and later confirmed, on fundus examination and/or X-rays, its
exact localization is mandatory to plan the proper removal. Following techniques may be used:
Radiographic localization. Different specialized radiographic techniques were used to localize
IOFBs, eg:
Limbal ring method:
i. A metallic ring of the corneal diameter is stitched at the limbus and X-rays are taken.
ii. One exposure is taken in the anteroposterior view.
iii. In the lateral view three exposures are made one each while the patient is looking straight
, upwards and downwards, respectively. T
iv. he position of the foreign body is estimated from its relationship with the metallic ring in
different positions
Ultrasonographic localization. It is being used increasingly these days. It can tell the position of
even non-radio opaque foreign bodies.
CT scan. the best method of IOFB localization
101 2. The complications of the penetrate injury (endophthalmitis, panophthalmitis), diagnostic
and treatment.

Endophthalmitis: inflammation of the inner structures of the eyeball i.e., uveal tissue and retina
associated with pouring of exudates in the vitreous cavity, anterior chamber and posterior
chamber.
Endophthalmitis caused by Perforating injuries can be:
infectious mostly caused by staphylococcus epidermidis and staphylococcus aureus (bacterial) or
Fungal endophthalmitis caused by aspergillus, fusarium, candida
or
Post-traumatic sterile endophthalmitis which occurs because of toxic reaction to retained
intraocular foreign body, e.g., pure copper.
Clinical Manifestation:
Acute endophthalmitis is characterized by severe ocular pain, redness, lacrimation, photophobia
and marked loss of vision.
Lids become red and swollen
Conjunctiva shows chemosis and congestion.
Cornea is edematous,cloudy and ringinfiltration 
may be formed.
Edges of wound become yellow and necrotic and 
wound may gape
Anterior chamber shows hypopyon; soon it 
becomes full of pus.
Iris, when visible, is edematous and muddy.
Pupil shows yellow reflex due to purulent 
exudation in vitreous.
Vitreous exudation
Intraocular pressure is raised in early stages, but in severe cases, the ciliary processes are
destroyed, and a fall in intraocular pressure may ultimately result in shrinkage of the globe.
Treatment:
Antibiotic therapy: Vancomycin , Steroid therapy ,
Supportive therapy: Cycloplegics, Antiglaucoma drugs
Vitrectomy operation should be performed if the patient does not improve with the above
intensive therapy for 48 to 72 hours or when the patient presents with severe infection with
visual acuity reduced to light perception.

Panophthalmitis: intense purulent inflammation of the whole eyeball including the Tenon’s
capsule. The disease usually begins either as purulent anterior or purulent posterior uveitis

Symptoms. Severe ocular pain and headache, Complete loss of vision,
Conjunctiva shows marked chemosis and ciliary as well as conjunctival congestion.
Cornea is cloudy and oedematous.

Anterior chamber is full of pus.

Vision is completely lost and perception of light is absent.
Intraocular pressure is markedly raised.

Globe perforation may occur at limbus, pus comes out and intraocular pressure falls.
Complications include:
 Orbital cellulitis
_ Cavernous sinus thrombosis
_ Meningitis or
encephalitis
Treatment
Anti-inflammatory and analgesics should be started immediately to relieve pain.

Broad spectrum antibiotics should be administered to prevent further spread of infection in the
surrounding structures.
Evisceration operation should be performed to avoid the risk of intracranial dissemination of
infection.
 102
3. Intraocular wounds, care for wounds and emergency.

Closed-globe injury is one in which the eyewall (sclera and cornea) does not have a full
thickness wound but there is intraocular damage.
It includes:
Contusion. It refers to closed-globe injury resulting from blunt trauma. Damage may occur at the
site of impact or at a distant site.
Lamellar laceration. It is a closed Globe injury characterized by a partial thickness wound of the
eyewall caused by a sharp object or blunt trauma.
Open-globe injury is associated with a full thickness wound of the sclera or cornea or both. It
includes rupture and laceration of eye wall.

Rupture refers to a full-thickness wound of eyewall caused by the impact of blunt trauma. The
wound occurs due to markedly raised intraocular pressure by an inside-out injury mechanism.
Laceration refers to a full-thickness wound of eyewall caused by a sharp object. The wound
occurs at the impact site by an outside-in mechanism. It includes:
Penetrating injury refers to a single laceration of eyewall caused by a sharp object.
Perforating injury refers to two full thickness lacerations (one entry and one exit) of the eyewall
caused by a sharp object or missile
(Treatment and management is specific to the areas affected, suturing if there are tears, and
antibiotics, cycloplegics are used, few specific ones that I found I have mentioned it below-)
Prophylaxis for tetanus infection is required for a patient with lacerations, particularly if dirty.
Corneal foreign bodies can be removed after adequate topical anaesthesia under magnification
with good illumination. Also antibiotic and eye padding for one day.
Globe rupture: A badly damaged globe should be enucleated. In less severe cases, repair should
be done under general anaesthesia. Postoperatively atropine, antibiotics and steroids should be
used.
Penetrating injury (open injury of the globe): Any open injury of the globe needs emergency
referral to an eye specialist. A shield only should be placed over the injured eye – eye pads must
not be used so as to avoid any pressure on the eye. A globe ruptured by blunt trauma (e.g. a blow
by a fist) should be treated in the same way as a penetrating injury.

103 4. Types of eye burning (thermal, chemical, radiation), primary care, treatment and
prognosis, complications and treatment.

RADIATIONAL INJURIES
1. Ultraviolet radiations. These may cause (i) photo-ophthalmia (ii) may be responsible for senile
cataract.
2. Infrared radiations. These may cause solar macular burns
3. Ionizing radiational injuries. These are caused following radiotherapy to the tumours in the
vicinity of the eyes. The common ocular lesions include (i) radiation keratoconjunctivitis; (ii)
radiation dermatitis of lids; and (iii) radiation cataract.
Treatment
Speed healing and protect the eye—pad the eye
Prevent infection—apply chloramphenicol ointment
Relieve pain—instill a cycloplegic drug and give oral analgesia if necessary.

THERMAL INJURIES
Thermal injuries are usually caused by fire, or hot fluids. The main brunt of such injuries lies on
the lids. Conjunctiva and cornea may be affected in severe cases.
Treatment for burns of lids is on general lines. When cornea is affected, it should be treated with
atropine, steroids and antibiotics.

CHEMICAL INJURIES
In general, the serious chemical burns mainly comprise alkali and acid burns.
Alkali burns
 : the most severe chemical injuries. Common alkalies responsible for burns are:
lime, caustic potash or caustic soda and liquid ammonia (most harmful).
Mechanisms of damage produced by alkalies includes:
Alkalies dissociate and saponify fatty acids of 
the cell membrane and, therefore, destroy the 

structure of cell membrane of the tissues.
They extract water from the cells, a factor which contributes to the total 
necrosis.
They combine with lipids of cells to form soluble 
compounds, which produce a condition of
softening and gelatinisation. 
The above effects result in an increased deep penetration of the
alkalies into the tissues.
Clinical picture. It can be divided into three stages:
1. Stage of acute ischaemic necrosis. In this stage;
i. Conjunctiva shows marked oedema, congestion, widespread necrosis and a copious purulent
discharge. 

ii. Cornea develops widespread sloughing of the epithelium, oedema and opalescence of the
stroma.
iii. Iris becomes violently inflamed and in severe cases both iris and ciliary body are replaced by
granulation tissue.

2. Stage of reparation. In this stage conjunctival and corneal epithelium regenerate, there
occurs corneal vascularization and inflammation of the iris subsides.

3. Stage of complications. This is characterised by development of recurrent corneal

ulceration and development of complicated cataract and secondary glaucoma.

Acid burns
: less serious than alkali burns. Common acids responsible for burns are: sulphuric
acid, hydrochloric acid and nitric acid.

Chemical effects. The strong acids cause instant coagulation of all the proteins which then act as
a barrier and prevent deeper penetration of the acids into the tissues. Thus, the lesions become
sharply demarcated.

Ocular lesions
1. Conjunctiva. There occurs immediate necrosis followed by sloughing. Late fibrosis
2. Cornea. It is also necrosed and sloughed out. The extent of damage depends upon the
concentration of acid and the duration of contact.
Treatment of chemical burns
1. Immediate and thorough wash with the available clean water or saline.
2. Chemical neutralization. It should be carried out when the nature of offending chemical is
known. For example, acid burns should be neutralized with weak alkaline solutions (such as
sodium bicarbonate) and alkali burns with weak acidic solutions (such as boric acid or mix)
3. Mechanical removal of contaminant. If any particles are left behind, particularly in the
case of lime, these should be removed carefully with swab stick.

4. Removal of contaminated and necrotic tissue.
5. Maintenance of favourable conditions for rapid and uncomplicated healing by frequent
application of topical atropine, corticosteroids and antibiotics.
6. Prevention of fibrosis between cojuctivas
7. Treatment of complications
:
Secondary glaucoma should be treated
Corneal opacity may be treated by keratoplasty.