OPHTHALMOLOGY

Previous years
Question – answer
 PREVIOUS YEARS : QUESTION ANSWER 2

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 OPHTHALMOLOGY 3

Contents

Groups Page no.

Group – A 5

Group – B 21

Group – C 43

Group – D 65

Old questions (before 2006) 87

Index : page no. 101

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References:
Comprehensive Ophthalmology, A K Khurana
Essentials of Ophthalmology, Samar K Basak
SOCH Simplified Ophthalmology Conceptual Handbook, Utsav Bansal
Textbook of anatomy : Head, Neck and Brain, Volume III, Vishram Singh

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Group – A
01. Discuss the anatomy of lacrimal apparatus with diagram. How is tear drained? 4+4+2 [2020]

Anatomy of lacrimal apparatus:

❖ The structures concerned with secretion and drainage of lacrimal (tear) fluid together form the lacrimal apparatus. The
lacrimal apparatus consists of the following structures:
1. Lacrimal glands.
2. Ducts of lacrimal glands.
3. Conjunctival sac.
4. Lacrimal puncta.
5. Lacrimal canaliculi.
6. Lacrimal sac.
7. Nasolacrimal duct (NLD).
❖ Lacrimal glands: These are serous acini, similar in structure to the salivary glands.
o Main lacrimal gland: The lacrimal gland is a J-shaped gland, consists of upper large orbital part and lower small
palpebral part. The two parts are continuous with each other around the lateral margin of the LPS.
• Orbital part:
✓ Almond shaped.
✓ Situated in the lacrimal fossa in the anterolateral part of the roof of the bony orbit.
✓ Superior surface is convex and lies in contact with the bone.
✓ Inferior surface is conceive and lies on LPS.
• Palpebral part:
✓ One-third of the size of the orbital part.
✓ Situated in the lateral part of the upper eyelid below the LPS.
✓ Extends up to the superior fornix of conjunctiva.
o Accessory lacrimal glands:
• Gland of Krause:
✓ Microscopic, situated beneath the palpebral conjunctiva near the fornices.
✓ About 42 in upper fornix and 6-8 in lower fornix.
• Gland of Wolfring: Situated near upper border of superior tarsus and lower border of inferior tarsus.
❖ Ducts of lacrimal gland:
o Approximately 12 in number.
o About 4 or 5 from orbital part and 6–8 from palpebral part.
o They open into the lateral parts of the superior fornix of the conjunctival sac.
❖ Conjunctival sac: It is a potential space between palpebral and bulbar conjunctiva.
❖ Lacrimal puncta:
o These are two small, rounded or oval openings on upper and lower lids, temporal to inner canthus.
o Situated upon a slight elevation called lacrimal papilla.
o Normally, puncta dip into the lacus lacrimalis.
❖ Lacrimal canaliculi:
o The two canaliculi join the puncta to the lacrimal sac.
o Each canaliculi has a vertical and a horizontal part, lie at 90° to each other.
o The superior canaliculus runs upwards and then bends downwards and medially to open into the lacrimal sac.
o The inferior canaliculus runs downwards and then bends upwards and medially to open into the lacrimal sac.
o At the bending each canaliculus presents a small dilatation called ampulla.
o These two can open separately or may join to form common canaliculus, which then opens into the lacrimal sac.
o A fold of mucosa in the opening forms the valve of Rosenmuller, which prevents reflux of tear.
❖ Lacrimal sac:
o Location:
• It is the upper dilated end of the nasolacrimal duct.
• Situated in the deep lacrimal groove bound by posterior lacrimal crest of lacrimal bone and anterior
lacrimal crest of frontal process of the maxilla.
• The sac is enclosed in the lacrimal fascia.

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o Parts:
• Fundus: Portion above the opening of canaliculus.
• Body: Middle part.
• Neck: Lower small part which is narrow and continuous with the nasolacrimal duct.
❖ Nasolacrimal duct (NLD):
o Extends from neck of lacrimal sac to inferior meatus of nose.
o Lies in a bony canal formed by maxilla, lacrimal bone and inferior turbinate.
o Runs downwards, backwards and laterally.
o Its lower opening presents an incomplete mucous fold called lacrimal fold or valve of Hasner, which prevents the
air from blowing the duct into the eye when one blasts his nose to clean nasal secretions.

Tear drainage:

❖ Secretion of tears:
o Basal secretion: Tears are co ntinuously secreted throughout the day by accessory glands.
o Reflex secretion:
• By main lacrimal glands.
• Secretion in response to sensations from the cornea and conjunctiva, by evaporation and tear film break.
• Hyperlacrimation due to irritative sensations from cornea and conjunctiva.
• Afferent pathway: Lacrimal nerve, a branch of ophthalmic division of trigeminal nerve.
• Efferent pathway: By secretomotor fibres to lacrimal glands.
❖ Elimination of tears:
o Pathway: From the lacrimal gland, the tears flow downwards laterally across the ocular surface → A variable
number of tears is lost by evaporation from ocular surface → Remained tears flow along superior and inferior
marginal strip → collects as lacus lacrimalis in inner canthus → Drained by lacrimal passage into nasal cavity.
o Lacrimal pump mechanism: 70% tear is drained via inferior and 30% via superior canaliculus by this mechanism.
• When the eyelids close:
✓ Contraction of pretarsal orbicularis oculi: Compresses the ampulla and shortens the canaliculi.
This movement propels tear towards the lacrimal sac.
✓ Contraction of preseptal orbicularis oculi: Distends the lacrimal sac and creates therein a -ve
pressure which draws tear into the lacrimal sac.
• When the eyelids open:
✓ Relaxation of pretarsal orbicularis oculi: Canaliculi and ampulla expand and reopen to draw
tear from lacus lacrimalis and marginal tear strips.
✓ Relaxation of preseptal orbicularis oculi (Horner's muscle): Lacrimal sac is collapsed and +ve
pressure forces tear to go down into nose through NLD.

02. Describe the anatomy of the lacrimal apparatus with labelled diagram. Enumerate the causes of watering of
the eye. 6+2+2 [2018]

Anatomy of lacrimal apparatus: Group A, question no. 01.

Causes of watering of eye:

❖ Watering of eye may occur due to two conditions:

1. Hyperlacrimation: Excessive secretion of tears.
2. Epiphora: Inadequate drainage of normally secreted tears.
❖ Causes of Hyperlacrimation:
o Primary lacrimation: Due to direct stimulation of lacrimal glands by tumour, cyst or strong parasympathetic drugs.
o Reflex lacrimation: Due to stimulation of sensory branches of trigeminal nerve.
• Affection of lids: Stye, hordeolum internum, acute meibomitis, trichiasis, concretions and entropion.
• Affection of conjunctiva: Any type of conjunctivitis.
• Affection of cornea: Corneal abrasion, corneal ulcer and non-ulcerative keratitis.

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• Affection of sclera: Episcleritis and scleritis.

• Affection of uveal tract: Iritis, cyclitis, iridocyclitis.
• Others: Acute glaucoma, endophthalmitis, panophthalmitis, orbital cellulitis.
o Central lacrimation: Psychical lacrimation in emotional state, voluntary lacrimation and hysterical lacrimation.
❖ Causes of epiphora:
o Physiological cause:
• Lacrimal pump failure due to lower lid laxity or orbicularis muscle weakness.
• Atonia of lacrimal sac.
o Mechanical obstruction:
• Eversion of lower punctum: Chronic conjunctivitis, chronic blepharitis and ectropion.
• Punctal obstruction:
✓ Congenital: Congenital absence of puncta.
✓ Acquired: Cicatricial closure; obstruction due to the foreign body, concretion or cilia; punctal
stenosis due to drugs like pilocarpine, idoxuridine etc.
• Canalicular obstruction:
✓ Congenial: Congenital obstruction of canaliculus.
✓ Acquired: Foreign body, trauma, idiopathic fibrosis, canaliculitis.
• Lacrimal sac obstruction:
✓ Congenital: Mucous membrane fold.
✓ Acquired: Traumatic stricture, dacryocystitis, dacryolithiasis, syphilis, TB and tumours.
• NLD obstruction:
✓ Congenital: Noncanalization, partial canalization, imperforated membranous valve.
✓ Acquired: Traumatic stricture, inflammatory stricture, idiopathic stenosis and tumours.

03. Write in brief the anatomy of lacrimal apparatus with labelled diagram. 5+5 [2008]

Anatomy of lacrimal apparatus: Group A, question no. 01.

➢ Important to note:
o Blood supply of main lacrimal gland:
• Artery: Lacrimal artery, a branch of ophthalmic artery.
• Vein: Ophthalmic vein
o Nerve supply of main lacrimal gland:
• Sensory supply: Sensory fibres of lacrimal nerve, a branch of ophthalmic division of trigeminal nerve.
• Sympathetic supply: T1 spinal segment → Superior cervical sympathetic ganglion (gives origin to post-
ganglionic sympathetic fibres) → Sympathetic plexus around internal carotid artery → Deep petrosal
nerve → Pterygopalatine ganglion → Zygomatic nerve → Zygomaticotemporal nerve → Lacrimal nerve
to lacrimal gland.
• Parasympathetic supply: Lacrimatory nucleus → Nervus intermedius → Geniculate ganglion → Greater
petrosal nerve → Pterygopalatine ganglion (gives origin to postganglionic parasympathetic fibres) →
Zygomatic nerve → Zygomaticotemporal nerve → Lacrimal nerve to lacrimal gland.

04. Name the extraocular muscles of the eyeball. Describe the attachments with a schematic diagram. Write the
functions of each muscle. 2+5+3 [2019]

Extraocular muscles:

❖ Rectus muscles:
1. Superior rectus (SR).
2. Inferior rectus (IR).
3. Medial rectus (MR).

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4. Lateral rectus (LR).

❖ Oblique muscles:
1. Superior oblique (SO).
2. Inferior oblique (IO).

Attachments of extraocular muscles:

❖ Rectus muscles:
o Origin: From a common tendinous ring (annulus of Zinn), which is attached at the apex of the orbit, encircling the
optic foramina and medial part of the superior orbital fissure.
• SR: From superior part and also the adjoining dura covering the optic nerve.
• IR: From inferior part.
• MR: From medial part.
• LR: From lateral part by two heads which join in a ‘V’ form.
o Insertion: Into the sclera at different distances from the limbus as under:
• SR: 7.7 mm.
• IR: 6.5 mm.
• MR: 5.5 mm.
• LR: 6.9 mm.
❖ Oblique muscles:
o SO:
• Origin: From body of sphenoid superomedial to the optic canal.
• Insertion: Into sclera behind the equator in posterior superior quadrant of eyeball between SR and LR.
o IO:
• Origin: From rough impression in anteromedial angle of the floor of orbit, lateral to the lacrimal groove.
• Insertion: Into sclera behind the equator in posterior superior quadrant of eyeball, a little below and
posterior to the insertion of SO.

Functions of extraocular muscles:

Muscles Primary action Secondary action Tertiary action

SR Elevation Intorsion Adduction
IR Depression Extorsion Adduction
MR Adduction – –
LR Abduction – –
SO Intorsion Depression Abduction
IO Extorsion Elevation Abduction

05. Describe the origin, insertion, nerve supply and action of extra ocular muscles. 2+2+3+3 [2009]

Attachments of extraocular muscles: Group A, question no. 04.

Nerve supply of extraocular muscles:

❖ Oculomotor nerve: The third cranial nerve supplies:

o Superior rectus.
o Inferior rectus.
o Medial rectus.
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o Inferior oblique.
❖ Trochlear nerve: The fourth cranial nerve supplies the superior oblique.
❖ Abducent nerve: The sixth cranial nerve supplies the lateral rectus. (All 3, SO4, LR6).

Functions of extraocular muscles: Group A, question no. 04

06. Describe the anatomy of the eyelids with a labelled diagram. 7+3 [2014]

Anatomy of eyelids:

❖ Gross anatomy: The eyelids, also called palpebrae, are movable curtains in front of the eyeball.
o Parts: Each eyelid is divided by a horizontal furrow into two parts:
• Peripheral orbital part.
• Central tarsal part.
o Palpebral fissure: The space between the two eyelids.
o Canthi:
• Lateral canthus: The lateral angle of the palpebral fissure where two eyelids meet.
• Medial canthus: The medial angle of the palpebral fissure where two eyelids meet.
o Lid margins: The free margin of each eyelid is divided into two parts:
• Lateral 5/6th : Ciliary part, which is flat and possesses eyelashes.
• Medial 1/6th : Lacrimal part, which is round and does not possess cilia.
❖ Structure: From anterior to posterior, each eyelid consists of the following layers:
o Skin: Elastic, fine and thinnest in the body.
o Subcutaneous areolar tissue: Very loose with no fat and readily distended by blood or oedema.
o Layer of striated muscle:
• Orbicularis oculi: Forms an oval sheet across the eyelids.
✓ Orbital part: Encircles the orbital margin.
✓ Preseptal part: Lies anterior to septum orbitale and loosely attached to it. At the junction of the
preseptal and pretarsal part, horizontal furrow is formed.
✓ Pretarsal part: Lies anterior to the tarsus and firmly attached to it. A portion of this part attaches
to the anterior lacrimal crest and posterior lacrimal crest (Horner’s muscle), helps in the tear
drainage. A small part of this also extends to the lid margin forming muscle of Rion.
• Levator palpebrae superioris (LPS): Only present in upper eyelids to rise them.
✓ Origin: Apex of orbit.
✓ Insertion: Three parts:
▪ Skin of lid.
▪ Anterior surface of tarsal plate.
▪ Conjunctiva of superior fornix.
o Submuscular areolar tissue: Layer of loose connective tissue with nerves and vessels.
o Fibrous layer: This is the framework of lid having two parts:
• Tarsal plate:
✓ Dense connective tissue.
✓ Upper and lower tarsal plates join with each other at medial and lateral canthi.
✓ They are attached with the orbital margins through medial and lateral palpebral ligaments.
• Septum orbitale:
✓ Thin membranous connective tissue.
✓ Centrally attached to tarsal plates and peripherally to periosteum of orbital margin.
✓ Perforated by nerves, vessels and LPS.
o Layer of non-striated muscle: Palpebral muscle of Muller.
• Origin: In upper lids from fibres of LPS and in lower lids from prolongation of inferior rectus muscle.
• Insertion: Peripheral margins of tarsal plate.
o Palpebral conjunctiva: Lines the lid and has three parts:
• Marginal: From lid margin to sulcus subtarsalis.
• Tarsal: Adherent to the tarsal plate.
• Orbital: From tarsal plate to fornix.
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❖ Glands:
o Meibomian glands: Modified sebaceous glands, present in stroma of tarsal plate.
o Glands of Zeis: Sebaceous gland opens into follicles of eyelashes.
o Glands of Moli: Modified sweat glands near the hair follicles, open into hair follicles or ducts of Zeis glands.
o Accessory lacrimal glands of Wolfring: Present near the upper border of tarsal plate.
❖ Blood supply:
o Arteries:
o Marginal arterial arcades: Lie in submuscualr plane in front of tarsal plate in both upper and lower lids.
o Superior arterial arcade: Lies near the upper border of tarsal plate in upper lid.
o Veins:
❖ Post tarsal venous plexus: Opens into ophthalmic veins.
❖ Pre tarsal plexus: Opens into subcutaneous veins.
o Lymphatics: Pre & post tarsal, lateral half of both drain into preauricular and medial half into submandibular LNs.
❖ Nerve supply:
o Motor nerves:
• Facial nerve: Orbicularis oculi.
• Oculomotor nerve: LPS.
• Sympathetic fibres: Muller's muscle, paralysis leads to Horner's syndrome.
o Sensory nerves: Derived from branches of trigeminal nerve.
• Upper lid: Lacrimal, supraorbital and supratrochlear nerves.
• Lower lid: Infraorbital nerve with infratrochlear branch.

07. Write in brief with a diagram structure of upper eyelids. 7+3 [2005]

Anatomy of upper eyelids: Group A, question no. 06.

08. Describe the anatomy of conjunctiva. [2011]

Anatomy of conjunctiva:

❖ Location: Conjunctiva is a translucent mucous membrane which lines the posterior surface of the eyelids and anterior
aspect of the eyeball. It stretches from the lid margin to the limbus and encloses a complex space called conjunctival sac
which is open in front at the palpebral fissure.
❖ Parts:
o Palpebral conjunctiva: Lines the posterior surface of the eyelids and has three parts:
• Marginal: From lid margin to sulcus subtarsalis.
• Tarsal: Adherent to the tarsal plate.
• Orbital: From tarsal plate to fornix.
o Bulbar conjunctiva: Lines the anterior aspect of the eyeball. It is separated from anterior sclera by episcleral tissue
and Tenon's capsule.
• Limbal conjunctiva:
✓ A 3mm ridge of bulbar conjunctiva around the cornea.
✓ Here the conjunctiva, Tenon's capsule and episcleral tissue fuse to form a dense tissue.
✓ It is strongly adherent to the underlying corneoscleral junction.
✓ Limbal epithelium is continuous with the corneal epithelium.
o Conjunctival fornix:
• Continuous circular cul-de-sac, which is broken medially by plica semilunaris and caruncle.
• Joins the bulbar with palpebral conjunctiva.
• Subdivided into superior, inferior, medial and lateral parts.
o Other parts:
• Plica semilunaris: Pinkish crescentic fold of conjunctiva in medial canthus representing nictitating mem-
brane as a vestigial organ.
• Caruncle: Small, ovoid, pinkish mass, just medial to plica semilunaris. It is a modified skin made of strati-

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fied squamous epithelium containing sweat glands, sebaceous glands and hair follicles.
❖ Structure: From outside to inside, each conjunctiva consists of the following layers:
o Epithelium: Non-keratinized multi-layered epithelial tissue, with structural variation from region to region.
• Marginal conjunctiva: 5 layered stratified squamous epithelium.
• Tarsal and orbital conjunctiva: 2 layered:
✓ Superficial layer: Cylindrical cells.
✓ Deep layer: Flat cells.
• Fornix and bulbar conjunctiva: 3 layered:
✓ Superficial layer: Cylindrical cells.
✓ Middle layer: Polyhedral cells.
✓ Deep layer: Cuboidal cells.
• Limbal conjunctiva: 2-3 layered stratified squamous epithelium.
o Adenoid layer: It is also called lymphoid layer because of presence of lymphocytes. It consists of fine connective
tissue reticulum in the meshes of which lie lymphocytes.
o Fibrous layer: It consists of a meshwork of collagenous and elastic fibres, containing vessels and nerves. This layer
in bulbar region blends with the underlying Tenon’s capsule.
❖ Glands:
o Mucin secretory glands:
• Goblet cells: Constitute about 10% of conjunctival epithelium.
• Crypts of Henle: Present in tarsal conjunctiva.
• Glands of Manz: Present in limbal conjunctiva.
o Accessory lacrimal glands:
• Gland of Krause: Microscopic glands.
✓ Situated beneath the palpebral conjunctiva near the fornices.
✓ About 42 in upper fornix and 6-8 in lower fornix.
• Gland of Wolfring: Situated near upper border of superior tarsus and lower border of inferior tarsus.
❖ Blood supply:
o Arteries:
• Peripheral arterial arcade of eyelid: Supplies palpebral conjunctiva and fornix.
• Marginal arterial arcade of eyelid: Supplies palpebral conjunctiva and fornix. Posterior conjunctival
arteries from both arterial arcades of eyelid supplies the bulbar conjunctiva.
• Anterior conjunctival arteries: Branch of anterior ciliary arteries, supply bulbar conjunctiva. Terminal
branches of anterior and posterior conjunctival arteries anastomose to form pericorneal plexus.
o Veins: Venous plexus of eyelids and anterior ciliary veins.
o Lymphatics: Superficial & deep, lateral half of both drain into preauricular & medial half into submandibular LNs.
❖ Nerve supply:
o Circumcorneal zone: Branches from long ciliary nerve.
o Rest of the conjunctiva: Branches from lacrimal, infratrochlear, supratrochlear, supraorbital and frontal nerves.

09. Describe the layers of cornea. What are the factors maintaining corneal transparency? 6+4 [2020]

Layers of cornea:

❖ Histologically the cornea consists of 6 layers. From anterior to posterior these are:
1. Epithelium.
2. Bowman's membrane.
3. Stroma (substantia propria).
4. Pre-Descemet's membrane (Dua's layer).
5. Descemet's membrane (posterior elastic lamina).
6. Endothelium.
❖ Epithelium: Composed of 5-6 layered stratified squamous non-keratinized epithelium cells and becomes continuous with
epithelium of bulbar conjunctiva. Damage of epithelium heals completely without any scar formation.
o Superficial 2 layers: Flattened cells with tight junctions prevent penetration of tear fluid into the stroma.
o Middle 2-3 layers: Wing or umbrella cells.
o Deep basal layer: Columnar cells.

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❖ Bowman’s membrane: This is an acellular collagenous layer, which maintains the integrity of cornea. This layer is unable
to regenerate and so damage heals by scarring.
❖ Stroma:
o Thickest layer (90% of corneal thickness).
o Formed by regular arrangement of collagen type I, V and VI on hydrophilic bed of proteoglycans like keratan
sulphate and chondroitin sulphate.
o Cells: Keratocytes (modified fibroblasts), wandering macrophages, histiocytes and a few lymphocytes.
❖ Dua's layer: Acellular and toughest layer of cornea.
❖ Descemet's membrane:
o This is the strong homogenous basement membrane of endothelium, which maintains the integrity of eyeball.
o Formed by collagen and glycoproteins and has the property of regeneration.
o Peripheral termination of DM at limbus is called Schwalbe's line/ring.
❖ Endothelium:
o Single layered flat polygonal (mainly hexagonal) epithelial cells which on slitlamp biomicroscopy appear as mosaic.
o Best examined by specular microscopy to see cell shape and endothelial cell count.
o Normal endothelial cell density of young adult is 3000 cells/mm2 and critical density is 500 cells/mm2.
o Do not proliferate and cell loss with age is compensated by polymegathism and migration of neighbouring cells.
o Function: Cells have Na+-K+ ATPase pump, which pumps water from stroma to aqueous and thus keeps cornea
dehydrated.

Factors maintaining corneal transparency:

❖ Anatomical factors:
o Tear film and corneal epithelium: Homogeneity of the refractive index throughout the epithelium.
o Lattice theory of Maurice: Peculiar arrangement of corneal lamella.
o Goldmann and Benedek theory: Peculiar refractive index of corneal lamella with variation less than 200 micron.
o Avascularity of cornea.
o Absence of lymphatics.
o Unmyelinated nerve fibres.
o Absence of antigen presenting cells in central cornea.
o Very less number of keratinocytes and other cells in stroma.
❖ Physiological factors: Factors that keep cornea in a relative dehydrated state with 78% water content.
o Barrier function of epithelium and endothelium.
o Endothelial pump: Endothelial cells have Na+-K+ ATPase pump, bicarbonate-dependent ATPase pump and Na+-H+
ATPase pump; which pumps water from stroma to aqueous and thus keeps cornea dehydrated.
o Evaporation from corneal surface.
o Normal intraocular pressure.
o Swelling pressure of stroma: Counters the imbibation effect of intraocular pressure.
o Corneal crystallins: Water soluble proteins of keratinocytes (transketolase and aldehyde dehydrogenase class IA1)
contribute to corneal transparency in cellular level.

10. Describe in brief the different layers of cornea with diagram mentioning the special clinical significance
related to each of them. [2007]

Layers of cornea: Group A, question no. 09.

11. Describe the anatomy of physiological lens. What is mechanism of accommodation? 5+5 [2013]

Anatomy of lens: Group A, question no. 12.

Mechanism of accommodation: Group A, question no. 12.

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12. Describe anatomy and physiology of lens and the mechanism of accommodation. 4+3+3 [2016]

Anatomy of lens:

❖ Gross anatomy:
o Shape: Biconvex. Posterior curvature is more than anterior.
o Appearance: Transparent, crystalline structure.
o Location: Between iris and the vitreous in a square shaped depression, the patellar fossa.
o Diameter: 9-10 mm.
o Thickness: Varies with age from 3.5 mm (at birth) to 5 mm (at extreme age).
o Equator: Area where the anterior and posterior surface meet.
o Refractive index: 1.39 (mean), 1.41 (nucleus, maximum in the eye), 1.38 (cortex).
o Total dioptric power: 15-16.
o Accommodation power: Varies with age from 14-15 D (at birth), 7-8 D (at 25 yrs.) and 1-2 D (at 50 yrs.).
❖ Attachments:
o Peripherally: Attached to the ciliary bodies by zonules of Zinn. These zonules have three parts i.e. pars orbicularis,
zonular plexuses, zonular fork. Zonuler fork again form three zonular limbs i.e. anterior, equatorial and posterior.
These limbs attach the lens with the ciliary bodies.
o Posteriorly: Attached to the anterior hyaloid surface of vitreous in a circular way by hyaloideocapsular ligament
of Weiger or reteolental ligament. The potential space between anterior hyaloid surface and posterior lens
capsule within the circular attachment is called space of Burger or Egglet's space.
❖ Structures:
o Capsule:
• Thin, transparent, hyaline membrane surrounding the lens.
• Thickest basement membrane in the body, formed by type IV collagen.
• Anterior thickness is more than posterior. Thickest at anterior pre-equatorial region and thinnest at
posterior pole.
o Epithelium:
• Single layered cuboidal cells lies deep to anterior capsule (absent posteriorly).
• Cells become columnar with a ‘nuclear bow' configuration in equator, and actively divide and elongate
to form new lens fibres throughout life.
o Lens fibres: Lied horizontally, front to back and concentrically like layers of an onion. These fibres arrange
compactly to form outer cortex and inner nucleus.
• Cortex: Peripheral part which comprises the youngest lens fibres.
• Nucleus: Central part which comprises the oldest lens fibres. It consists of different zones of dis-
continuity, seen in slit-lamp. Depending upon the period of development, the different zones of nucleus
from inside to outside are:
✓ Embryonic nucleus: Upto 3 months of gestation. Consists of primary lens fibres.
✓ Foetal nucleus: From 3 months of gestation to birth. Fibres meet around sutures which are
anteriorly Y-shaped and posteriorly inverted Y-shaped.
✓ Infantile nucleus: From birth to puberty.
✓ Adult nucleus: From puberty to rest of the life.
❖ Blood and nerve supply: It has no blood supply and no innervation.

Physiology of lens:

❖ Factors maintaining lens transparency:

o Aquaporin MIP26 or aquaporin 0: Controls transport of water through water channel and glycerol through
glycerol channel, thus maintain transparency of lens. Aquaporin 0 or MIP mutation leads to cataract.
o Antioxidant mechanism and high concentration of reduced glutathione in lens maintains the lens proteins in a
reduced state and ensues the integrity of cell membrane pump.
o Electrochemical balance maintain by pump mechanism.
❖ Antioxidant mechanism:
o Superoxide dismutase: Breaks superoxide anion (O2-) to produce hydrogen peroxide.
o Catalase: Breaks peroxide to water.
o Glutathione peroxidase and glutathione reductase: Major free radical scavenger in lens.
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o Vitamin C and E.
o Low oxygen level around the lens: Lost after vitrectomy, leading to increased incidence of nuclear cataract.
❖ Carbohydrate metabolism:
o Glucose transported into lens by both simple & facilitated diffusion, mainly from aqueous and partly from vitreous.
o Glucose transportation occurs at both, anterior and posterior surface of lens.
o Metabolized by:
• >80%: Anaerobic glycolysis.
• 3%: Kreb's cycle (aerobic).
• 5%: HMP shunt.
• 5%: Sorbitol pathway.
❖ Electrochemical balance:
o Lens is electronegative, with a potential of -70 mV across an intact lens → Lens has higher levels of K+ and amino
acids and lower levels of Na+, Cl- and water than the surrounding aqueous and vitreous → Thus the flow of
electrolytes into the lens is directed by an electrical gradient.
o Lens maintains its electrolyte and water balance via membrane transport processes mainly across the anterior
lens capsule and epithelium:
• Cation balance:
✓ Na+-K+ ATPase dependent Na+ extrusion and K+ intake at the anterior epithelium which creates
a concentration gradient for diffusion at the posterior surface (pump and leak theory).
✓ Sodium enters preferentially at poles.
✓ Potassium exits preferentially from equator.
✓ Ascorbic acid and myo-inositol: Active transport via Na+ dependent SVCT2.
✓ Amino acid: Active transport dependent on Na+ gradient across lens.

Mechanism of accommodation:

❖ The mechanism by which near objects are brought to focus on the retina is called accommodation.
❖ Accommodation triad:
o Convergence of eye by medical rectus.
o Miosis by sphincter pupillae.
o Increase in anterior curvature of lens.
❖ Von Helmholtz's capsular theory:
o Before accommodation:
• Large diameter of ciliary ring.
• Zonules are stretched and intertwined.
• Anterior capsule is stretched and straight.
• Equatorial diameter 10 mm.
• Lens is compressed.
o After accommodation: Contraction of ciliary muscles.
• Decreased diameter of ciliary ring.
• Relaxation of zonules.
• Relaxation of anterior capsule.
• Decreased equatorial diameter of lens.
• Thickness of lens is increased and lens becomes more cover or conoidal. The reason of attaining this
shape is the configuration of anterior lens capsule which is thinner in centre and thicker in periphery.
❖ Schachar’s theory:
o During accommodation ciliary muscle contraction tenses the anterior zonulae, most especially the equatorial
zonular fibres → The lens would then be stretched equatorially (i.e. the lens edge moves toward the sclera), but
the biomechanical properties of the lens are such that the central part of the lens rounds up and moves anteriorly,
increasing its refracting power.
o According to this theory, presbyopia results from growth in the equatorial diameter of the lens, such that the peri-
lenticular space is reduced and ciliary muscle contraction can no longer tense zonules and expand lens coronally.

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➢ Important to note:
o Anatomical factors maintaining lens transparency:
• Avascularity of lens.
• No innervation.
• Single layered epithelium.
• Semipermeable lens capsule.
• Characteristics of lens fibres:
✓ Tightly packed nature of lens cells.
✓ Narrow lens fibre membrane.
✓ Loss of organelles.

13. Discuss the theories of aqueous humor formation, circulation and drainage. 4+3+3 [2015]

Formation of aqueous humor:

❖ Aqueous humour is derived from plasma of capillary network of ciliary processes through 3 mechanisms:
1. Ultrafiltration (20%).
2. Active secretion (70%).
3. Diffusion (10%).
❖ Ultrafiltration: Most of the plasma substances pass out from the capillary wall and loose connective tissue by ultrafiltration
and accumulate behind the epithelium of ciliary body as plasma filtrate or dialysate.
❖ Active secretion:
o From stroma into epithelium:
• Transportation of dialysate into the pigment epithelium.
• Transportation of Na+ and Cl- from stroma into the epithelial cells by paired Na+-H+ and Cl--HCO3- anti-
ports.
o From non-pigmented epithelium into posterior chamber:
• Mechanism of transportation:
✓ Na+-K+ ATPase pump.
✓ Calcium and voltage gated ion channels.
✓ Carbonic anhydrase enzyme system.
• Substance transported: Sodium, chlorides, potassium, ascorbic acid, amino acids and bicarbonates.
❖ Diffusion:
o Active transport of the substances across the non-pigmented epithelium results in an osmotic gradient leading to
the movement of other plasma constituents from epithelium into the posterior chamber.
o As the aqueous humour passes from posterior chamber to Schlemm's canal, again diffusion occurs from the
surrounding structures into the canal. That’s why anterior chamber aqueous resembles plasma more closely than
posterior chamber aqueous.

Circulation of aqueous humor:

❖ Aqueous humour secretion → Posterior chamber → Via pupil against slight physiological resistance → Anterior chamber
→ Angel of anterior chamber, i.e. iridocorneal angle → Aqueous outflow.

Drainage of aqueous humor:

❖ From anterior chamber, the aqueous is drained out by two routes:

1. Trabecular (conventional) outflow (70-80%).
2. Uveoscleral (unconventional) outflow (20-30%).
❖ Trabecular outflow: Free flow of aqueous occurs from trabecular meshwork upto juxtacanalicular tissue which along with
inner wall of Schlemm's canal (SC) appears to provide some resistance. The outflow occurs by an active pump mechanism.
o Components of active pump:

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• Aqueous outflow pump: Operates through oscillatory pressure transients caused by the ocular pulse,
blinking and eye movement.
• Trabecular meshwork flexibility: Trabecular meshwork because of its flexibility can actively move
outward and recoil back in response to oscillatory pressure transients.
• Aqueous valves: Valves present circumferentially in the SC allow one way passage of aqueous from
juxtacanalicular space to inside SC and not vice-versa.
o Mechanism of active pump:
• From juxtacanalicular space to SC: Cardiac diastole → Slightly decreased IOP due to less blood flow to
choroidal vasculature → Inward retraction of trabecular meshwork → Negative pressure formation inside
SC → Opening of aqueous valves → Flow of aqueous into the canal.
• From SC to collector channels and aqueous veins: Cardiac systole → Slightly increased IOP due to more
blood flow to choroidal vasculature → Outward distention of trabecular meshwork → Positive pressure
formation inside SC → Closure of aqueous valves → Aqueous is pushed from SC to collector channel and
then to aqueous veins.
• From aqueous veins to episcleral veins:
✓ By the same cardiac systolic mechanism.
✓ Pressure gradient between IOP (16 mm Hg) and episcleral venous pressure (10 mm Hg) also
helps in this process.
✓ Drains into cavernous sinus via anterior ciliary vein and superior ophthalmic vein.
❖ Uveoscleral outflow: Aqueous inside ciliary body through iris root, ciliary body face and uveal trabecular meshwork →
Aqueous between bundles of ciliary muscles into the suprachoroidal space → Aqueous drained by venous circulation of
ciliary body, choroid and sclera.

14. Describe with a schematic diagram of pupillary light reflex. Mention the drugs acting on pupil. 6+4 [2017]

Pupillary light reflex:

❖ Light reflex: When light is shone in one eye, both the pupils constrict. This reflex is initiated by rods and cones.
o Direct light reflex: Constriction of the pupil to which light is shone is called direct light reflex.
o Consensual light reflex: Constriction of the other pupil is called consensual (indirect) light reflex.
❖ Pathway:
o Afferent fibres: Extend from retina to the pretectal nucleus in the midbrain. These travel along the optic nerve to
the optic chiasma where fibres from the nasal retina decussate and travel along the opposite optic tract to
terminate in the contralateral pretectal nucleus. While the fibres from the temporal retina remain uncrossed and
travel along the optic tract of the same side to terminate in the ipsilateral pretectal nucleus.
o Internuncial fibres: Connect each pretectal nucleus with Edinger-Westphal nuclei of both sides. This connection
forms the basis of consensual light reflex.
o Efferent pathway: Consists of the parasympathetic fibres which arise from the Edinger-Westphal nucleus in the
mid-brain and travel along the third (oculomotor) cranial nerve. The preganglionic fibres enter the inferior division
of the third nerve and via the nerve to the inferior oblique reach the ciliary ganglion to relay. Post-ganglionic fibres
travel along the short ciliary nerves to innervate the sphincter pupillae.

Drugs acting on pupil:

❖ Cycloplegic and mydriatic drugs: These drugs cause paralysis of acco-

mmodation and dilate the pupil.
o Antimuscarinic ganglion blocker:
• Atropine sulphate 1% ointment.
• Homatropine hydrobromide 2% drops.
• Cyclopentolate hydrochloride 1% drops.
• Tropicamide 0.5%, 1% drops
o Alpha-1 adrenergic agonist: Phenylephrine 5%, 10% drops.
o Indirect sympathomimetic: Hydroxyamphetamine.

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❖ Miotic drugs: These drugs cause contraction of ciliary muscles and con-
strict the pupil.
o Direct acting cholinergic drug: Muscarinic agonist drugs like
pilocarpine.
o Cholinesterase inhibitor:
• Reversible: Physostigmine, neostigmine.
• Irreversible: Echothiophate iodide, demecarium, diiso-
propylflurophosphate (DFP3).
o Dual-action parasympathomimetic: Carbachol.

15. Describe the pathway of light reflex with a diagram. [2012]

Pupillary light reflex: Group A, question no. 14.

16. Discuss pupillary reactions with special reference to their basis and clinical significance. [2010]

Pupillary reactions:

❖ Light reflex: Group A, question no. 14.

❖ Near reflex: This occurs on looking at a near object. It consists of two components:
1. Convergence reflex: Contraction of pupil on convergence.
2. Accommodation reflex: Contraction of pupil associated with accommodation.
o Pathway of convergence reflex: Its afferent pathway is still not elucidated. It is assumed that the afferents from
the medial recti travel centrally via the third nerve to the mesencephalic nucleus of the fifth nerve, to a
presumptive convergence centre in the tectal or pretectal region. From this the impulse is relayed to the Edinger-
Westphal nucleus and the subsequent efferent pathway of near reflex is along the 3rd nerve. The efferent fibres
relay in the accessory ganglion before reaching the sphincter pupillae.
o Pathway of accommodation reflex: The afferent impulses extend from the retina to the parastriate cortex via the
optic nerve, chiasma, optic tract, lateral geniculate body, optic radiations, and striate cortex. From the parastriate
cortex the impulses are relayed to the Edinger-Westphal nucleus of both sides via the occipito-mesencephalic
tract and the pontine centre. From the Edinger-Westphal nucleus the efferent impulses travel along the 3rd nerve
and reach the sphincter pupillae and ciliary muscle after relaying in the accessory and ciliary ganglions.
❖ Psychosensory reflex: It refers to dilatation of the pupil in response to sensory and psychic stimuli. It is very complex and
its mechanism is still not elucidated.

Clinical significance:

❖ Amaurotic light reflex:

o Absence of direct light reflex on affected side and absence of consensual light reflex on the normal eye.
o Indicates lesions of optic nerve or retina of affected side.
❖ Efferent pathway defect:
o Absence of both direct and consensual light reflex on affected eye and presence of both direct and consensual
light reflex on normal eye.
o Indicates effect of parasympathetic drugs (atropine, homatropine), internal ophthalmoplegia or 3rd nerve palsy.
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❖ Wernicke’s hemianopic pupil:

o Absence of ipsilateral direct and contralateral consensual light reflex when light is thrown on the temporal half of
the retina of the affected side and nasal half of opposite side, but presence of reflex when light is thrown on the
nasal half of the retina of the affected side and temporal half of opposite side.
o Indicates lesion of optic tract.
❖ Marcus Gunn pupil:
o Paradoxical response of a pupil to light.
o Indicates relative afferent pathway defect (RAPD) due to incomplete optic nerve lesions or severe retinal diseases.
❖ Argyll Robertson pupil (ARP):
o Absence of light reflex but presence of near reflex in both pupil.
o Indicates lesion in the region of tectum usually due to neurosyphilis.
❖ Adie's tonic pupil:
o Absence of light reflex, and very slow and tonic near reflex of the anisocoric affected pupil.
o Indicates post-ganglionic parasympathetic pupillomotor damage.

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Note:

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Note:

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Group – B
01. Morgagnian cataract. [2020, 2011]

❖ Morgagnian cataract is a form of hypermature senile cataract (HMSC). When the mature cataract is left in situ, in some
patients the stage of hypermaturity sets in as morgagnian cataract.
❖ Appearance of the lens:
o Cortex: The cortex liquefies into milky white fluid and the lens is converted into a bag containing the fluid.
o Nucleus: The small brownish nucleus settles at the bottom, altering it’s position with change in position of head.
o Capsule: The capsule is wrinkled and leaky in nature. Sometimes, calcium deposits may also be seen.
❖ Clinical features:
o Symptoms: Patient comes with profound visual loss.
o Signs:
• Visual acuity: Only perception of light is present.
• Colour of lens: Milky white.
• Irish shadow: absent.
• Distant direct ophthalmoscopy with dilated pupil: No red glow, milky white pupil.
• Slit-lamp examination: Focus above the nucleus shows a triangular area bounded anteriorly and
posteriorly by the anterior and posterior lens capsule and the base of the triangle formed by the lens
nucleus. This is called the triangle sign.
• Refraction or retinoscopy: Not possible.
❖ Diagnosis:
o On the basis of clinical signs and symptoms.
o Ultrasonography is found to be normal.
❖ Management: Surgical removal of the cataractous lens followed by intraocular lens implantation is the treatment of choice.
o Extracapsular cataract extraction (ECCE), small incision cataract surgery (SICS) or phacoemulsification can be
performed for the cataract extraction.
o Intraocular lens scaffold technique is used to prevent posterior capsule rupture during phacoemulsification.
❖ Complications:
o Phacoanaphylactic uveitis: Lens proteins may leak into the anterior chamber causing antigen-antibody reaction,
leading to phacoanaphylactic uveitis.
o Phacolytic glaucoma: Leaked lens proteins are engulfed by the macrophages. The swollen macrophages clog the
trabecular meshwork leading to increase in IOP. This leads to phacolytic glaucoma, a type of secondary open angle
glaucoma.

02. Phlyctenular conjunctivitis. [2020, 2017, 2003]

❖ Also known as microbial allergic conjunctivitis.

❖ Aetiopathogenesis:
o Causative agents:
• Tuberculous protein: Most common cause previously.
• Staphylococcal protein: Most common in recent cases.
• Rarely proteins of Moraxella Anlxenfeld bacillus and certain parasites.
o Predisposing factors:
• Age group of 3-15 years.
• More in girls.
• Undernourishment.
• Overcrowded and unhygienic conditions.
• More in spring and summer season.
o Pathology: Endogenous microbial proteins → type IV hypersensitivity reaction → nodule formation in
conjunctival epithelium → necrosis and ulceration in tip of the nodule → granulation tissue formation → healing
with minimal scar formation.
❖ Clinical features:
o Symptoms:
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• Mild discomfort, irritation, redness, photophobia and reflex watering.

• These are associated with mucopurulent conjunctivitis due to secondary bacterial infection.
o Signs:
• Simple phlyctenular conjunctivitis: 1-2 typical pinkish white nodules on bulbar conjunctiva near limbus.
• Necrotizing phlyctenular conjunctivitis: Large phlycten with necrosis and ulceration near limbus.
• Miliary phlyctenular conjunctivitis: Multiple phlycten arranged haphazardly or in ring form near limbus.
• Keratitis: Secondary corneal involvement may cause ulcerative or infiltrative type phlyctenular keratitis.
❖ Diagnosis: Based on history of predisposing factors and clinical features.
❖ Differential diagnosis: Needs to be differentiated from episcleritis, scleritis and conjunctival foreign body granuloma.
❖ Management:
o Local therapy:
• Topical steroids as eye drop of dexamethasone or betamethasone.
• Antibiotic drops and ointments against secondary infection.
• Atropine (1%) eye ointment in case of corneal involvement.
o Specific therapy:
• Antitubercular treatment in case of tubercular aetiology.
• Systemic antibiotics and surgical measures in septic focus like tonsillitis, adenoiditis or caries teeth.
• Complete eradication of the parasite in case of parasitic aetiology.
o General management: High protein diet supplemented with vitamin A,C and D.

➢ Important to note:
o Ulcerative phlyctenular keratitis: May occur in the following three forms:
• Scrofulous ulcer: Shallow marginal ulcer formed due to breakdown of small limbal phlycten. Such an
ulcer usually clears up without leaving any opacity.
• Fascicular ulcer: Has a prominent parallel leash of blood vessels. This ulcer usually remains superficial
but leaves behind a band-shaped superficial opacity after healing.
• Miliary ulcer: In this form multiple small ulcers are scattered over a portion of or whole of the cornea.
o Diffuse infiltrative phlyctenular keratitis: Appear in the form of central infiltration of cornea with characteristic
rich vascularization from the periphery, all around the limbus. It may be superficial or deep.

03. Uses of atropine in ophthalmology. [2020]

❖ Pharmacology:
o Mechanism of action: Atropine is an anticholinergic or anti-muscarinic ganglion blocker.
o Mode of action: It acts as an cycloplegic and mydriatic agent.
o Route of administration: Generally used as 1% atropine sulphate eyedrop or ointment.
❖ Therapeutic use:
o Indications:
• Spasm of accommodation.
• Uveal tract pathologies: Iridocyclitis, trauma to the uveal components.
• Conjunctivitis: Acute purulent conjunctivitis, acute membranous conjunctivitis, contact dermoconjuncti-
vitis, phlyctenular keratoconjunctivitis, ophthalmia neonatorum.
• Corneal pathologies: Interstitial keratitis, neuroparalytic keratitis, herpes zoster ophthalmicus, corneal
opacities, corneal ulcer, corneal wounds.
• Against post operative complication of cataract surgery like oculo-cardiac reflex due to local anaesthesia.
• Injuries: Sympathetic ophthalmitis, chemical burn injuries, indirect globe rupture.endophthalmitis.
o Action:
• Gives comfort and rest to the eye ball by relieving spam of iris sphincter and ciliary muscles.
• Prevents the formation of synechiae and may break the already formed synechiae.
• Reduces exudation by decreasing hyperaemia and vascular permeability.
• Increases the blood supply to anterior uvea by relieving pressure on the anterior ciliary arteries. As a
result, more antibodies reach the target tissues.
o Mydricain: A mixture of atropine, adrenaline and procaine, used for more powerful cycloplegic effect.

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❖ Diagnostic use in retinoscopy:

o Used in children below the age of 5 years.
o After thrice daily use of the 1% ointment for 3 days, retinoscopy is done in the 4th day.
o Action lasts of 10-20 days.

04. Panophthalmitis. [2019, 2014]

❖ It is an intense purulent inflammation of the whole eyeball including the Tenon's capsule. The disease usually begins either
as purulent anterior or purulent posterior uveitis and soon a full-fledged picture of panophthalmitis develops, following
through a very short stage of endophthalmitis.
❖ Aetiology:
o Causative organism: Staphylococcus epidermidis and Staphylococcus aureus (most common), Streptococcus,
Pseudomonas, Pneumococci and Cyanobacterium.
o Mode of infection: May be exogenous, endogenous or secondary infection from surrounding structures.
❖ Clinical features:
o Symptoms:
• Severe ocular pain and headache.
• Complete loss of vision.
• Profuse watering.
• Purulent discharge.
• Marked redness and swelling of the eyes.
• Associated constitutional symptoms are malaise and fever.
o Signs:
• Lids show a marked oedema and hyperaemia.
• Eyeball is slightly proptosed, ocular movements are limited and painful.
• Conjunctiva shows marked chemosis and ciliary as well as conjunctiva! 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 limb us, pus comes out and intraocular pressure falls.
o Complications:
• Orbital cellulitis.
• Cavernous sinus thrombosis.
• Meningitis or encephalitis.
❖ Treatment:
o Anti-inflammatory and analgesics: Should be started immediately to relieve pain.
o Broad spectrum antibiotics: To prevent further spread of infection in the surrounding structures.
o Evisceration operation: To avoid the risk of intracranial dissemination of infection.

05. Hyphema: causes and management. [2019, 2004]

❖ The condition of collection of blood in the anterior chamber is called hyphaema.

❖ Causes:
o Blunt trauma: This is the most common cause of a hyphaema. Injury to the iris, ciliary body, trabecular
meshwork and their vasculature can tear the vessels and result in the accumulation of blood within anterior
chamber.
o Iatrogenic cause:
• Cataract surgery: Hyphaema is a common early postoperative complication after ECCE and SICS.
• Uveitis-glaucoma-hyphaema (UGH) syndrome: Rarely the placement of an IOL within the anterior
chamber can result in chronic inflammation, secondary iris neovascularization and recurrent hyphaemas.
• Laser: A hyphaema resulting from an ocular laser procedure is a possible adverse event.
o Spontaneous hyphaema:

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• Secondary to neovascularization: Diabetes mellitus, ischemia, cicatrix formation, rubeosis iridis.

• Ocular neoplasms: Retinoblastoma, angioma, iris melanoma.
• Uveitis: Herpes zoster iritis, Gonococcal iritis.
• Vascular anomalies: Juvenile xanthogranuloma.
• Coagulation problems: Haemophilia, von Willebrand disease, use of substances that alter platelet or
thrombin function (e.g. ethanol, aspirin, warfarin).
❖ Management:
o Spontaneous: Most of the hyphaemas are absorbed spontaneously and requires no treatment.
o General measures:
• Use of eye shield.
• Limited activity and 45° had elevation to settle the hyphaema inferiorly in the anterior chamber as it can
cause central visual obstruction.
• Observation for one week as this is the highest risk time frame for rebleeding.
o Medical management:
• Large hyphaema with increased IOP is treated with acetazolamide and hyperosmolar agents.
• Topical cycloplegic agents are also useful for patients with significant ciliary spasm or photophobia.
• Treatment of the underlying pathology is done.
o Surgical management:
• Anterior chamber washout: Anterior chamber irrigation and aspiration through a small incision.
• Hyphaema evacuation with closed vitrectomy instrumentation.
• Clot irrigation with a filtering procedure like trabeculectomy.
• Anterior chamber paracentesis for temporalizing control of elevated intraocular pressure.

06. Astigmatism. [2019, 2000]

❖ Absence of point focus is called astigmatism. Generally it’s of two types:

1. Regular astigmatism.
2. Irregular astigmatism.
❖ Regular astigmatism: When there are two principle meridians i.e. a step meridian and a flat meridian forming two foci.
o Types of regular astigmatism based on location of two foci with respect to retina:
• Simple: When one focus is on retina. It’s also of two types:
✓ Simple myopic astigmatism.
✓ Simple hypermetropic astigmatism.
• Compound: When both the foci are on the same side of retina. It’s also of two types:
✓ Compound myopic astigmatism.
✓ Compound hypermetropic astigmatism.
• Mixed: When one focus is in front of the retina and the other one is behind the retina.
o Types of regular astigmatism based on orientation of two principle meridians:
• With the rule: Steep meridian is vertical and flat meridian is horizontal, like a rugby ball.
• Against the rule: Steep meridian is horizontal and flat meridian is vertical, like an egg against gravity.
• Oblique: Two meridians are at right angle to each other but no one is horizontal.
• Bi-oblique: Two principle meridians are not at 90° to each other.
❖ Irregular astigmatism: When there are more than two foci and hence no geometrical analysis is impossible. This can be
due to corneal transplant, keratoconus or scarred corneas.
❖ Clinical features:
o Symptoms: Asthenopia, blurred or defective vision, elongation of objects.
o Signs: Half closure of lid, head tilt, oval or tilted optic disc, different power in two meridians.
❖ Diagnosis: By retinoscopy, keratometry, astigmatic fan test, Jackson's cross cylinder test.
❖ Management:
o Cylindrical lens: Positive/convex along steep axis and negative/concave along flat axis.
o Contact lens: Rigid gas permeable toric contact lens.
o Surgery: Toric IOL or corneal incision on steep axis by phacoemulsification.
o LASIK.

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07. Endophthalmitis. [2018]

❖ An inflammatory condition of the inner layers (fluids and tissue) of the eyeball, sparing sclera is called endophthalmitis.
❖ Aetiology:
o Infective endophthalmitis:
• Acute postoperative: Within 7 days after surgery. Staphylococcus epidermidis (CONS) is most common
cause. Staphylococcus aureus and Streptococcus can also cause endophthalmitis.
• Delayed onset postoperative/saccular: More then 6 weeks after surgery. Propionibacterium acnes is the
most common cause. Aspergillus, a fungus can also cause this.
• Post traumatic: Bacillus cereus.

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• Endogenous bacterial: In Asia the most common cause is Klebsiella. Can occur by a cutaneous infection
of Staphylococcus also.
• Endogenous fungal: Candida having roth spots and retinal haemorrhage with white or pale centre.
o Non-infective (sterile) endophthalmitis:
• Postoperative sterile endophthalmitis: Due to toxic reaction with chemicals.
• Post traumatic sterile endophthalmitis: Due to toxic reaction with retained foreign body.
• Phacoanaphylactic endophthalmitis: Due to lens protein in Morgagnian cataract.
• Intraocular tumour necrosis: Masquerade syndrome.
❖ Clinical features:
o Symptoms: Pain, redness, lacrimation, photophobia and loss of vison.
o Signs: Lid redness and swelling, circumcorneal congestion, corneal oedema, anterior chamber hypopyon,
amaurotic cat's eye reflex (Hallmark) due to vitreous turbidity.
❖ Treatment:
o Approach to treat:
• If no perception of light: Frill excision or evisceration.
• If perception of light only: Immediate pars plana vitrectomy with intravitreal antibiotics.
• If hand motion or better vision: Vitreous tap → culture → intravitreal antibiotics.
o Antibiotics: Vancomycin and ceftazidine are used.
o Antifungals: Voreconazole, amphotericin B, caspofungin.
❖ Prevention:
o Povidone Iodine (5% periocular) into the conjunctival fornices for at least 3 minutes prior to surgery is the single
best methode.
o Preoperative topical antibiotic use decreases the risk.
o lntracameral cefuroxime should be considered in high-risk cases (i.e. diabetes and vitreous loss).

08. Keratic precipitate. [2018, 2009]

❖ Keratic precipitates (KP) are collections of inflammatory cells and proteinaceous materials on the corneal endothelium.
❖ Features:
o Pathognomonic sign of anterior uveitis.
o ARLT’s triangle: Most commonly located inferiorly in a triangular pattern with the apex pointing up as a result of
gravity and normal convection flow of aqueous.
o The composition and morphology of KPs varies with the severity, duration and type of uveitis.
❖ Types:
o Mutton fat KPs:
• Seen in granulomatous uveitis.
• Composition: Epithelioid cells and macrophages.
• Appearance: Large, thick, fluffy, lardaceous, greasy or waxy.
• Number: Usually few, 10-15.
o Small and medium KPs (granular KPs):
• Seen in non-granulomatous uveitis.
• Composition: Lymphocytes.
• Appearance: Small, discrete, dirty, irregular arrangement.
• Number: Numerous.
o Fine KPs (stellate KPs):
• Seen in Fuchs heterochromic iridocyclitis, herpetic iritis, CMV retinitis, toxoplasmosis.
• Appearance: Fine, fibrillar, diffuse distribution. Typically cover entire corneal endothelium and form
endothelial dusting.
o Old KPs:
• Seen in cases of healed uveitis.
• Appearance: Pigmented, crenated margins, ground glass appearance due to hyalinization.

09. Treatment of myopia. [2020, 2018]

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❖ Myopia is a type of refractive error in which parallel rays of light coming from infinity are focused in front of the retina
when accommodation is at rest.
❖ Optical treatment:
o Spectacles: Concave or minus spheres.
o Contact lenses: In cases of high myopia, to avoid peripheral distortion and minification by spectacles.
o Orthokeratology: A non-surgical reversible method of moulding the cornea with overnight wear of unique rigid
gas permeable contact lens.
❖ Cornea based surgical treatment:
o Radial keratotomy (RK):
• Aim is to flatten the central cornea and steepen the peripheral cornea.
• Obsolete, unpredictable procedure with chance of astigmatism and regression.
o Photorefractive keratotomy (PRK): Photoablation using excimer laser to flatten the central cornea.
o Laser in-situ keratomileusis (LASIK):
• Procedure:
✓ Anterior corneal tissue flap creation with the help of femtosecond laser and elevation of flap.
✓ Photoablation using excimer laser to flatten the central cornea.
✓ Replacing the flap after the laser correction.
• Prerequisites:
✓ More than 20 years of age.
✓ Stable refraction for more than 1 year.
✓ Absence of corneal pathology.
✓ Corneal thickness less than 450 µm is an absolute contraindication.
o Small incision lenticular extraction (SMILE):
• Also called refractive lenticular extraction (ReLEx) or all-femtolaser-vision-correction.
• A bladeless, flapless technique in which a lenticule of corneal stroma is extracted with femtosecond laser.
o Intracorneal ring (ICR) implantation:
• ICR implantation into the peripheral cornea results in a vaulting effect that flattens the central cornea.
• This is an unpredictable reversible procedure with a chance of keratitis.
❖ Lens based surgical treatment:
o Refractive lens exchange (RLE): Clear lens extraction (Fucala's operation) followed by IOL implantation of
appropriate power is being recommended as a refractive surgery to correct myopia.
o Phakic refractive lens (PRL) or implantable contact lens (ICL):
• A special type of IOL is implanted in the anterior chamber, anterior to the natural crystalline lens.
• Can form endophthalmitis, iridocyclitis, cataract or secondary glaucoma.

10. Buphthalmos. [2019, 2017]

❖ Buphthalmos means ‘bull like eyes'. This is a visible enlargement of the eyeball detected before 3 years of age. As it
results due to retention of aqueous humour, it is also called hydrophthalmos.
❖ Aetiology: Conditions which can cause raised IOP in early childhood:
o Primary congenital or developmental glaucoma (most common).
o Sturge-Weber syndrome.
o Neurofibromatosis.
o Aniridia etc.
❖ Pathogenesis: Increased IOP results in increase in size of eyeball due to extreme softness and elasticity of infantile eyeball.
❖ Clinical features:
o Symptoms: Classical symptoms of primary congenital glaucoma like tearing, photophobia and irritability.
o Signs:
• Corneal signs:
✓ Increased corneal diameter.
✓ Hazy cornea.
✓ Thinning of cornea and ruptures of descemet's membrane known as Haab's striae.
✓ Presence of corneal oedema.
• Deep anterior chamber.
• Axial myopia due to increased axial length.
• Increase in the size of the globe.
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• Increased intraocular pressure.

❖ Evaluation or diagnosis: Complete examination under general anaesthesia is performed in each clinical suspected case.
o Measurement of IOP with Perkin's applanation tonometer or tonopen.
o Measurement of corneal diameter with callipers.
o Slit-lamp examination.
o Ophthalmoscopy to evaluate optic disc.
o Gonioscopic examination with Koeppe's lens.
❖ Management: Aim is to reduce IOP to prevent progressive corneal opacification and glaucomatous optic atrophy and
thereby preserve existing vision.
o Medical management: Topical Beta blockers, carbonic anhydrase inhibitors or prostaglandin analogues.
o Surgical management:
• Goniotomy: Openings are created in the trabecular meshwork, thus reducing resistance to outflow.
• Trabeculoctomy: The trabecular meshwork is incised by cannulating Schlemm's canal with a probe.
• Trabeculectomy: A section of the trabecular meshwork and Schlemm's canal is removed underneath a
partial thickness scleral flap, thus creating a fistula draining aqueous to the subconjunctival space.
• Combined trabeculoctomy and trabeculectomy: Done with antimetabolites as a standard procedure.
• Glaucoma drainage implants: Required in incalcitrant cases.

11. Nutritional blindness. [2017, 2002, 1999]

❖ Ocular manifestations of vitamin A deficiency, including not only the structural changes affecting the conjunctiva, cornea
and occasionally retina, but also the biophysical disorders of retinal rods and cones function are referred to as nutritional
blindness or xerophthalmia.
❖ Aetiology:
o Dietary deficiency of vitamin A.
o Defective absorption of vitamin a from gut.
o Accompanied by protein-energy malnutrition (PEM) and infections.
❖ Modified WHO classification:
o XN: Night blindness. This is the earliest symptom in children.
o X1A: Conjunctival xerosis. It consists of one or more patches of dry, lustreless, nonwettable conjunctiva described
as ‘emerging like sand banks at receding tide' when the child ceases cry.
o X1B: Bitot's spot. It is a raised, silvery white, foamy, triangular patch of keratinized epithelium, usually situated
bilaterally and temporally on the bulbar conjunctiva in the interpalpebral area.
o X2: Corneal xerosis. The earliest change in cornea is punctate kerayopathy in lower nasal quadrant, followed by
haziness and/or granular pebbly dryness.
o X3A: Corneal ulceration/keratomalacia affecting less than 1/3rd of corneal surface. This occurs in the late stage
due to colliquative necrosis. Peripheral small circular ulcers with steep margins and sharp demarcation are seen.
o X3B: Corneal ulceration/keratomalacia affecting more than 1/3rd of corneal surface. This results in blindness.
o XS: Corneal scar due to xerophthalmia. This occurs due to healing of stromal defect, may or may not cover pupil.
o XF: Xerophthalmic fundus. It is characterized by typical seed-like, raised, whitish lesions scattered uniformly over
the part of the fundus at the level of optic disc.
❖ Treatment:
o Local ocular therapy: For X1A, artificial tear is advised in every 3-4 hours and for X3, full-fledged treatment of
bacterial corneal ulcer is indicated.
o Vitamin A therapy: Applied in all active stages i.e. from XN to X3B. Oral administration is recommended.
• All patients above the age of 1 year (except women of reproductive age): 200,000 lU of vitamin A orally
or 100,000 IU by intramuscular injection should be given immediately on diagnosis and repeated the
following day and 4 weeks later.
• Children under the age of 1 year and children of any age who weigh less than 8 kg: They should be
treated with half the doses for patients of more than 1 year of age.
• Women of reproductive age, pregnant or not:
✓ Those having night blindness (XN), conjunctival xerosis (X1A) and Bitot's spots (X1B) should be
treated with a daily dose of 10,000 lU of vitamin A orally (1 sugar coated tablet) for 2 weeks.
✓ For corneal xerophthalmia, administration of full dosage schedule is recommended.
o Treatment of underlying conditions: PEM and other nutritional disorders, diarrhoea, dehydration and
electrolyte imbalance, infections and parasitic conditions should be considered simultaneously.

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12. Staphyloma. [2016, 2012, 2008, 2002]

❖ Staphyloma refers to a localized bulging of weak and thin outer tunic of the eyeball (cornea or sclera), lined by uveal tissue
which shines through the thinned out fibrous coat.
❖ Types: Based on location, staphylomas can be divided into 5 types.
o Anterior staphyloma:
• Cause: Ectasia of pseudocornea after sloughing corneal ulcer and corneal injuries.
• Bulging coat: Cornea.
• Lining uveal tissue: Iris.
• Iris is plastered behind the lens in this cases.
o Intercalary staphyloma:
• Cause: Ectasia of weak scar tissue, following healing of peripheral corneal ulcer and perforating injuries.
• Bulging coat: Limbus. Secondary angle closure glaucoma may cause progression of bulge if not treated.
• Lining uveal tissue: Iris root and anterior most part of ciliary body.
• Defective vision occurs due to marked corneal astigmatism.
• Treatment: Localized staphyloectomy under heavy dose of oral steroids.
o Ciliary staphyloma:
• Cause: Scleritis, perforating injuries, end stage primary or secondary glaucoma and developmental
glaucoma.
• Bulging coat: Sclera, 2-3 mm away from limbus.
• Lining uveal tissue: Ciliary body.
o Equatorial staphyloma:
• Cause: Scleritis, high or pathological myopia and chronic uncontrolled glaucoma.
• Bulging coat: Sclera in equatorial region. Most commonly occurs at the regions of sclera which are
perforated by vortex veins.
• Lining uveal tissue: Choroid.
o Posterior staphyloma:
• Cause: Pathological myopia (most common), posterior scleritis and perforating injuries.
• Bulging coat: Sclera behind the equator.
• Lining uveal tissue: Choroid.
• Investigation: Ophthalmoscopy and B scan ultrasound. The area is excavated with retinal vessels dipping
in it. Its floor is focused with minus lenses in ophthalmoscope as compared to its margins.

13. Phacolytic glaucoma. [2016, 2008]

❖ Phacolytic glaucoma, also known as lens protein glaucoma, is a lens-induced secondary open angle glaucoma.
❖ Pathogenesis: It is a type of secondary open angle glaucoma, in which trabecular meshwork is clogged by the lens
proteins, macrophages which have phagocytosed the lens proteins and inflammatory debris. Leakage of the lens proteins
occurs through an intact capsule in the hypermature (Morgagnian) cataractous lens.
❖ Clinical features:
o Symptoms:
• Acute attack severe pain in the eye radiating along the branches of 5th nerve.
• Nausea, vomiting and prostrations.
• Rapidly progressive impairment of vision, redness, photophobia and lacrimation.
• Coloured halos during an acute attack.
o Signs:
• Lids may be oedematous.
• Conjunctiva is chemosed and congested (both conjunctival and ciliary vessels are congested).
• Cornea becomes oedematous and insensitive.
• Pupil is semidilated, vertically oval and fixed. It is non-reactive to both light and accommodation.
• IOP is markedly elevated, usually between 40 and 70 mm of Hg.
• Anterior chamber may become deep and aqueous may contain fine white protein particles, which
settle down as pseudohypopyon.
• Anterior chamber angle is open on gonioscopy.
• Lens has hypermature cataract (Morgagnian cataract).
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• Optic disc is oedematous and hyperaemic.

❖ Management:
o Medical therapy to lower the IOP.
o Extraction of the hypermature cataractous lens with PCIOL implantation.

14. Paracentesis. [2016]

❖ In general paracentesis means the perforation of a cavity of the body or of a cyst or similar outgrowth, especially with a
hollow needle to remove fluid or gas. In eye, paracentesis is normally done in anterior chamber.
❖ Procedure of anterior chamber paracentesis:
o Preoperative acetazolamide, topical antibiotic and pilocarpine is administered.
o Patient is positioned in the slit lamp.
o Slit is positioned on anterior chamber and peripheral cornea.
o The cornea at 9 o’clock for right eye and 3 o’clock for left eye is punctured with a sterilized instrument.
o Aspiration of aqueous is done.
o Instrument:
• Paracentesis needle.
• 15° side port blade.
• MVR or V lance blade.
• Keratomes.
❖ Indications:
o Acute angle closure glaucoma or acute secondary glaucoma.
o As a step in phacoemulsification.
o To treat corneal ulcer with impending perforation.
o In central retinal arterial occlusion (CRAO) as an aggressive treatment procedure.
o When total hyphaema persists for more than 4 days.
o During application of iris hooks.
o Amsler's sign: In Fuch's heterochromic iridocyclitis on gonioscopy, fine-radial twig-like vessels are seen bridging
over the angle, which may bleed on paracentesis. This is called Amsler's sign.
❖ Complications:
o Risk of infringement of iris, lens or corneal endothelium that can cause malignant glaucoma.
o Rapid decompression can cause intraocular haemorrhage, decompression retinopathy or hyohaema.
o Rarely exogenous endophthalmitis.

15. Myopia. [2015, 2011, 2009, 2003]

❖ When parallel rays of light coming from infinity are focused in front of the retina when accommodation is at rest is called
myopia.
❖ Aetiological classification:
o Axial myopia: Due to increased axial length of eye ball. It is the commonest form. Seen in:
• Pathological myopia.
• Buphthalmos or congenital glaucoma.
• Posterior staphyloma.
o Curvature myopia: Due to increased curvature of cornea or lens or both. Seen in:
• Corneal pathologies like keratoconus, keratoglobous.
• Lens pathologies like lenticonous, intumescent cataract, diabetic cataract, spherophakia.
o Index myopia: Due to increased refractive index of lens nucleus. Seen in nuclear sclerosis.
o Positional myopia: Due to anterior positioning of lens. Seen in:
• Weill-Marchesani syndrome.
• Anterior dislocation of lens.
o Consecutive myopia: When an IOL is implanted such that the patient is still myopic after surgery.
❖ Clinical features: Defective vision of varying degree based on clinical varieties. AOA has defined 3 grades of myopia:
o Low myopia: ≤ -3D.
o Moderate myopia: Between -3D to -6D.
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o High myopia: ≥ -6D.

❖ Classification based on clinical varieties:
o Congenital myopia (high myopia).
o Simple or developmental myopia (most common), a physiological error not associated with any disease of eye
(low or moderate myopia).
o Pathological or degenerative or progressive myopia (high myopia).
o Acquired or secondary myopia which can be post-traumatic, post-keratitic, drug-induced, pseudomyopia, space
myopia, night myopia etc.
❖ Treatment: Group B, question no. 09.

16. Vision 2020. [2015, 2007]

❖ Vision 2020 : Right to Sight was a global initiative launched by WHO in 1999 to eliminate avoidable blindness from major
causes like:
o Cataract.
o Trachoma.
o Childhood blindness.
o Refractive errors.
o Onchocerciasis.
with a target to reduce blindness to <0.3% of population.
❖ India adopted this initiative in 2004 and included the following causes:
o Cataract.
o Childhood blindness.
o Refractive errors.
o Corneal blindness.
o Glaucoma.
o Diabetic retinopathy.
❖ Human resource development and infrastructure and technology development at various levels of health system were
made.
❖ Proposed structure:

Centre
of excellence
20
----------------------------------
Training centres
200 (1 for 5 million)
-----------------------------------------------------
Service centres 2000 (1 for 5 lakhs)
-----------------------------------------------------------------
Vision centres 20000 (1 for 50 thousand)

o Centre of excellence:
• Professional leadership.
• Strategy development.
• Continued medical education (CME).
• Laying of standard and quality assurance.
• Research.
o Training (tertiary) centres:
• Tertiary eye care including retinal surgery, corneal transplant etc.
• Training and CME.
o Service (secondary) centres:
• Cataract surgery and other common eye surgeries.
• Facilities for refraction.
• Referral services.
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o Vision (primary) centres:

• Refraction and prescription of glasses.
• Primary eye care.
• School eye screening programme.
• Screening and referral services.

17. Visual field changes in PAOG. [2015]

❖ Visual field defects appear only after about 40% of axons have been damaged and subsequently the field defects usually
run parallel to the changes at the optic nerve head and continue to progress if IOP is not controlled. These can be described
as early and late field defects.
❖ Nomenclature of glaucomatous field defects: Visual field defects in glaucoma are initially observed in Bjerrurn's area (10-
20 degrees from fixation) and correlate with optic disc changes. The natural history of the progressive glaucomatous field
loss, more or less, takes the following sequence:
o Isopter contraction: It refers lo mild generalised constriction of central as well as peripheral field. It is the earliest
visual field defect occurring in glaucoma. However, it is of limited diagnostic value, as it may also occur in many
other conditions.
o Baring of blind spot: It is also considered to be an early glaucomatous change, but is very nonspecific and thus of
limited diagnostic value. Baring of the blind spot means exclusion of the blind spot from the central field due to
inward curve of the outer boundary of 30° central field.
o Small wing-shaped paracentral scotoma: It is the earliest clinically significant field defect. It may appear either
below or above the blind spot in Bjerrum's area.
o Seidel's scotoma: With the passage of time paracentral scotoma joins the blind spot to form a sickle-shaped
scotoma known as Seidel's scotoma.
o Arcuate or Bjerrum's scotoma: It is formed at a later stage by the extension of Seidel's scotoma in an area either
above or below the fixation point to reach the horizontal line. Damage to the adjacent fibres causes a peripheral
breakthrough.
o Ring or double arcuate scotoma: It develops when the two arcuate scotomas join together.
o Roenne's central nasal step: It is created when the two arcuate scotomas run in different arcs and meet to form
a sharp right-angled defect at the horizontal meridian.
o Peripheral field defects: These appear sometimes at an early stage and sometimes only late in the disease. The
peripheral nasal step of Roenne's results from unequal contraction of the peripheral isopter.
o Advanced glaucomatous field defects: The visual field loss gradually spreads centrally as well as peripherally, and
eventually only a small island of central vision (tubular vision) and an accompanying temporal island are left. With
the continued damage, these islands of vision also progressively diminish in size until the Liny central island is
totally extinguished. The temporal island of the vision is more resistant and is lost in the end leaving the patient
with no light perception.

➢ Important to note: For better under standing of the actual field defects, it is mandatory to have a knowledge of their
anatomical basis.
o Distribution of retinal nerve fibres:
• Fibres from nasal half of the retina come directly to the optic disc as superior and inferior radiating fibres
(SRF and IRF).
• Fibres from the macular area come horizontally as papillomacular bundle (PMB).
• Fibres from the temporal retina arch above and below the macula and papillomacular bundle as superior
and inferior arcuate fibres with a horizontal raphe in between (SAF and IAF).
o Arrangement of nerve fibres within optic nerve head: Those from the peripheral part of the retina lie deep in the
retina but occupy the most peripheral (superficial) part of the optic disc. While fibres originating closer to the
nerve head lie superficially in the retina and occupy a more central (deep) portion of the disc.
• Superior and inferior arcuate nerve fibres (SAP and IAF) occupy the superior and inferior temporal
portions of optic nerve head, respectively, and are most sensitive to glaucomatous damage; accounting
for the early loss in the corresponding regions of the visual field.
• Macular fibres are most resistant to the glaucomatous damage and explain the retention of the central
vision till end.

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18. Symblepharon. [2014]

❖ Symblepharon is condition where lids become adherent with the eyeball as a result of adhesions between the palpebral
and bulbar conjunctiva.
❖ Aetiology: It results from healing of kissing raw surfaces upon the palpebral and bulbar conjunctiva. Common causes are:
o Thermal or chemical burns.
o Membranous conjunctivitis.
o Conjunctival injuries or ulcerations.
o Ocular pemphigus.
o Stevens-Johnson syndrome.
❖ Clinical features:
o Restricted ocular movement.
o Diplopia due to restricted ocular motility.
o Lagophthalmos i.e. inability to close the lids due to adhesions.
o Cosmetic disfigurement.
❖ Types: Depending upon the extent of adhesions, symblepherons are of 3 types:
o Anterior symblepharon: Adhesions present only in the anterior part.
o Posterior symblepharon: Adhesions present in the fornices.
o Total symblepharon: Adhesions involving whole of the lid.
❖ Complications:
o Dryness.
o Thickening and keratinisation of conjunctiva due to prolonged exposure.
o Corneal ulceration (exposure keratitis).
❖ Treatment:
o Prophylaxis: During the stage of raw surfaces, the adhesions may be prevented by:
• Sweeping a glass rod coated with lubricant around the fornices several times a day.
• Therapeutic soft contact lens of large size.
o Curative treatment by symblepharectomy: The raw area created may be covered by:
• Mobilising the surrounding conjunctiva in mild cases.
• Conjunctival or buccal mucosal graft is required in severe cases.
• Amniotic membrane transplantation (AMT) also gives good results.

19. Pathological myopia. [2014, 2011]

❖ Pathological myopia, also known as degenerative or progressive myopia, is a rapidly progressive error which starts in
childhood at 5-10 years of age and results in high myopia during early adults, associated with degenerative changes in eye.
❖ Aetiology:
o Hereditary (major) factors:
• Familial.
• Race: More in Chinese, Japanese, Arabs and Jews.
• Sex: More in female than male.
• Autosomal dominant 18p11.31 and 12q21.23.
• Sex-linked recessive.
• Heredity- linked growth of retina.
o Factors affecting general growth processes (minor):
• Nutritional deficiency.
• Debilitating diseases.
• Endocrine disturbances.
• Indifferent general health.
❖ Pathogenesis: Aetiological factors → more growth of retina → stretching of sclera → features of pathological myopia like
increased axial length, degeneration of choroid, retina and vitreous.
❖ Clinical features:
o Symptoms:
• Progressive defective vision with refractive error varying from -10D to -40D.
• Muscae volitantes.
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• Difficulty in night vision.

o Signs:
• Prominent eyeball.
• Blue sclera.
• Large cornea.
• Deep anterior chamber.
• Primary open angle glaucoma.
• Fundus findings in central retina:
✓ Temporal crescent.
✓ Tessellated appearance of fundus.
✓ Cracks of Bruch's membrane.
✓ Myopic choroid neovascular membrane (CNVM) with Foster-Fuchs' spot due to haemorrhage.
• Fundus findings in peripheral retina:
✓ Retinal degeneration with retinal breaks.
✓ Posterior vitreous detachment forming Weiss' reflex.
✓ Cystoid degeneration.
✓ Total retinal atrophy.
❖ Complications:
o Retinal detachment.
o Complicated posterior subcapsular cataract.
o Vitreous and choroidal haemorrhage.
o Strabismus focus convergence.
❖ Treatment: Group B, question no. 09.

20. Entropion. [2013, 1994]

❖ Entropion refers to inward rolling and rotation of the lid margin towards the globe.
❖ Aetiological classification:
o Congenital entropion: Rare condition, may be associated with microphthalmos.
Treatment: Plastic reconstruction of lid crease.
o Spastic entropion: Corneal irritation or light bandaging. Seen in old people and affects lower lid.
Treatment: Treat cause of blepharospasm, botulinum toxin to relieve spasm and surgeries (similar to senile
entropion).
o Senile (involutional) entropion: Seen in elderly and affects the lower lid due to horizontal laxity, vertical lid
instability, over-riding of pretarsal orbicularis or laxity of orbital septum.
Treatment: Modified Wheelers operation, Weiss operation, plication of inferior lid retractors (Lester Jones
operation) or Bick procedure.
o Cicatricial entropion: Seen with trachoma, burns, membranous conjunctivitis. Affects upper lid.
Treatment: Wedge resection, modified Burrows operation – tarsal fracture, Jaesche Arlt's operation.
o Mechanical entropion: Due to lack of support by the globe to the lids in case of phthisis bulbi, endophthalmitis
and after enucleation or evisceration operation.
❖ Clinical features:
o Symptoms: Occur due to rubbing of cilia against the cornea and conjunctiva.
• Foreign body sensation.
• Irritation and lacrimation.
• Photophobia.
o Signs:
• Inturning of lid margins: On examination, lid margin is found inturned. Depending upon the degree of
inturning, it can be divided into three grades:
✓ Grade I entropion: Only the posterior lid border is in rolled.
✓ Grade II entropion: Includes inturning up to the inter-marginal strip.
✓ Grade III entropion: The whole lid margin including the anterior border is inturned.
• Signs of causative disease: Scarring of palpebral conjunctiva in cicatricial entropion and horizontal lid
laxity in involutional entropion.
• Signs of complications: Recurrent corneal abrasions, superficial corneal opacities, corneal vascularization
and corneal ulceration.

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21. Clinical features of VKC. [2013]

❖ Vernal keratoconjunctivitis (VKC), also known as spring catarrh, is a recurrent, bilateral, interstitial, self-limiting, allergic
inflammation of the conjunctiva having a periodic seasonal incidence.
❖ Clinical course of disease is often self-limiting and usually burns out spontaneously after 5-10 years.
❖ Symptoms:
o Marked intolerable burning and itching sensation, when patient comes in a warm humid atmosphere. Itching is
more marked with palpebral form of disease.
o Other associated symptoms include mild photophobia, lacrimation, stringy (ropy) discharge and heaviness of lids.
❖ Signs of conjunctivitis: Signs can be described in following three clinical forms:
o Palpebral form: Usually upper tarsal conjunctiva of both eyes is involved.
• Typical lesion is the presence of hard, flat topped, papillae arranged in a ‘cobble-stone’ or ‘pavement
stone’ fashion along with conjunctival hyperaemia.
• In severe cases, papillae may hypertrophy to produce cauliflower-like excrescences of ‘giant papillae’.
o Bulbar limbal form:
• Dusky red triangular congestion of bulbar conjunctiva in palpebral area.
• Limbal papillae occur as gelatinous, thickened confluent accumulation of tissue around the limbus.
• Presence of discrete whitish raised dots along the limbus (Horner-Tranta's spots).
o Mixed form: It shows combined features of both palpebral and bulbar forms.
❖ Signs of vernal keratopathy: Corneal involvement in VKC, more frequent with palpebral form.
o Punctate epithelial keratitis stained with rose bengal and fluorescein dye.
o Frank epithelial erosions.
o Vernal corneal plaques.
o Ulcerative vernal keratitis (shield ulceration).
o Subepilhelial scarring occurs in the form of a ring scar.
o Pseudogerontoxon can develop in recurrent limbal disease and is characterised by a classical ‘cupid's bow’ outline.
❖ Other signs:
o Dennie-Morgan line: An extra lower lid crease.
o Maxwell-Lyon sign: Pseudomembrane formation due to ropy discharge, when the upper eyelid is everted and
exposed to heat.
o Keratoconus is common.

22. Acute dacryocystitis. [2013]

❖ Acute dacryocystitis is an acute suppurative inflammation of the lacrimal sac, characterised by presence of a painful
swelling in the region of sac.
❖ Aetiology:
o Acute dacryocystitis may develop in two ways:
• As an acute exacerbation of chronic dacryocystitis.
• As an acute peridacryocystitis due to direct involvement from the neighbouring infected structures such
as: paranasal sinuses, surrounding bones and dental abscess or caries teeth in the upper jaw.
o Causative organisms: Streptococcus haemolyticus, Pneumococcus and Staphylococcus.
❖ Clinical features: This can be divided into 3 stages:
o Stage of cellulitis:
• It is characterised by a red, hot, firm and painful swelling in the region of lacrimal sac associated with
epiphora and constitutional symptoms such as fever and malaise.
• Redness and oedema also spread to the lids and cheek.
o Stage of lacrimal abscess:
• Continued inflammation → occlusion of the canaliculi due to oedema → sac filled with pus → distension
and rupture of anterior wall of the sac → lacrimal abscess formation.
• It usually points below and to the outer side of the sac.
o Stage of fistula formation:
• External fistula: When the lacrimal abscess is left unattended, it discharges spontaneously, leaving an
external fistula below the medial palpebral ligament.
• Internal fistula: Rarely the abscess may open up into the nasal cavity forming an internal fistula.

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❖ Complications:
o Acute conjunctivitis.
o Conversion of corneal abrasion into corneal ulceration.
o Lid abscess.
o Osteomyelitis of lacrimal bone.
o Orbital cellulitis.
o Facial cellulitis and acute ethmoiditis.
o Rarely cavernous sinus thrombosis and very rarely generalized septicaemia.
❖ Treatment:
o During cellulitis stage: Systemic and topical antibiotics to control infection and systemic anti-inflammatory
analgesic drugs and hot fomentation to relieve pain and swelling.
o During stage of lacrimal abscess: Above treatment along with pus drainage by a small incision. Later on depending
upon condition of the lacrimal sac either DCT or OCR operation should be carried out to stop recurrence.
o Treatment of external lacrimal fistula: Systemic antibiotics followed by fistulectomy along with DCT or OCR.

23. Evisceration. [2014, 2012]

❖ Evisceration is the removal of the contents of the eyeball leaving behind the sclera. Frill evisceration is preferred over
simple evisceration. In it, only about 3 mm frill of the sclera is left around the optic nerve.
❖ Indications:
o Panophthalmitis.
o Expulsive choroidal haemorrhage.
o Bleeding anterior staphyloma.
❖ Surgical steps of frill evisceration:
o Separation of conjunctiva and Tenon's capsule: Conjunctiva is incised all around the limbus with the help of spring
scissors. Undermining of the conjunctiva and Tenon's capsule is done combinedly, all around up to the equator,
using blunt-tipped curved scissors. This manoeuvre exposes the extraocular muscles.
o Removal of cornea: A cut at the limbus is made with a razor blade fragment or with a No. 11 scalpel blade and
then the cornea is excised with corneoscleral scissors.
o Removal of intraocular contents: The uveal tissue is separated from the sclera with the help of an evisceration
spatula and the contents are scooped out using the evisceration curette.
o Separation of extraocular muscles: The rectus muscles are pulled out one by one with the help of a muscle hook
and a 3-0 silk suture is passed near the insertion of each muscle. The muscle is then cut with the help of tenotomy
scissors leaving behind a small stump carrying the suture. The inferior and superior oblique muscles are hooked
out and cut near the globe.
o Removal of sclera: Using curved scissors the sclera is excised leaving behind only a 3 mm frill around optic nerve.
o Closure of conjunctiva and Tenon's capsule: These are done separately. Tenon's capsule is sutured horizontally
with 6-0 vicryl or chromic catgut. Conjunctiva is sutured vertically so that conjunctival fornices are retained deep
with 6-0 silk sutures which are removed after 8-10 days.
o Post-surgical procedures: After completion of surgery, antibiotic ointment is applied, lids are closed and dressing
is done with firm pressure using sterile eye pads and a bandage.

24. Biometry. [2018, 2012]

❖ Biometry is the process of measuring the power of the cornea (keratometry) and the length of the eye, and using this data
to determine the ideal intraocular lens power.
❖ The basic formulas for determining IOL power introduced earlier the regression formula called SRK (Sanders, Retzlaff and
Kraff) formula is:
P = A - 2.5L - 0.9K
Where,
P = The power of IOL.
A = Constant, which is specific for each lens type.
L = The axial length of the eyeball in mm, which is determined by A-scan ultrasonography.
K = Average corneal curvature, which is determined by keratornetry.
Assumption: PC-IOL is placed in the capsular bah so that the patient is emmetropic from distance.
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❖ For accurate IOL power calculation, various new formulae are available for use in different eyes (emmetropic, myopic,
hypermetropic). These include:
o SRK-T.
o Holladay-1.
o Holladay-2.
o Hoffer-Q.
o Haigis.
o Barret.
o Olsen.
o Hiel-RBF.
The newer biometers have in-built software for the newer formulae.
❖ Limitations: All IOL power calculation formulae give spherical power only. Nowadays for correcting associated astigmatism
toric-IOLs are also used, for which online toric power calculators are also available.
❖ Equipment for biometry:
o A-scan ultrasonic biometer: The ultrasound machine equipped with A-scan and IOL power calculation software is
called Biometer.
o Optical biometers: These are non-contact optical devices based on the principle of partial coherence
interferometry (PCI). These are quick and more accurate devices. Commercially available optical biometers are:
• IOL Master Tm (Zeiss Humphrey system).
• Lenstar.

25. Vernal conjunctivitis. [2011, 2007, 2005]

❖ Vernal conjunctivitis, also known as spring catarrh, is a recurrent, bilateral, interstitial, self-limiting, allergic inflammation
of the conjunctiva having a periodic seasonal incidence.
❖ Aetiopathogenesis:
o Predisposing factors:
• Age: 4-20 years.
• Sex: More in boys than girls.
• Season: Common in summer, also known as ‘warm weather conjunctivitis’.
• Climate: Tropical > temperate > cold climate.
• Other atopic manifestations: Eczema, asthma.
• Family history.
o Pathology: Allergens in conjunctiva → Th2 lymphocyte alteration and exaggerated IgE response ( type I and II
hypersensitivity) → inflammation of all layers of conjunctiva along with conjunctival vessels → multiple papillae
formation in tarsal conjunctiva.
❖ Clinical features: Group B, question no. 21.
❖ Diagnosis: Based on history of predisposing factors and clinical features.
❖ Differential diagnosis: Needs to be differentiated from atopic keratoconjunctivitis, trachoma with papillary hypertrophy.
❖ Management:
o Cool compresses.
o Topical Antihistamines.
o Topical Mast cell stabilizers: Sodium cromoglycatea, nedocromil, lodoxamide, pemirolast.
o Topical dual action drugs: Azelastine 0.05%, ketotifen, olopatadine 2%, bepelastine, alcaftadine. These are the
drugs of choice.
o Oral Antihistamines: Only in severe cases as they may also decrease tear production.
o Topical steroids: Usually added as initial therapy in acute exacerbations. Taper after episode subsides.
o Mucolytic agent: Acetylcysteine 10% or 20%.
o Antibiotics and steroids for shield ulcer.
o Surgical excision for extraordinarily large papillae.

26. Clinical features and management of chronic dacryocystitis. [2010]

❖ Chronic dacryocystitis i.e. chronic inflammation of the lacrimal gland is the most common variety of adult dacryocystitis.
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❖ Clinical features: Clinical features of chronic dacryocystitis can be divided into four stages:
o Stage of chronic catarrhal dacryocystitis: Mild inflammation of the lacrimal sac associated with blockage of NLD.
• Symptoms: Watering eye, sometimes associated with mild redness in the inner canthus.
• Signs:
✓ Syringing of the lacrimal sac: Regurgitation of clear fluid or fibrinous mucoid flakes regurgitate.
✓ Dacryocystography: Blocked NLD, a normal-sized lacrimal sac with healthy mucosa.
o Stage of lacrimal mucocele: Chronic stagnation causing distension of lacrimal sac.
• Symptoms: Constant epiphora associated with a swelling just below the inner canthus. Encysted
mucocele may be seen.
• Signs:
✓ Regurgitation test: Regurgitation of milky or gelatinous mucoid fluid from the lower punctum.
✓ Dacryocystography: Distended sac with blocked NLD.
o Stage of chronic suppurative dacryocystitis: Due to pyogenic infection, conversation of mucocele into ‘pyocoele’.
• Symptoms: Epiphora, associated recurrent conjunctivitis and swelling at the inner canthus with mild
erythema of the overlying skin. Encysted pyocoele may be seen.
• Signs: Regurgitation test: Registration of a frank purulent fluid from the lower puncntm.
o Stage of chronic fibrotic sac: Small fibrotic sac formation by thickening of mucosa.
• Symptoms: Persistent epiphora and discharge.
• Signs: Dacryocystography: Very small sac with irregular folds in the mucosa.
❖ Management:
o Conservative treatment: Probing and lacrimal syringing in early cases only.
o Balloon catheter dilation: Also known as balloon dacryocystoplasry. Used in patient with partial NLD obstruction.
o Dacryocystorhinostomy (DCR): It is the operation of choice as it re-establishes the lacrimal drainage. Post-
operative topical antibiotic application and repeated lacrimal syringings are done.
o Dacryocystectomy (DCT): Performed if DCR is contraindicated. Indications of DCT are:
• Too old patient.
• Markedly shrunken and fibrosed sac.
• Tuberculosis, syphilis, leprosy or mycotic infections of sac.
• Tumours of sac.
• Gross nasal diseases like atrophic rhinitis.
o Conjunctivodacryocystorhinostomy (CDCR): It is performed in the presence of blocked canaliculi.

27. Various methods of visual acuity determination. [2010]

❖ Visual acuity should be tested in all cases, as it may be affected in numerous ocular disorders. In real sense acuity of vision
is a retinal function of the macular area concerned with the appreciation of form sense.
❖ Distant visual acuity:
o Snellen's test types: The fact that two distant points can be visible as separate only when they subtend an angle
of 1 minute at the nodal point of the eye, forms the basis of Snellen's test-types.
Description: It consists of a series of black capital letters on a white board, arranged in lines, each progressively
diminishing in size. The lines comprising the letters have such a breadth that they will subtend an angle of 1 min
at the nodal point. Each letter of the chart is so designed that it fits in a square, the sides of which are five times
the breadth of the constituent lines. Thus, at the given distance, each letter subtends an angle of 5 min at the
nodal point of the eye. The letters of the top line of Snellen's chart should be read clearly at a distance of 60 m.
Similarly, the letters in the subsequent limes should be read from a distance of 36, 24, 18, 12, 9, 6 and 5 m
respectively, by a person with normal vision.
o Other tests which are based on the same principle as Snellen's test types:
• Simple picture chart: Used for children more 2 years.
• Landolt's C-chart: Used for illiterate patients.
• B-chart: Used for illiterate patients.
o LogMAR visual acuity charts: LogMAR stands for Logarithm of the Minimum Angle of Resolution. A LogMAR chart
comprises rows of letters and has equal number of letters in each line. It is used at a distance of 4 meters. It is
designed to enable a more accurate estimate of acuity as compared to other charts, for this reason, it is now
recommended in research settings.
❖ Near visual acuity: 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. In near vision charts, a series of different sizes of printer type are arranged in
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increasing order and marked accordingly. Commonly used near vision charts are:
o Jaeger's chart: ln this chart, prints are marked from 1 to 7 and accordingly patient's acuity is labelled as JI to J7
depending upon the print he can read.
o Roman test types: According to this chart, the near vision is recorded as N5, N8, N10, N12 and N18 (Printer's point
system).
o Snellen's near vision test types: Prepared by reducing, thickness of Snellen's distance vision chart.

28. Esotropia. [2010]

❖ Esotropia, also known as concomitant convergent squint, denotes inward deviation of one eye and is the most common
type of squint in children. It can be unilateral or alternating.

→ Essential infantile esotropia

→ Non-accomodative esotropia
→ Acquired non-accomodative esotropia
→ Esotropia
→ Refractive accommodative esotropia
→ Accomodative esotropia
→ Non-refractive accommodative esotropia

❖ Essential infantile esotropia:

o Most common type of congenital esotropia.
o Present by 4-6 months of age.
o No refractory error.
o Large angle esodeviation (> 30 pd).
o Alternate fixation in primary gaze or cross fixation.
o BSV does not develop and amblyopia may be seen.
o Treatment:
• Prevent amblyopia by occlusion therapy.
• Early surgery: Treatment of choice (by 12 months of age). MR recession and LR resection is done.
• Botulinum Toxin A into medial rectus → chemodenervation → temporary paralysis.
❖ Acquired non-accomodative esotropia: This group includes all those acquired primary esodeviations in which amount of
deviation is not affected by the state of accommodation. lt includes:
o Essential acquired or late onset esotropia: Most common variant and is of three types:
• Basic type.
• Convergence excess type.
• Divergence insufficiency type.
o Acute concomitant esotropia.
o Cyclic esotropia.
o Nystagmus blockage syndrome.
o Esotropia in myopia and microtropia.
❖ Refractive accommodative esotropia:
o Normal AC/A ratio (accommodative convergence / accommodation).
o Due to hypermetropia from +2D to +7D as increased accommodative effort to clearly focus on the near work
(increased accommodation) → increased convergence occurs as a part of near reflex (increased accommodative
convergence).
o Esotropia in distance ≥ near.
o Treatment:
• Spectacles: Full cycloplegic correction. Unifocal convex spectacles.
• Orthoptic exercises.
• Surgeries: Recession and resection, bimedial recession.
❖ Non-refractive accommodative esotropia:
o High AC/A ratio.
o Due to either increased convergence or decreased accommodation.
o Esotropia at distance < near.
o Treatment:
• Spectacles: Full cycloplegic correction. Bifocals with near add.
• Surgeries: Bimedial recession is surgery of choice. FADEN (retro equatorial myoexy) can also be done.
• Miotics: Echothiophate, DEP.
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29. Hypermature cataract. [2009, 2004, 1999]

❖ When the mature cataract is left in situ, the stage of hypermaturity sets in. The hypermature cataract may occur in any of
the following two forms:
1. Morgagnian hypermature cataract.
2. Sclerotic type hypermature cataract.
❖ Morgagnian hypermature cataract:
o Appearance of the lens:
• Cortex: Liquefies into milky white fluid and the lens is converted into a bag containing the fluid.
• Nucleus: Small brownish nucleus settles at bottom, altering its position with change in position of head.
• Capsule: The capsule is wrinkled and leaky in nature. Sometimes, calcium deposits may also be seen.
o Symptoms: Patient comes with profound visual loss.
o Signs:
• Visual acuity: Only perception of light is present.
• Colour of lens: Milky white.
• Irish shadow: Absent.
• Distant direct ophthalmoscopy with dilated pupil: No red glow, milky white pupil.
• Slit-lamp examination: Focus above the nucleus shows a triangular area bounded anteriorly and
posteriorly by the anterior and posterior lens capsule and the base of the triangle formed by the lens
nucleus. This is called the triangle sign.
• Refraction or retinoscopy: Not possible.
❖ Sclerotic type hypermature cataract:
o Appearance of lens:
• Cortex: Cortex becomes degenerated and lens becomes shrunken due to leakage of water.
• Capsule: Anterior capsule is wrinkled and thickened due to proliferation of anterior cells.
o Symptoms: Patient comes with profound visual loss.
o Signs:
• Visual acuity: Only perception of light is present.
• Colour of lens: Dirty white with hyper white spots and calcific plaques.
• Irish shadow: Absent.
• Distant direct ophthalmoscopy with dilated pupil: No red glow, dirty white pupil.
• Slit-lamp examination: Shrunken cataractous lens with thickened anterior capsule, deep anterior
chamber and tremulous iris (iridodonesis).
• Refraction or retinoscopy: Not possible.
❖ Management: Surgical removal of the cataractous lens followed by intraocular lens implantation is the treatment of choice.
o Extracapsular cataract extraction (ECCE), small incision cataract surgery (SICS) or phacoemulsification can be
performed for the cataract extraction.
o Intraocular lens scaffold technique is used to prevent posterior capsule rupture during phacoemulsification.
❖ Complications:
o Phacoanaphylactic uveitis: Due to leakage of lens protein in anterior chamber leading to Ag-Ab reaction.
o Lens induced glaucoma:
• Phacolytic glaucoma in morgagnian type.
• Phacotopic glaucoma in sclerotic type.
o Subluxation or dislocation of lens due to degeneration of zonules, mostly seen in sclerotic type.

30. Complications of myopia. [2008, 2005]

❖ When parallel rays of light coming from infinity are focused in front of the retina when accommodation is at rest is called
myopia.
❖ Complications:
o Peripheral retinal detachment: Myopia → longer axial length → mechanical stretching and thinning of retinal
layer → increased chance of peripheral retinal tear → retinal detachment and degeneration.
o Central retinal degenerative changes:
• Posterior staphyloma.

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• Lacquer cracks.
• Chorioretinal atrophy.
o Myopic macular degeneration (maculopathy): It may show further complication like atrophic changes or
choroidal neovascular membrane (CNV) formation, which leads to loss of central vision.
o Complicated cataract: The exact mechanism of cataract formation in myopia is not still fully known. Mostly
posterior subcapsular cataract, nuclear cataract and occasionally cortical cataract are seen. Cataract is one of the
most common cause of blindness in case of pathological myopia.
o Choroidal haemorrhage: Myopia → longer axial length → mechanical stretching and thinning of choroidal layer
→ concomitant vascular changes → increased chance of choroidal haemorrhage.
o Vitreous haemorrhage: Myopia along with choroidal haemorrhage, can also precipitate vitreous haemorrhage.
o Strabismus focus convergence.
o Primary open angle glaucoma: Myopia → longer axial length and vitreous chamber depth → higher cup-disc ratio
(CDR) → increased optic nerve fibre layer defects and greater deformability of the lamina cribrosa → higher
susceptibility to glaucomatous optic disc changes. Glaucoma is one of the most common cause of blindness in
case of pathological myopia.

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Note:

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Group – C
01. Describe the clinical features and management of acute iridocyclitis. 5+5 [2020, 2013, 2011, 2004]

Clinical features of acute iridocyclitis:

❖ Acute iridocyclitis is a sudden symptomatic inflammation of the uveal tissue from iris up to pars plicata of ciliary body i.e.
anterior uveal tissue.
❖ Symptoms:
o Pain: Ocular pain along with the distribution of 5th nerve, especially towards forehead and scalp, worse at night.
o Redness: Due to circumcorneal congestion.
o Photophobia and blepharospasm: Due to a reflex between sensory fibres of 5th nerve and motor fibres of 7th
nerve, supplying the orbicularis oculi muscle.
o Lacrimation: Due to lachrymatory reflex.
o Defective vision: Acute slight blurring of vision due to ciliary spasm, corneal haze, vitreous haze, pupillary block.
❖ Signs:
o Lid oedema.
o Circumcorneal congestion.
o Corneal signs:
• Corneal oedema.
• Keratic precipitates (KPs): KPs are the pathognomonic sign. These are proteinaceous cellular deposits
occurring at the back of cornea. In acute cases, small and medium KPs (granular KPs) are mostly seen.
o Anterior chamber signs:
• Aqueous cells: It is an early feature. They indicate disease activity and their number reflects severity.
Cells are counted under slit-lamp beam and graded as per ‘Standardization of Uveitis Nomenclature
(SUN)’ as below:
– = < 1 cell. +1 = 6-15 cells. +3 = 26-50 cells.
± = 1-5 cells. +2 = 16-25 cells. +4 = > 50 cells.
• Aqueous flare: It is the earliest sign and occurs due to leakage of protein particles into the aqueous from
the damaged blood vessels. This can also be graded as per SUN as below:
0 = No aqueous flare. +3 = Marked flare (iris and lens details hazy).
+1 = Faint i.e. just detectable. +4 = Intense flare ( fibrin or plastic aqueous).
+2 = Moderate flare with clear iris and lens details.
• Hypopyon: Pus in anterior chamber, e.g. dense immobile hypopyon in HLA-B27 acute anterior uveitis,
shifting mobile hypopyon in Behcet's disease.
• Hyphaema: Blood in anterior chamber.
o Iris signs:
• Loss of normal pattern due to oedema and waterlogging of iris.
• Muddy in colour.
• Iris nodules: Koeppe's nodule in pupillary border, Busacca's nodule in body of iris.
• Posterior synechiae: Adhesion between the posterior surface of the iris and anterior capsule of lens or
anterior hyaloid face due organisation of the fibrin-rich exudates. Posterior synechiae is of three types:
segmental, annular (ring or 360°) and total.
o Pupillary sign:
• Narrow pupil: Due to irritation of sphincter pupillae by toxins.
• Entropion pupil: Eversion of pupil margin due to contraction of fibrous exudate on anterior iris surface.
• Pupillary reaction: Sluggish or absent due to oedema or hyperaemia of iris.
• Irregular pupil: Seen in segmental synechiae. Dilatation with mydriatic results in festooned pupil.
• Seclusio pupillae: No circulation of aqueous humour from posterior to anterior chamber due to annular
synechiae.
• Occlusio pupillae: Occlusion of pupil by exudates in total synechiae.
o Changes in the lens:
• Pigment dispersal on anterior capsule.
• Pigment deposition in acute plastic type uveitis.
o Exudates and inflammatory cells may be seen in anterior vitreous.

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o IOP may be:

• Normal.
• Increased in secondary glaucoma after seclusio pupillae.
• Decreased after acute ciliary shock.

Management of acute iridocyclitis:

❖ Nonspecific treatment:
o Local therapy:
• Cycloplegics: 1% atropine sulphate eye ointment or drop is instilled 2-3 times a day. In case of atropine
allergy, 2% homatropine or 1% cyclopentolate eye drop can be used. These can:
✓ Give comfort and rest to the eye by relieving spasm of iris sphincter and ciliary muscle.
✓ Prevent synechiae formation and break preformed synechiae.
✓ Reduce exudation by decreasing hyperaemia and vascular permeability.
✓ Increase antibody concentration and toxin absorption by increasing blood supply to anterior
uvea by repeating pressure on the anterior ciliary arteries.
• Corticosteroids: Dexamethasone, betamethasone, hydrocortisone or prednisolone eye ointment or drop
or anterior sub-Tenon injection is used to decrease inflammation, allergy and fibrosis.
• Broad spectrum antibiotics: Used with topical steroids to provide an umbrella cover for them.
o Systemic therapy:
• Corticosteroids: If topical therapy is unresponsive.
• NSAIDs: Aspirin is used when systemic steroid therapy is contraindicated. Phenylbutazone or oxyphenbu-
tazone are used in uveitis with rheumatoid disease; naproxen in uveitis with ankylosing spondylitis.
• Immunosuppresants: Cyclophosphamide, azathioprine, methotrexate are used in extremely severe case.
• Antibiotics: Azithromycin, tetracycline or erythromycin is used to treat chlamydial infection and uveitis
with Reiter's syndrome.
o Physical measures:
• Hot fomentation: To reduce pain, venous stasis and increase circulation.
• Dark goggles: To give comfort against photophobia.
❖ Specific treatment of cause: In case of relapse or if nonspecific treatment is unresponsive, underlying cause should be
diagnosed and treated as such.
❖ Treatment of complications:
o Inflammatory glaucoma: Drugs to reduce IOP (0.5% timolol, acetazolamide) are indicated.
o Post-inflammatory glaucoma: As it occurs due to ring synechiae, laser or surgical iridectomy is done.
o Complicated cataract: Lens extraction. Presence of KPs is considered a contraindication for intraocular surgery.
o Retinal detachment: Tractional detachment requires vitrectomy.
o Phthisis bulbi: Removal by enucleation, especially when it is painful.

02. Describe the clinical features of iridocyclitis. Differentiate it from acute PACG? 5+5 [2008, 2000, 1998, 1994]

Clinical features of acute iridocyclitis: Group C, question no. 01.

Difference between iridocyclitis and acute PACG: See bellow, important to note.

➢ Important to note: Difference between acute conjunctivitis, acute iridocyclitis and acute PACG:

Features Acute conjunctivitis Acute iridocyclitis Acute PACG

Onset Gradual Gradual Sudden
Pain in eye Mild discomfort Moderate Severe
Pain along Vth nerve Absent Along 1st division of Vth nerve Along the entire Vth nerve
Discharge Mucopurulent Watery Watery
Coloured halos May be present Absent Present
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Vision Good Slightly impaired Markedly impaired

Congestion Superficial conjunctival Deep ciliary Deep ciliary
Tenderness Absent Marked Marked
Pupil Normal Small and irregular Large and vertically oval
Media Clear Hazy due to KPs, aqueous flare Hazy due to corneal oedema
Anterior chamber Normal May be deep Very shallow
Iris Normal Muddy Oedematous
IOP Normal Normal Raised
Constitutional symptoms Absent Little Prostration and vomiting

03. Write about the preoperative workup of a patient planned for cataract surgery. How do you assess the visual
prognosis in such a case? 5+5 [2019, 1998]

Preoperative workup in cataract surgery:

❖ Aim of preoperative workup:

o To detect underlying local or systemic pathology, which can affect the management adversely.
o To prevent intraoperative or postoperative complications.
o To calculate the power of IOL.
❖ Ocular examinations:
o Examination of pupil: Pupil should be examined to check:
• Light reactions and RAPD.
• Ability of the pupil to dilate adequately.
o Examination of anterior segment: Done by slit-lamp biomicroscopy.
• Corneal examination: To note any scarring, endothelial status (guttata).
• Specular microscopy: In patients with suspicion of endothelial dystrophy, it should be done for
endothelial cell count and morphology. Special care is needed if cell count below is 1500 cell/mm 2
(normal 2000-2500).
• KPs: Presence of KPs suggest management of subtle uveitis before surgery.
• Lens examination: Morphology, maturity of cataract and grading of nuclear sclerosis is important for
planning of phacoemulsification surgery.
• Other signs: Posterior synechiae, pseudoexfoliation, iridodonesis, pigment of anterior lens capsule and
anterior chamber depth would also be evaluated before surgery.
o Examination of IOP: After applanation tonometry, if IOP is found to be increased, it needs priority management.
o Examination of lids and conjunctiva: As in presence of any pathogen, surgery cannot be carried out, examination
should be done to rule out conjunctival infections, blepharitis, meibomitis etc. In doubtful cases, conjunctival swab
culture and sensitivity should be carried out.
o Examination of lacrimal apparatus: To rule out lacrimal sac infections. Lacrimal syringing should be done in
patients with history of persistent watering. If chronic dacryocystitis is discovered, DCR or DCT should be done
before surgery.
o Examination of fundus: Should be carried out with special attention on macula to rule out other causes of
decreased vision. Indirect ophthalmoscopy may be useful in hazy media.
o Examination of retina: Objective tests like USG, ERG, EOG and VEG (visually evoked response) are done to rule
out any retinal pathology.
❖ Calculation of intraocular lens power: Group B, question no. 24.

Assessment of visual prognosis in cataract surgery:

❖ Ocular examination:
o Visual status assessment:
• Visual acuity: Should be noted unaided, best corrected and with pin hole testing for good prognosis.
• Perception of light (PL): Must be noted. Absence of PL indicates nil visual prognosis.
• Projection of light rays (PR):

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✓ It is a crude but an important and easy test for function of the peripheral retina. It is tested in a
semi-dark room with the opposite eye covered. A thin beam of light is thrown in the patient's
eye from four directions (up, down, medial and lateral) and the patient is asked to look straight
ahead and point out the direction from which the light seems to come.
✓ Inaccurate PR may be due to old retinal detachment, visual pathway detects, advanced
glaucoma, large area of chorio-retinal atrophy and indicated poor prognosis.
✓ Sometimes in dense cataract PR may be inaccurate with good visual prognosis.
• Potential visual acuity tests: These may be required in the presence of dense opaque media (advanced
stages of cataract) includes:
✓ Laser interferometry (LI).
✓ Potential acuity meter (PAM) test.
o Macular function tests: These are important to predict the visual prognosis in patients with very dense cataracts.
Normal macular function indicates good prognosis. A few simple macular functions tests are as below:
• Two-light discrimination test: The patient is asked to look through an opaque disc perforated with two
pin-holes behind which a light is held. The holes are 2 inches apart and kept about 2 feet away from the
eye. If the patient can perceive two lights, it indicates normal macular function.
• Maddox rod test: The patient is asked to look at a distant bright light through a Maddox rod. An accurate
perception of red line indicates normal function.
• Colour perception: It indicates that some macular function is present and optic nerve is relatively normal.
• Purkinje’s entoptic view of retina: Patient can see his whole retinal vessels, after pressing the lower
lid with an illuminated bulb. An intelligent patient may be able to detect a patch of choroiditis or macular
degeneration.
• Blue-field entoptoscopy: It allows the observation of one’s own leukocytes (flying corpuscles) flowing in
macular retinal capillaries.
• Illuminated Amsler’s grid test: Assessed macular function in eyes with visual acuity of 6/60 or less.
• Modified photostress test: This is with the help of an indirect ophthalmoscope with at least 6 volts of
illumination. A prolonged recovery time indicates a maculopathy.
❖ General systemic examination: Also called pre-anaesthetic check-up (PAC). This is done to exclude the presence of
systemic diseases which can affect visual prognosis. These diseases are:
o Hypertension.
o Diabetes mellitus.
o Cardiac problems.
o Obstructive lung disorders.
o Any potential source of infection in the body such as septic gums, urinary tract infection etc.

04. Describe the symptoms, signs and management of Retinoblastoma. 5+5 [2019]

Clinical features of retinoblastoma:

❖ Manifestations of intraocular stage:

o Quiescent presentations:
• Leucocoria: Also called yellow-white pupillary reflex or amaurotic cat's eye appearance, is the most co-
mmon presenting feature (60%).
• Squint: Convergent squint is the second most common presentation (20%).
• Others: Nystagmus, defective vision.
o Painful red eye presentations: Quiescent stage, if left untreated, may present severe pain, redness and watering
due to:
• Acute secondary glaucoma: It may occur due to:
✓ Tumour pushing the lens-iris diaphragm forward.
✓ Tumour cells clogging the trabecular meshwork.
✓ Neovascular glaucoma.
Presentations like buphthalmos, proptosis, conjunctival congestion, hazy cornea, ↑ IOP are also seen.
• Apparent intraocular inflammation: Acute uveitis with pseudohypopyon and/or hypopyon is the presen-
ting mode (retinoblastoma masquerading as iridocyclitis).
• Orbital inflammation: Mimicking preseptal or orbital cellulitis like presentation occurs with necrotic
tumours.
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o Growth pattern: In early stage, before the appearance of leucocoria, ophthalmoscopic examination reveals many
types of growth patterns of retinoblastoma.
• Endophytic: Most common, from retina grows into the vitreous.
• Exophytic: From retina grows towards choroid, leading to serous retinal detachment and diffuse retinal
thickening.
• Mixed: Growth having features of both.
• Diffuse infiltrating: Tumour shows just a placoid thickness of retina and not a mass.
❖ Manifestations of extraocular extensions:
o Globe bursts through the sclera near the limbus or optic disc, due to progressive enlargement of tumour.
o Marked proptosis due to rapid fungation and involvement of extraocular tissues.
❖ Manifestations of distant metastasis:
o Direct extension: Spreads to CSF i.e. subarachnoid space via optic nerve. Brain is the most common organ for
metastasis.
o Lymphatic spread: Preauricular and neighbouring LNs.

Management of retinoblastoma:

❖ International classification of retinoblastoma (ICRB): This classification is followed to decide the treatment modality.

Group Risk Specifications

Group A Very low Size < 3 mm, confined to retina, located > 3 mm from fovea and > 1.5 mm from the optic disc.
Group B Low Size > 3 mm and any size tumours located < 3 mm from fovea and < 1.5 mm from the optic disc.
Group C Moderate Focal seeds characterized by subretinal and or vitreous seeds ≤ 3 mm from retinoblastoma.
Group D High Diffuse seeds characterized by subretinal and or vitreous seeds > 3 mm from retinoblastoma.
Extensive retinoblastoma characterized by any of the following: tumour touching the lens,
neovascular glaucoma, tumour anterior to anterior vitreous face involving ciliary body and anterior
Group E Very high segment, diffuse infiltrating tumour, opaque media with haemorrhage, tumour necrosis with
aseptic orbital cellulitis, invasion of postlaminar optic nerve, choroid, sclera, orbit and anterior
chamber or phthisis bulbi.

❖ Conservative tumour destructive therapy to salvage eyeball: Treatment of choice for group A to D.
o Chemotherapy: Treatment of choice for group A to C.
• CVE regimen: 3 weekly 6 cycles of carboplatin on day 1, vincristine on day 1 and etoposide on day 1 & 2.
• Intra arterial chemotherapy by ophthalmic artery cannulation is done for targeted therapy.
o Focal treatment:
• Laser photocoagulation by diode laser.
• Cryotherapy only for peripheral tumours.
o Radiation:
• Brachytherapy.
• External beam radiation therapy (EBRT).
❖ Enucleation: Treatment of choice for group E. Indicated when patient is presented with:
o Neovascular glaucoma.
o Tumour filling more than half of the vitreous.
o Optic nerve involvement.
Eyeball should be enucleated along with maximum length of the optic nerve taking special care not to perforate the eyeball.
If optic nerve shows invasion, postoperative treatment should include:
o External beam radiotherapy (5,000 rads): This should be applied to the orbital apex.
o Chemotherapy: Consisting of CVE regimen which may be combined with cyclosporin.
❖ Palliative therapy: It is given in following cases where prognosis for life is dismal in spite of aggressive treatment:
o Retinoblastoma with orbital extension.
o Retinoblastoma with intracranial extension.
o Retinoblastoma with distant metastasis.
Palliative therapy should include combination of:
o Chemotherapy by CVE regimen.
o Surgical debulking of the orbit or orbital exenteration.
o External beam radiotherapy (EBRT).

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05. How do you prepare a patient before cataract surgery? How to predict the outcomes of surgery? 5+5 [2016]

Preoperative preparations of cataract surgery: Group C, question no. 03.

Prediction of outcome of cataract surgery: Group C, question no. 03.

06. What is chronic dacryocystitis? Describe the steps of dacryocystorhinostomy. 5+5 [2016]

Chronic dacryocystitis: Group B, question no. 26.

Dacryocystorhinostomy: Group D, question no. 27.

07. Enumerate the causes of night blindness. Write down the clinical features and management of Vitamin A
deficiency. 4+6 [2013, 2012]

Night blindness: Group D, question no. 03.

Clinical features and management of vitamin A deficiency: Group B, question no. 11.

08. What is keratoplasty? What are its types? How will you collect the donor cornea and how will you preserve
it? 2+2+4+2 [2017]

Keratoplasty: Group D, question no. 28.

Types of keratoplasty: Group D, question no. 28.

Method of collection of donor cornea: Group D, question no. 30.

Methods of corneal preservation:

❖ Short-term storage (24 hours to 96 hours) methods:

o Moist chamber method: The whole globe after enucleation can be preserved in a moist chamber at 4°C in a
refrigerator upto 24 hours.
o McCarey Kaufman (M-K) medium: Most commonly used.
• Colour: Pink.
• Components: Tissue culture (TC)-199, 5%, Dextran-40, HEPES buffer (pH-7.4) and gentamycin 0.1 mg/mL.
• Preservation time: Donor corneo-scleral rim can be preserved upto 96 hours.
• Corneo-scleral rim can be excised in-situ from the cadaver or can be prepared in the laboratory from the
enucleated eyeball ( transported in moist chamber) and is immediately stored in the storage medium.
❖ Intermediate-term storage (upto 2 weeks) methods:
o Optisol GS: It comprises of 2.5% chondroitin sulphate, 1 % dextran, ascorbic acid, vitamin B12, ATP precursors and
the antibiotics gentamycin and streptomycin.
o Other similar media: Cornisol, Eusol and Life-GE medium.
❖ Long-term storage (up to months to years) methods:
o Glycerine preservation: It can be done for 3-4 weeks.
o Organ culture method: Storage at 30°C to 37°C is useful for preservation up to 35 days.
o Cryopreservation: Corneal button preservation at -70°C can be done up to 1 year.

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09. Enumerate the postoperative complication of cataract surgery. Give treatment of any one. 6+4 [2017]

Complications of cataract surgery: Group D, question no. 29.

Treatment of PCO: Group D, question no. 08.

10. What are the effects in the eye in vitamin A deficiency? How do you prevent it? 7+3 [2000]

Effects of vitamin A deficiency: Group B, question no. 11.

Prevention of vitamin A deficiency:

❖ Short-term approach: WHO recommend periodic administration of vitamin A supplements.

o Infants 6-12 months old and any older children less than 8 kg: 100,000 IU orally every 3-6 months.
o Children 1-6 years old: 200,000 IU orally every 6 months.
o Lactating mothers: 20,000 lU orally once at delivery or during the next 2 months. This will raise the concentration
of vitamin A in the breast milk and therefore, help to protect the breastfed infant.
o Infants less than 6 months old, not being breastfed: 50,000 IU orally should be given before they attain the age
of 6 months.
A revised schedule of vitamin A supplements being followed in India under 'Child Survival and Safe Motherhood (CSSM)'.
o First dose (1 lakh IU): At 9 months of age along with measles vaccine.
o Second dose (2 lakh IU): At 18 months of age along with booster dose of DPT/OPV.
o Third dose (2 lakh IU): At 2 years of age.
❖ Medium-term approach: It includes food fortification with vitamin A.
❖ Long-term approach: It should be the ultimate aim.
o Promotion of adequate intake of vitamin A rich foods such as green leafy vegetables, papaya and drumsticks.
o Nutritional health education.

11. Outline the management of bacterial corneal ulcer and treatment of non-healing ulcer. Mention the compli-
cations of corneal ulcers. 5+3+2 [2015]

Management of bacterial corneal ulcer:

❖ Clinical evaluation:
o History taking: To know the mode of onset.
o General physical examination: To rule out anaemia and immunocompromised state.
o Ocular examinations:
• Diffuse light examination: For gross lesion of lids, conjunctiva and cornea.
• Regurgitation and syringing: To rule out lacrimal sac infection.
• Slit-lamp examination: The site, size, shape, depth, margin, floor and vascularization of the ulcer is noted.
Also presence of KPs, depth of anterior chamber, colour and pattern of iris, condition of lens are noted.
❖ Laboratory investigation:
o Routines laboratory investigation: Hb, TLC, DLC, ESR, blood sugar, complete urine and stool examination is done.
o Microbiological investigation: To identify the causative organism.
• Gram and Giemsa stain for causative bacterias.
• Culture on blood agar for aerobic organisms.
• 10% KOH, calcofluor white (CFW) stain and SDA media for fungus identification.
❖ Treatment:
o Definitive treatment:
• Topical antibiotic: Cefazoline (5%) and tobramycin (1.3%) or vancomycin (5%).
• Systemic antibiotic: Usually not required.

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o Adjuvant or concurrent therapy:

• Cycloplegic drugs: 1% atropine or 2% homatropine eye drop is used:
✓ To reduce pain from ciliary spasm.
✓ To prevent the formation of posterior synechiae from secondary iridocyclitis.
✓ To reduce exudation by decreasing hyperaemia and vascular permeability.
✓ To increase the blood supply to anterior uvea by relieving pressure on the anterior ciliary
arteries. As a result, more antibodies reach the target tissues.
• Systemic analgesic and anti-inflammatory drugs: Paracetamol and ibuprofen to relieve the pain and
decrease oedema.
• Vitamin: A, C and B complex help in early healing of ulcer.
o Physical and general measures:
• Local fomentation: Local application of dry heat to give comfort, reduce pain and increase vasodilation.
• Dark goggles: To prevent photophobia.
• Rest, good diet and fresh air may have a soothing effect.

Treatment of non-healing corneal ulcer:

❖ Main treatment: Group C, question no. 11.

❖ Additional treatment:
o Removal of known cause: A thorough search for any already missed cause not allowing healing should be made
and when found, such factors should be eliminated. Common causes of non-healing ulcers are:
• Local causes: Raised IOP, concretions, misdirected cilia, impacted foreign body, dacryocystitis,
inadequate therapy, wrong diagnosis, lagophthalmos and excessive vascularization of ulcer.
• Systemic causes: DM, severe anaemia, malnutrition, chronic debilitating diseases, systemic steroid use.
o Mechanical debridement of ulcer: This is done to remove necrosed material by scraping floor of the ulcer with a
spatula under local anaesthesia to hasten the healing.
o Cauterisation of the ulcer: This may also be considered in non-responding cases. Cauterisation may be performed
with pure carbolic acid or 10-20% trichloroacetic acid.
o Bandage soft contact lens: This may also help in healing.
o Peritomy: Severing of perilimbal conjunctival vessel may be performed when excessive corneal vascularization is
hindering healing.

Complications of corneal ulcers:

❖ Complications:
o Toxic iridocyclitis: Due to absorption of toxins in the anterior chamber.
o Secondary glaucoma: Due to fibrous exudates blocking the angle of anterior chamber.
o Descemetocele or keratocele: Herniation of Descemet’s membrane as a transparent vesicle.
o Perforation of ulcer: This may lead to:
• Prolapse of iris.
• Subluxation or anterior dislocation of lens.
• Anterior capsule cataract.
• Corneal fistula with continuous leakage of aqueous.
• Purulent uveitis, endophthalmitis or even panophthalmitis.
• Intraocular haemorrhage in form of vitreous or expulsive choroidal haemorrhage.
o Corneal scarring: This occurs after healing and may lead to permanent visual impairment ranging from slight
blurring to total blindness.

12. Write the clinical features and management of uncomplicated bacterial corneal ulcer. 5+5 [2008, 2001]

Clinical features of bacterial corneal ulcer: Group D, question no. 22.

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Management of bacterial corneal ulcer: Group C, question no. 11.

13. Describe the clinical features, complications and treatment of progressive corneal ulcer? 3+2+5 [1999]

Clinical features of progressive corneal ulcer: Group D, question no. 22.

Complications of progressive corneal ulcers: Group C, question no. 11. (except corneal scarring).

Treatment of progressive corneal ulcers:

❖ Main treatment: Group C, question no. 11.

❖ Additional treatment:
o No strain: The patient is advised to avoid sneezing, coughing and straining during stool and to take strict bed rest.
o Pressure bandage: This should be applied to give some external support.
o Lowering of IOP: Done by simultaneous use of acetazolamide 250 mg QID orally, intravenous mannitol (20%) drip
stat, oral glycerol twice a day, 0.5% timolol eye drops twice a day and even paracentesis with slow evacuation of
aqueous from the anterior chamber may be performed if required.
o Tissue adhesive glue: Such as cyanoacrylate is helpful in preventing perforation.
o Bandage soft contact lens: This may also be used.
o Conjunctival flap: The cornea may be covered completely or partly by a conjunctival flap to give support to the
weak tissue.
o Amniotic membrane transplantation: This may also be considered as an option.
o Penetrating therapeutic keratoplasty (tectonic graft): This may be undertaken in suitable cases, when available.

14. Discuss aetiology, clinical feature, complication, management of herpes zoster ophthalmicus. 2+3+2+3 [2003]

Aetiology of herpes zoster ophthalmicus:

❖ Risk factors: Immunocompromised states like disseminated TB, cancer, leukaemia, AIDS, immunocompromised organ
transplant recipient and lymphoma.
❖ Causative organism: Varicella-zoster virus (VZV).
❖ Pathogenesis: VZV infection in childhood → dormant virus in sensory ganglion of V th nerve → reactivation of virus in later
life due to any immunocompromised state → virus travels down along the branches of ophthalmic division of V th nerve.

Clinical features and complications of herpes zoster ophthalmicus:

❖ General features:
o Frontal nerve is more frequently affected than the lacrimal and nasociliary nerves.
o Ocular complications occurs in about 50% cases.
o Hutchinson's rule: Ocular involvement is frequent if the side or tip of nose presents vesicles (cutaneous
involvement of nasociliary nerve).
o Lesions are strictly limited to one side of the midline of head along the course of nerve.
❖ Acute phase lesions:
o General features: Sudden fever, malaise and severe neuralgic pain along the course of nerve.
o Cutaneous lesions: Red and oedematous skin after 3-4 days of the onset of disease → vesicle formation → pustule
formation → crusting ulcer formation after bursting → permanent pitted scar formation after healing.
o Ocular lesions:
• Conjunctivitis, episcleritis and scleritis, iridocyclitis.
• Zoster keratitis: Epithelial keratitis, nummular keratitis, disciform keratitis or keratouveitis with endo-
thelitis.
• Secondary glaucoma: Due co trabeculitis in early stages and synechial angle closure in late stages.

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• Acute retinal necrosis, anterior segment necrosis and phthisis bulbi may occur rarely.
o Associated neurological complications: Motor nerve palsies, optic neuritis and encephalitis.
❖ Chronic phase lesions:
o Post-herpetic neuralgia: Persistence of mild to moderate pain after subsidence of eruptive phase. But sometimes,
it may persist for years with little diminution of intensity. There occurs some anaesthesia of the affected skin,
which when associated with continued post-herpetic neuralgia is called anaesthesia dolorosa.
o Lid lesions: Ptosis, trichiasis, entropion and notching occur as sequelae of scarring.
o Conjunctival lesions: Chronic mucous secreting conjunctivitis.
o Corneal lesions: Neuroparalytic ulceration, exposure keratitis and mucous plaque keratitis.
o Chronic scleritis and uveitis.
❖ Relapsing phase lesions:
o Keratitis: Nummular keratitis, mucous plaque keratitis.
o Episcleritis and scleritis.
o Secondary glaucoma.

Treatment of herpes zoster ophthalmicus:

❖ Systemic therapy:
o Oral antiviral drugs: Acyclovir 800 mgb5 times a day for 10 days or valaciclovir 500 mg TDS for 10 days.
o Analgesics: Mephenamic acid + paracetamol or pentazocin or pethidine (for severe pain).
o Systemic steroids: Indicated to inhibit development of neuralgic complications.
o Cimetidine: Indicated to reduce pain and pruritis.
o Amitriptyline: To relieve the accompanying depression in acute phase.
❖ Local therapy for skin lesions:
o Antibiotic-corticosteroid skin ointment or lotions.
o No calamine lotion as it promotes crust formation.
❖ Local therapy for ocular lesions:
o For keratitis, scleritis and iridocyclitis: Topical steroid, cycloplegic and 3% acyclovir are indicated.
o For secondary infection: Topical antibiotics.
o For secondary glaucoma: Topical timolol or betaxolol drop and oral acetazolamide.
o For mucous plaques: Topical mucolytics e.g. acetyl cysteine.
o For persistent epithelial defects: Lubricating artificial drops and bandage soft contact lens.
❖ Surgical treatment: For neuroparalytic corneal ulcer.
o Lateral tarsorrlraphy.
o Amniotic membrane transplantation (AMT) or conjunctival flap for non-healing cases.
o Tissue adhesive with bandage contact lens for corneal perforation.
o Keratoplasty for visual rehabilitation.

15. Describe symptoms, signs and management of acute attack of angel closure glaucoma. 5+5 [2018, 2005, 1998]

Clinical features of acute angle closure glaucoma:

❖ An attack of acute rise in IOP in patient with primary angle closure (PAC) is a sight-threatening emergency. It may occur
due to pupillary block causing sudden closure of the angle and cannot terminate without treatment.
❖ Symptoms:
o Pain: Sudden onset of very severe pain in the eye which radiates along the branches of 5th nerve.
o Associated systemic symptoms: Nausea, vomiting and prostrations.
o Associated ocular symptoms: Rapidly progressive impairment of vision, redness, photophobia, lacrimation and
coloured halos around light.
o Past history: About 5% patients give history of typical previous intermittent attacks of subacute angle-closure.
❖ Signs:
o Lids: Oedematous.
o Conjunctiva: Chemosis of conjunctiva and congestion (both conjunctival and ciliary).
o Cornea: Oedematous and insensitive.

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o Anterior chamber: Very shallow. Aqueous flare or cells may be seen in anterior chamber.
o Angle of anterior chamber: Completely closed as seen on gonioscopy (Shaffer grade 0).
o Iris: Discoloured.
o Pupil: Semidilated, vertically oval and fixed. It is non-reactive to both light and accommodation.
o IOP: Markedly elevated, usually between 40 and 70 mm of Hg.
o Optic disc: Oedematous and hyperaemic.
o Fellow eye: Shallow anterior chamber and occludable angle.

Management of acute angle closure glaucoma:

❖ Immediate medical therapy:

o Systemic hyperosmotic agents: Mannitol 20% IV or glycerol 50% oral.
o Systemic anti-glaucoma drugs: Acetazolamide 500 mg IV stat followed by 250 mg tablet 3 times a day.
o Topical anti-glaucoma drugs:
• Beta-blockers: Timolol or betaxolol.
• Alpha adrenergic agonists: Brimonidine.
• Prostaglandin analogues: Latanoprost.
• Miotic therapy: Pilocarpine 2% QID should be started after 1 hour of commencement of treatment when
IOP is lowered, as at higher IOP sphincter is ischaemic and unresponsive to pilocarpine.
o Analgesics and antiemetics: To subside symptoms.
o Compressive gonioscopy: Compressive gonioscopy with a 4 mirror goniolens may help relieve pupil block and is
essential to determine if the trabecular blockage is reversible.
o Topical steroid: Prednisolone or dexamethasone eye drops to reduces inflammation.
❖ Definitive therapy:
o Peripheral iridotomy (PI): Gonioscopy should be performed as soon as cornea becomes clear. PI should be
performed if PAS are seen in < 270° angle. PI re-establishes communication between posterior and anterior
chamber, so it bypasses the pupillary block and immediately relieves the crowding of the angle.
• Laser peripheral iridotomy (LPI) (with Nd:YAG laser or Argon Laser) is most preferred mode.
• If lasers are not available surgical Pl should be done.
o Filtration surgery i.e. trabeculectomy: This should be performed in cases:
• Where IOP is not controlled with the maximum medical therapy following an attack of acute PAC.
• When gonioscopy reveals PAS > 270° angle.
• When peripheral iridotomy is not effective.
Mechanism: Filtration surgery provides an alternative to the angle for drainage of aqueous from anterior chamber
into subconjunctival space.
o Clear lens extraction by phacoemulsification with IOL implantation has recently been recommended in the pres-
ence of phacomorphic etiology (diagnosed on UBM).
❖ Prophylactic treatment in the normal fellow eye: Prophylactic PI should be performed on the fellow asymptomatic eye
(PACS) as early as possible as chances of acute attack are 50% in such eyes.
❖ Long-term glaucoma surveillance and IOP management in both eyes: This is must to prevent glaucomatous blindness:
o Eyes treated with PI (both affected and fellow eye) may develop PACG at any time. So, it should be treated as and
when required.
o Filtration surgery may fail anytime during the course and hence need to be repeated with antimetabolites.

16. What are causes of rainbow halos? Outline the management of one such case having pain. 3+7 [2015, 2011]

Causes of rainbow halos:

❖ Perception of abnormal colours by a patient is called coloured halos.

❖ Causes:
o Acute congestive glaucoma.
o Corneal oedema e.g. bulbous keratopathy.
o Early stage or immature cataract.
o Mucopurulent conjunctivitis.
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Management: Group C, question no. 15.

17. A patient comes with rainbow haloes. How will you diagnose the case? [2013]

Diagnosis of rainbow haloes:

❖ The coloured halos in glaucoma must be differentiated from those found in acute purulent conjunctivitis and early
cataractous changes.
o Coloured halos in conjunctivitis: This can be eliminated by irrigating the discharge.
o Coloured halos of glaucoma and immature cataract: These may be differentiated by Fincham's test in which a
stenopaeic slit is passed across the pupil. During this test, glaucomatous halo remains intact, while a halo due to
cataract is broken up into segments.

18. What is Aphakia? What is the difference between aphakia and pseudophakia? How do you manage a case of
uniocular aphakia after cataract operation due to trauma (on a patient of 20 years of age)? 2+3+5 [2001]

Aphakia:

❖ Aphakia literally means 'absence of crystalline lens' from the eye. However, from the optical point of view, it may be
considered a condition in which the lens is absent from the pupillary area causing a high degree of hypermetropia. It may
be due to:
o Congenital absence of lens.
o Surgical aphakia after removal of lens (most common cause).
o Aphakia due to absorption of lens matter after trauma in children.
o Traumatic extrusion of lens from the eye.
o Posterior dislocation of lens in vitreous.

Difference between aphakia and pseudophakia:

❖ Difference between aphakia and pseudophakia:

Features Aphakia Pseudophakia

Definition Absence of crystalline lens from pupillary area. Aphakia corrected by IOL implantation.
Cause Group C, question no. 19. Surgery.
Refractive status High degree of hypermetropia. Emmetropia, consecutive myopia or hypermetropia
based on the power of implanted IOL.
Accommodation Lost totally. Present.
Purkinje's image 2 in number. 4 in number.
Erythropsia and Present. Absent.
Cyanopsia

Management of aphakia:

❖ Optical principle: Correct the refractive error by convex lenses of appropriate power so that image is formed on the retina.
❖ Modalities for correcting aphakia:
o Spectacles: Most common. Roughly, about +10D with cylindrical lenses for surgically induced astigmatism are
required to correct aphakia in previously emmetropic patients. An addition of +3 to +4 D is required for near vision
to compensate the loss of accommodation.

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Disadvantages of spectacles are:

• Image is magnified by 30%, so not useful in unilateral aphakia (produce diplopia).
• Problem of spherical and chromatic aberrations of thick lenses.
• Field of vision is limited.
• Prismatic effect of thick glasses.
• 'Roving ring Scotoma' (Jack in the box phenomenon).
• Cosmetic blemish especially in young aphakes.
o Contact lenses:
Advantages of contact lenses over spectacles include:
• Less magnification of image.
• Elimination of aberrations and prismatic effect of thick glasses.
• Wider and better field of vision.
• Cosmetically more acceptable.
• Better suited for uniocular aphakia.
Disadvantages of contact lenses are:
• More cost.
• Cumbersome to wear, especially in old age and in childhood.
• Corneal complications may be associated.
o IOL implantation: This is the best available method of correcting aphakia.
• Primary IOL implantation is done during cataract surgery.
• Secondary IOL implantation is done in already aphakic patients.
o Refractive corneal surgery: Hyperopic LASIK may be tried in cases where secondary IOL cannot be implanted.

19. A patient attended OPD with painful red congested eye with semi-dilated pupil. What is the diagnosis and
what investigation will you do to confirm? Write in brief the management of the patient? 1+4+5 [2004]

Diagnosis:

❖ Primary angle closure glaucoma.

Confirmation of diagnosis: Group C, question no. 02.

Management: Group C, question no. 15.

20. A child of 3 years age presented with a white reflex behind the pupil. Discuss the differential diagnosis and
management in brief. 3+7 [2004, 1996]

Differential diagnosis of white reflex:

❖ White pupillary reflex, also known as leucocoria, can occur in many pathological conditions:
o Retinoblastoma: Most common.
o Pseudoganglioma: Various conditions other than retinoblastoma, which present as leucocoria are collectively
called as pseudoganglioma. A few common conditions are:
• Congenital cataract.
• Inflammatory deposits in vitreous following a plastic cystitis or choroiditis.
• Coloboma of the choroid.
• Retrolental fibroplasia or retinopathy of prematurity.
• Persistent hyperplastic primary vitreous (PHPV).
• Parasitic endophthalmitis (toxocara endophthalmitis).
• Exudative retinopathy of Coats.

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Management:

❖ Management of white reflex includes the treatment of the cause:

o Retinoblastoma: Group D, question no. 11.
o Congenital cataract: This can be dealt with extracapsular cataract extraction technique involving anterior
capsulorrhexis and irrigation aspiration of the lens matter (lens aspiration) or lensectomy.
o Coloboma of choroid: Treatment of the complications are done as no definitive treatment is present.
o Retrolental fibroplasia:
• Laser treatment: Laser photocoagulation using diode laser 810 nm or frequency doubled Nd: YAG (532
nm) with LIO (laser indirect ophthalmoscope) delivery should be carried out in all patients with high-risk
pre-threshold, threshold and aggressive posterior ROP.
• Post-laser treatment and follow-up:
✓ Immediate follow-up: Antibiotic and steroid eye drops should be prescribed for a week. Post-
laser treatment follow-up should be done weekly for 3 weeks and if required retreatment should
be done.
✓ Subsequent follow-up: Examination should be continued at 3, 6 and 12 weeks after treatment.
✓ Long-term follow-up: Must for timely management of complications if any.
• Surgical treatment: Patients with stage IVa, IVb and V require lens sparing vitrectomy along with
endolaser photocoagulation and retinal reattachment measures.
o PHPV: This can be dealt with pars plana lensectomy and excision of the membranes with anterior vitrectomy. The
surgery is done only for complications and the only goal is to save the eye and maintain existing visual acuity.
o Parasitic endophthalmitis: Group B, question no. 07.
o Coats disease: Photocoagulation or cryotherapy is done to check the progression of the disease in early stage.
However, once the retina is detached, treatment becomes increasingly difficult and success rate declines to 33%.

21. Write causes of red eye. Give differential diagnosis and treatment options for each. 2+3+5 [2012]

Causes of red eye: Group. D, question no. 25.

Differential diagnosis: Group C, question no. 02.

Management:

❖ Management of acute conjunctivitis:

o Bacterial: Chloramphenicol 0.5% eye drops, gentamicin 0.3% eye drops and tetracycline 1% eye ointment should
be prescribed. Intensive instillation should be done for first day or until symptoms and signs reduce.
o Viral: Cold compresses are given to relieve discomfort.
o Allergic: Reassurance is given. Antihistamines (eye drops or orally), steroid eye drops, cromolyn sodium 4% eye
drop and lodoxamide 0.1% eye drop should be prescribed.
❖ Management of acute iridocyclitis: Group C, question no. 01.
❖ Management of acute congestive glaucoma: Group C, question no. 16.

22. Write down the diagnosis and follow up of POAG. 6+4 [2010]

Diagnosis of POAG:

❖ Intraocular pressure (IOP):

o Procedures:
• Tonometry: The gold standard for IOP measurement is Goldmann Applanation Tonometry (GAT).
• Central corneal thickness (CCT): A thinner cornea may lead to measurements that underestimate true
IOP and vice versa. A correction factor should be applied to the IOP reading in patients with CCT less than

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545 or more than 600 microns. A low CCT (< 545 microns) is an independent risk factor for conversion of
ocular hypertension to POAG.
• Other methods:
✓ Reichert ocular response analyser (ORA): It is a non-contact tonometer that measures a
biomechanical attribute of the cornea termed hysteresis.
✓ Pascal Dynamic Contour Tonometer (DCT): It uses principle of contour matching instead of
applanation to reduce the effect of corneal biomechanics.
o Aim: POAG is diagnosed based on signs of glaucomatous optic neuropathy regardless of the level of IOP. Patients
can be classified as normal tension glaucoma (NTG) or high tension glaucoma (HTG) based on the IOP.
• NTG: IOP ≤ 21 mm Hg.
• HTG: IOP > 21 mm Hg.
❖ Anterior chamber angle:
o Procedures: The anterior chamber angle is assessed by slit lamp (Van Herick technique) and with gonioscopy.
Newer techniques include ultrasound biomicroscopy (UBM) and anterior segment optical coherence tomography.
o Aim: To rule out causes of secondary open-angle glaucoma.
❖ Optic disc: Gold standard for diagnosis of POAG.
o Procedures:
• Confocal scanning laser topography (CSLT) i.e. Heidelberg retinal tomograph (HRT).
• Advanced imaging techniques like optical coherence tomography (OCT) and scanning laser polarimetry
i.e. nerve fibre analyser (NFA).
o Aim: To found the glaucomatous optic disc changes.
• Early changes:
✓ Vertically oval, asymmetrical or large cup with cap-disc ratio > 0.4.
✓ Pallor areas on disc.
✓ Atrophy or defect of regional nerve fire layer (RNFL).
• Advanced changes:
✓ Marked cupping.
✓ Thinning of neuro-retinal rim (NRR).
✓ Nasal shifting of retinal vessels.
✓ Pulsations of retinal arterioles.
✓ Lamellar dot sign.
• Glaucomatous optic atrophy.
❖ Visual field:
o Procedures: Automated static threshold perimetry (e.g. Humphrey field analysis) is useful for diagnosis and gold
standard for monitoring of POAG.
o Aim: To find the glaucomatous visual field changes.
Visual field changes: Group B, question no. 17.

Follow up of POAG:

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❖ Medical follow up:

o Target IOP: It is popular practice to define a target IOP for IOP lowering. This would be based on current evidence,
the stage of the patient’s POAG and other risk factors for progression. A reasonable initial target is for at least
20%-30% reduction in IOP. A larger reduction may well be needed for patients presenting with advanced disease.
o Monotherapy: This should be initiated with topical prostaglandins (latanoprost, bimatoprost or travoprost) or
topical beta blocker (0.5% timolol or betaxolol). IOP should be checked after 15 days. If the drug chosen is
ineffective or intolerable it should be replaced by drug of second choice.
o First review: First review after commencing a new therapy should occur within 6-8 weeks, though the patient
should understand to present sooner if they develop any side-effects. At each review, the patient needs the
following assessed:
• Any subjective change in vision or any side-effects.
• IOP, is it within target.
• Signs of progression: Standard automated perimetry, optic disc assessment (clinical +/- HRT, OCT)
o If the patient has no side effects, the IOP is within target level and there are no signs of progression, then a
routine 3-4 month review can be arranged.
o Combination therapy: If the initial therapy significantly reduced IOP, but not to target level, then a combination
of two drugs-one drug which decreases aqueous production (timolol or other beta blocker or brimonidine or
dorzolamide) and other drug which increase aqueous outflow (latanoprost or brimonidine or pilocarpine) may be
used.
o If there are signs of progression despite target IOP, the target should be lowered further, and the patient more
closely followed.
o If target IOP is not reached despite fully tolerated topical medications, laser or surgical therapy should be done.
❖ Surgical follow up:
o Early surgical follow up: It includes close monitoring of prognosis and complications associated with the surgery.
o Longer term surgical follow up: It is similar to the assessment described above under medical follow up.

23. Describe the anatomy of the angle of anterior chamber of eye ball. Write in short your plan for medical
treatment of open angle glaucoma? 5+5 [2001]

Anatomy of angle of anterior chamber:

❖ Contents of the angle of anterior chamber: Clinically by gonioscopy, angle structures seen from behind forward are:
o Root of iris.
o Anterior most part of ciliary body as ciliary body band (CBB).
o Scleral spur (SS).
o Trabecular meshwork (TM): It is a circular sponge work of connective tissue lines by trabeculocytes. It behaves as
a sieve-like structure through which aqueous humour leaves the eye into Schlemm's canal. It consists of three
layers, which from inside out are:
• Uveal meshwork.
• Corneoscleral meshwork.
• Juxtacanalicular or endothelial meshwork.
o Schwalbe's line (SL): Prominent end of Descemet’s membrane of cornea.
Angle of anterior chamber plays an important role in process of aqueous drainage. The angle width varies in different
individuals and plays a vital role in the pathomechanism of different types of glaucoma.

Medical treatment of open angle glaucoma:

❖ Antiglaucoma drugs for POAG: Group D, question no. 15.

❖ Medical follow up: Group C, question no. 23.

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➢ Important to note: Shaffer's system of grading the angle width:

Grade Angle width Configuration Risk of closure Structure seen on gonioscopy

4 40° Wide open Closure impossible SL, TM, SS, CBB
3 30° Open angle Closure impossible SL, TM, SS
3 20° Moderately narrow Closure possible SL, TM
1 10° Very narrow High risk of closure SL
S < 10° Slit angle Closure imminent No structure visible
0 0° Closed Closed No structure visible

24. What is IOP? Mention conditions where IOP is low. 4+6 [2009]

IOP:

❖ Definition: Intraocular pressure (IOP) is the internal pressure exerted by the intraocular fluids on the coats of the eyeball.
❖ Measures:
o The normal intraocular pressure (IOP) is between 10 and 20 mm Hg.
o Two main factors, concerned with the maintenance of IOP are the rate of secretion of aqueous humour and its
rate of outflow from the eye. Most (75%) of the resistance to outflow is in the trabecular meshwork immediately
adjacent to the canal of Schlemm.
o Coefficient of facility of outflow: The ease with which the fluid exits, is indicated as the coefficient of the facility
of outflow (‘C’), and in the normal eyes is more than 0.2 µl/min/mm Hg of pressure within the eye. It is measured
clinically by tonography.
o Under normal conditions, the rate of aqueous production is relatively constant, so that, in clinical practice, the
main determinants of IOP are the resistance of exit channels and the outflow pressure.
o Intraocular pressure = Outflow pressure + episcleral venous pressure.

Conditions for low IOP:

❖ Physiological conditions:
o Diurnal variation: A characteristic diurnal variation is seen, with a minimum around 6.00 PM, and a peak on
waking in the morning.
o Venous pressure: Low episcleral venous pressure increases aqueous outflow and reduces the IOP.
o Arterial pressure: Low systemic blood pressure decreases IOP.
o Osmotic pressure of blood: When plasma osmolarity rises (as with intravenous mannitol or oral glycerol), the IOP
falls. Whereas, reduced osmolarity (as with water drinking provocative test) raises IOP.
❖ Mechanical conditions:
o Anterior chamber: The IOP may be low if the anterior chamber is deep.
o Angle of anterior chamber: Grade 4 angle may be sometimes associated with low IOP.
❖ Pharmacological conditions: IOP lowering drugs: Group D, question no. 15.
❖ Pathological conditions:
o Ruptured globe.
o Phthisis bulbi.
o Retinal or choroidal detachment.
o Iridocyclitis.
o Ocular ischemia.
o Postoperative wound leak.
o Traumatic ciliary body shut down.

25. A 7 years old boy was hit by a cricket ball in one eye. Enumerate possible damage in each of the ocular
structures. Describe options for treatment of each of the injuries. [2014, 2012, 2005, 2000, 1999]

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Damage by blunt trauma:

❖ Eyelids:
o Lid lacerations.
Treatment: Reapproximation of skin edges with small interrupted sutures.
o Lid swelling and ecchymosis (black eye – panda bear sign).
Treatment: Cold compression for first 24 hours and warm compression after 24 hours.
o Emphysema of the eyelid.
Treatment: Usually resolves spontaneously.
❖ Conjunctiva:
o Conjunctival lacerations.
Treatment: Observation, surgical repair for large lacerations.
o Chemosis and subconjunctival haemorrhage.
Testament: Usually resolves spontaneously.
❖ Cornea:
o Simple corneal abrasion: Very painful and diagnosed by fluorescein staining.
Treatment: Topical antibiotic and patching.
o Recurrent corneal erosions (recurrent keratalgia): Recurrent pain and lacrimation on opening the eye in morning
due to abnormally loose attachment of epithelium to the underlying Bowman's membrane.
Treatment: Removal of loosely attached epithelium by debridement and application of ‘pad and bandage’ for 48
hours for firm healing.
o Partial corneal tears (lamellar corneal laceration).
Treatment: Topical antibiotic and patching.
o Tears in Descemet’s membrane: Usually vertical.
Treatment: Observation, surgical repair for large tears.
o Acute corneal oedema: Due to traumatic dysfunction of endothelial cells.
Treatment: Usually resolves spontaneously.
o Blood staining of cornea: Reddish brown or greenish cornea due to hyphaema and raised IOP.
Treatment: Usually resolves spontaneously, but whole process may take even more than 2 years.
❖ Sclera:
o Lamellar scleral laceration.
Treatment: Surgical repair is done as far posteriorly as possible. Far posterior rupture is generally left unsutured.
Strict observation of IOP should be done.
❖ Anterior chamber:
o Traumatic hyphaema: Blood in the anterior camber.
Treatment: For small hyphaemas, conservative treatment including prevention of rebleeding and rise in IOP is
done. For large non-resolving hyphaemas, anterior chamber washout is done.
o Exudates following traumatic uveitis.
Treatment: Usually resolves spontaneously.
❖ Pupil:
o Traumatic miosis or mydriasis: Miosis occurs due to irritation of ciliary nerves and may be associated with spasm
of accommodation. Mydriasis may be permanent and may be associated with cycloplegia.
Treatment: Supportive care is given as these conditions usually resolves spontaneously.
❖ Iris:
o Iris laceration: This may be in the form of:
• Rupture of pupillary margin.
• Radiating tears in the iris stroma.
• Iridodialysis: Detachment of iris from its root at the ciliary body. It results in a D-shaped pupil and a
biconvex area is seen at the periphery.
• Antiflexion: Rotation of detached portion of iris following extensive iridodialysis, in which posterior
surface faces anteriorly.
• Retroflexion: Condition when whole of the iris is doubled back into the ciliary region and becomes
invisible.
• Traumatic aniridia or iridemia: Completely torn iris sinks to the bottom of AC in form of a minute ball.
Treatment:
• Repair is conducted in aphakic or pseudophakic eyes, as the risk of capsular tear is high in phakic eyes.
• It is recommended to block the eye, either via a peribulbar or retrobulbar block.
• Miochol or moistat should be used to pharmacologically constrict the pupil as much as possible.

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❖ Ciliary body:
o Angle recession: Tear between longitudinal and circular muscle fibres of the ciliary body. Gonioscopy reveals
deepening of the anterior chamber and widening of the ciliary body band. Later on, it is complicated by glaucoma.
Treatment: Treatment is same as POAG. Use of topical aqueous suppressants in the initial medical treatment is
preferred including beta-antagonists, alpha-agonists and carbonic anhydrase inhibitors.
❖ Inflammatory changes:
o Traumatic iridocyclitis, haemophthalmitis, post-traumatic iris atrophy, pigmentary changes, traumatic choroiditis.
Treatment: Atropine, antibiotic and steroid administration. In ruptures of pupillary margins and subluxation of
lens, atropine is contraindicated.
❖ Lens:
o Vossius ring: Circular ring of brown pigment on anterior capsule. It occurs due to striking of contracted pupillary
margin against the crystalline lens. It is always smaller than the size of the pupil.
Treatment: No treatment is needed as it is diagnostically important with least clinical importance.
o Concussion cataract: Due to imbibition of aqueous and partly due to direct mechanical effect of the injury on lens
fibres. It may appear in the form of:
• Discrete subepithelial opacities (most common).
• Early rosette cataract (punctate).
• Late rosette cataract.
• Traumatic zonular cataract.
• Diffuse (total) concussion cataract.
• Early maturation of senile cataract.
Treatment: General line surgical management of cataract by ICCE or ECCE.
o Traumatic absorption of lens.
Treatment: Management of aphakia is done by spectacle, contact lens, IOL or hyperopic LASIK.
o Subluxation or dislocation of lens: Due to partial and complete rupture of zonules respectively.
Treatment:
• Anterior dislocation is managed by removal of lens through lomba route as early as possible.
• Posterior dislocation is managed by removal of lens by pars plana vitrectomy technique.
❖ Vitreous:
o Liquefaction and appearance of clouds of fine pigmentary opacities.
Treatment: Though no treatment is required, monitoring is essential to rule out complications.
o Detachment of vitreous either anteriorly at base or posterior (PVD) may occur.
Treatment: Uncomplicated detachment requires no treatment, where as complicated PVD requires management
of the complications.
o Vitreous haemorrhage.
Treatment:
• Conservative treatment: Bed rest and elevation of head to allow the blood to settle down.
• Vitrectomy by pars plana route to clear the vitreous.
o Vitreous herniation at anterior chamber due to subluxation or dislocation of lens.
Treatment: Lens subluxation or dislocation is treated.
❖ Choroid:
o Rupture of choroid: It is concentric to the optic disc and situated temporal to it. Rupture may be single or multiple.
Treatment: Eevaluation is done for formation of choroidal neovascular membrane (CNVM).
o Subretinal choroidal or chorioretinal haemorrhage.
Treatment: Surgical removal.
o Choroidal detachment.
Treatment: Eye drops are given to reduce inflammation and dilate pupil.
❖ Retina:
o Commotio retinae: Old questions, question no. 16.
o Retinal haemorrhage: Flame shaped and pre-retinal D-shaped (subhyaloid) haemorrhage may be seen.
Treatment: Surgical removal.
o Retinal tears.
Treatment: Photocoagulation or cropexy is doen.
o Traumatic proliferative retinopathy.
o Retinal detachment.
Treatment: Surgery is difficult and requires pars plana vitrectomy.
o Concussion changes in macula.
❖ IOP:

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o Traumatic glaucoma.
Treatment:
• Medical therapy with topical 0.5% timolol and oral acetazolamide.
• Treatment of associated causative mechanism: Atropine and steroids for control of inflammation.
• Surgical intervention according to the situation.
o Traumatic hypotony: It may follow temporary damage to the ciliary body (ciliary shock) or there may occur
permanent damage to the ciliary body which may even result in phthisis bulbi.
Treatment: Surgical replacement of permanently damaged ciliary tissue with normal tissue.
❖ Refraction:
o Myopia: This may follow ciliary spasm or rupture of zonules or anterior shift of the lens.
Treatment: Optical treatment is done by concave lens.
o Hypermetropia and loss of accommodation: These may result from damage to the ciliary body (cycloplegia).
Treatment: Optical treatment is done by convex lens.

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Note:

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Note:

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Group – D
01. Syringing of lacrimal passage. [2020, 2012]

❖ Lacrimal syringing test is performed in clinical evaluation of a case of watering eye.

❖ Anaesthesia: Topical anaesthesia with 4% xylocaine.
❖ Procedure:
o Lower Punctum is dilated with the help of a Nettleship punctum dilator →
o Blunt tipped, curved 26 gauge cannula is inserted into the punctum and the lower canaliculi →
o Saline is injected for irrigation.
❖ Observation and inference:
o Free flow of saline through the lacrimal passages into the nasal cavity and throat.
Inference: Lacrimal passage is patent with no obstruction. Cause of watering may be hypersecretion or lacrimal
pump failure.
o Saline flows through the lacrimal passage with considerable pressure in the syringe.
Inference: There is partial obstruction in the passage. Jones dye test is done in these cases.
o No saline passes into the nose.
• Reflux of saline through the same punctum.
Inference: Obstruction in the same or common canaliculus.
• Reflux of saline through the opposite punctum.
Inference: Obstruction in the lower sac or in the nasolacrimal duct.

02. Vitreous haemorrhage. [2020, 2010]

❖ Vitreous haemorrhage usually occurs from the retinal vessels. It is usually presented as:
o Sub-hyaloid haemorrhage: Pre-retinal haemorrhage between ILM and posterior hyaloid membrane.
o Integral haemorrhage:
• Anterior vitreous haemorrhage.
• Mid vitreous haemorrhage.
• Posterior vitreous haemorrhage.
• Total vitreous haemorrhage.
❖ Aetiology:
o Trauma: Most common cause of VH in children.
o Eales' disease: An inflammatory disease, most common cause of VH in young adults.
o Proliferative diabetic retinopathy: Most common cause of VH in older adults.
o Vascular disorders: Hypertensive retinopathy, CRVO, BRVO.
o Blood dyscrasias: Retinopathy of anaemia, prematurity, leukaemia, polycythaemia, sickle cell retinopathy.
o Bleeding disorders: Purpura, haemophilia, scurvy.
o Others: Retinal tear, PVD, RD, exudative age-related macular degeneration, neoplasms, Coat's diseases, radiation
retinopathy, retinal capillary aneurysm, retinal macro-aneurysm, Terson syndrome.
❖ Clinical features:
o Symptoms:
• Floaters of sudden onset when the haemorrhage is small.
• Sudden painless loss of vision in large haemorrhage.
o Signs:
• Distant direct ophthalmoscopy: Black shadow in red glow in small VH and no red glow in large VH.
• Direct and indirect ophthalmoscopy: Blood in vitreous in small VH and no visible fundus in large VH.
• Slit-lamp examination: Normal anterior segment and a reddish mass in the vitreous.
❖ Diagnosis: With the help of B-scan ultrasonography.
❖ Fate of haemorrhage:
o Complete absorption without organization within 4-8 weeks.
o Organization with formation of a yellowish-white debris in persistent or recurrent bleeding.
o Complications like khaki cell glaucoma, a secondary open angle glaucoma.
o Retinitis proliferans with complications like tractional retinal detachment.
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❖ Management:
o Conservative treatments: Like bed rest and elevation of patient’s head along with observation:
• 6 months for normal patient.
• 3 months for type II DM.
• 1 month for type I DM.
o Pars plana vitrectomy if absorption does not occur within the observation period.
o Treatment of the cause.

03. Night blindness. [2019]

❖ Night blindness:
o It is also known as nyctalopia.
o It is a common symptomatic disturbance of the vision.
o This can occur due to rod dysfunction, media opacities or advanced POAG.
❖ Rod dysfunction: Night (scotopic) vision is a function of rods. Therefore, the conditions in which functioning of these nerve
endings are deranged will result in night blindness. These include:
o Vitamin A deficiency: In modified WHO classification of xerophthalmia, night blindness is given the grade XN (1st
grade) as it is the earliest symptom of xerophthalmia.
o Retinitis pigmentosa: In this tapetotmretinal degeneration night blindness is presented as the earliest feature.
This may present several years before the visible changes in the retina.
o Other tapetoretinal degenerations.
o Congenital high myopia.
o Familial congenital night blindness.
o Oguchi's disease.
❖ Media opacities: Night blindness may also develop in conditions of the ocular media interfering with the light rays in dim
light (i.e. with dilated pupils). These include:
o Paracentral lenticular opacities like in case of peripheral cortical cataract.
o Corneal opacities.
❖ Advanced posterior open angle glaucoma (POAG): In advanced cases of primary open angle glaucoma, dark adaptation
may be so delayed that patient gives history of night blindness.

04. Internal hordeolum. [2019, 1998, 1994]

❖ Internal hordeolum is a supportive inflammation of the meibomian gland associated with the blockage of the duct.
❖ Aetiology:
o Predisposing factors:
• Age: More in children and young adults, though can happen in any age.
• Patients with eye strain: Due to muscle imbalance or refractive errors.
• Metabolic factors: Chronic debility, excessive carbohydrate and alcohol intake.
o Associated features:
• Habitual rubbing of the eyes or fingering of the kids and nose.
• Chronic blepharitis.
• Diabetes mellitus.
o Causative organism:
• Primary Staphylococcus aureus infection of meibomian gland.
• Secondary infection in a chalazion (infected chalazion).
❖ Clinical features:
o Symptoms: Acute pain associated with swelling of the lid, mild watering and photophobia.
o Signs: Localized, firm, red, tender swelling of the lid associated with marked oedema. Maximum tenderness,
swelling and pus point away from lid margin.
❖ Differential diagnosis: It should be differentiated from external hordeolum on the basis of:
o Pain: More intense pain in internal hordeolum due to the swelling being embedded deeply in dense fibrous tissue.
o Pus point: In internal hordeolum pus usually points on the tarsal conjunctiva as a yellowish area on everting the
lid and not on the root of cilia, which is seen in external hordeolum. Sometimes, pus point may be seen at the
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opening of involved meibomian gland or rarely on the skin.

❖ Treatment:
o Hot compression: 2-3 times a day.
o Pus drainage: By vertical incision from the tarsal conjunctiva.
o Topical antibiotics: Eye drops 3-4 times a day and eye ointment at bed time to control infection.
o Systemic antibiotics: For early control of infection.
o Systemic anti-inflammatory and analgesics: To relieve pain and reduce oedema.

05. Alkali burn of eye. [2018]

❖ Alkali burns are among the most severe chemical injuries known to the ophthalmologists. Common alkalies responsible for
burns are lime (most common), caustic potash or caustic soda and liquid ammonia (most harmful).
❖ Mechanisms of damage:
o Alkalies dissociate and saponify fatty acids of the cell membrane and therefore destroy the structure of cell
membrane of the tissue.
o Being hygroscopic, they extract water from the cells, a factor which contributes to the total necrosis.
o They combine with lipids of cells to from soluble compounds which produce a condition of softening and
gelatinization.
The above effects result in an increased deep penetration of the alkalies into the tissues. Therefore these burns spread
widely and their action continues for some days.
❖ Clinical features:
o Stage of acute ischaemic necrosis:
• Conjunctiva: Marked oedema, congestion, widespread necrosis and a copious purulent discharge.
• Cornea: Marked oedema, widespread sloughing of the epithelium and opalescence of the stroma.
• Iris: Marked inflammation with granulation tissue deposition in severe cases.
o Stage of reparation: Conjunctival and corneal epithelium regenerates. Inflammation of iris subsides.
o Stage of complication: Symblepharon, recurrent corneal ulcer, complicated cataract, secondary glaucoma is seen.
❖ Treatment:
o Immediate treatment: Copious early with normal saline and removal of all foreign particles by double eversion
of the eyelid to normalize the pH and reduce the duration of contact of chemical should be done under slit-lamp.
o Early acute phase treatment: Medical treatment:
• Topical antibiotics to prevent superinfection.
• Cycloplegics for comfort.
• Preservative free lubricating eye drops.
• Topical sodium citrate 10% 2 hourly to prevent proteolysis.
• Topical steroids for initial 7-10 days → Pred acetate 1% QID.
• Topical ascorbic acid (10%) hourly + systemic vitamin C 2g QID Improves wound healing by promoting
collagen synthesis.
• Doxycycline to inhibit MMPs.
o Surgical treatment: Intermediate and late treatment: Usually needed for grade III and IV injuries.
• Amniotic membrane transplantation (AMT) promotes epithelization and reduces lid friction due to the
expression of TGß 1 and EGF.
• Limbal stem cell transplantation autograft or allograft (if bilateral injury).
• Tenoplasty advancement of conjunctiva and Tenon's capsule to limbus.
• Keratoplasty or Boston prosthesis.

➢ Important to note:
o Roper-Hall classification of ocular surface burn:

Grade Prognosis Cornea Limbal ischemia

I Excellent Corneal epithelial damage with clear cornea No limbal ischemia
II Good Corneal haze, iris details visible <⅓
III Guarded Total epithelial loss, stromal haze, iris details obscured ⅓ to ½
IV Poor Cornea opaque, iris and pupil obscured >½

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o Dua's classification of ocular surface burn:

Clinical findings (clock hours

Grade Prognosis Conjunctival involvement Analogue scale
of limbal involvement)
I Very good 0 clock hours 0% 0/0.0%
II Good ≤ 3 clock hours ≤ 30% 0.1-3/1-30%
III Good > 3-6 clock hours > 30-50% 3.1-6/31-50%
IV Good to guarded > 6-9 clock hours > 50-75% 6.1-9/51-75%
V Good to poor > 9-12 clock hours > 75- < 100% 9.1-11.9/75.1-99.9%
VI Very poor 12 clock hours involved Total conjunctiva (100%) involved 12/100%

06. Enucleation. [2018, 2011]

❖ Enucleation surgery means excision of the eyeball.

❖ Indications:
o Absolute indications: Retinoblastoma, malignant melanoma.
o Relative indications: Painful blind eye, non-responsive to conservative measure mutilating ocular injuries,
anterior staphyloma, phthisis bulbi.
o Indication for eye donation: Most common indication, done in the cadaveric eye.
❖ Anaesthesia: Local anaesthesia in adults and general anaesthesia in children.
❖ Surgical techniques:
o Separation of conjunctiva and Tenon's capsule: Conjunctiva is incised all around the limbus with the help of spring
scissors. Undermining of the conjunctiva and Tenon's capsule is done combinedly, all around up to the equator,
using blunt-tipped curved scissors. This manoeuvre exposes the extraocular muscles.
o Separation of extraocular muscles: The rectus muscles are pulled out one by one with the help of a muscle hook
and a 3-0 silk suture is passed near the insertion of each muscle. The muscle is then cut with the help of tenotomy
scissors leaving behind a small stump carrying the suture. The inferior and superior oblique muscles are hooked
out and cut near the globe.
o Cutting of optic nerve: The eyeball is prolapsed out by stretching and pushing down the eye speculum. The eyeball
is pulled out with the help of sutures passed through the muscle stumps. The enucleation scissors is then
introduced along the medial wall up to the posterior aspect of the eyeball. Optic nerve is felt and then cut with
the scissors while maintaining a constant pull on the eyeball.
o Removal of eyeball: The eyeball is pulled out of the orbit by incising the remaining tissue adherent to it and
haemostasis is achieved by packing the orbital cavity with a wet pack and pressing it back.
o Inserting an orbital implant: Preferably an orbital implant (made up of PMMA Medpor or hydroxyapatite) of
appropriate size should be inserted into the orbit and sutured with the rectus muscles.
o Closure of conjunctiva and Tenon's capsule: These are done separately. Tenon's capsule is sutured horizontally
with 6-0 vicryl or chromic catgut. Conjunctiva is sutured vertically so that conjunctival fornices are retained deep
with 6-0 silk sutures which are removed after 8-10 days.
o Post-surgical procedures: After completion of surgery, antibiotic ointment is applied, lids are closed and dressing
is done with firm pressure using sterile eye pads and a bandage.
❖ Fitting of artificial prosthetic eye: Conformer may be used postoperatively so that the conjunctiva! fornices are retained
deep. A proper sized prosthetic eye can be inserted for good cosmetic appearance after 6 weeks when healing of the
enucleated socket is complete.

07. Presbyopia. [2017, 2005]

❖ The condition of progressive failing near vision due to age-related decrease in the amplitude of accommodation or increase
in punctum proximum is called presbyopia. It (eye sight of old age) is not a refractive error but a physiological condition.
❖ Causes:
o Age-related presbyopia:
• Age-related changes in the lens:
✓ Decreased elasticity of lens capsule.

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✓ Progressive increase in size and hardness (sclerosis) of lens substance, less easily moulded.
• Age-related decline in ciliary muscle power.
o Premature presbyopia:
• Uncorrected hypermetropia.
• Premature sclerosis of crystalline lens.
• General debility causing presenile weakness of colliery muscles.
• Chronic simple glaucoma.
❖ Symptoms:
o Difficulty in near vision, at first in dim light and after in good light also.
o Asthenopic symptoms due to fatigue of ciliary muscles after doing any near vision work.
o Intermittent diplopia due to disturbed relationship between accommodation and convergence (rare).
❖ Treatment:
o Optical treatment: Unifocal, bifocal or varifocal, i.e. progressive convex glass spectacles.
o Surgical treatment:
• Cornea based procedures:
✓ Monovision conductive keratoplasty (CK).
✓ Monovision LASIK.
✓ Presbyopic bifocal LASIK or LASIK by Presbyopia Avalos Rozakis method (LASIK-PARM).
✓ Presbyopic multifocal (PML) LASIK.
✓ Presbyond laser blended vision.
✓ Corneal inlays (Kamra inlay).
• Lens based procedures:
✓ Multifocal or accommodating IOL.
✓ Monovision with IOL.
• Sclera based procedure:
✓ Anterior ciliary sclerotomy (ACS).
✓ Scleral spacing procedures and scleral ablation.
✓ Scleral expansion.

➢ Important to note:
o Rough guide for presbyopia:
• 45 years: +1 to +1.25D.
• 50 years: +1.5 to +1.75D.
• 55 years: +2 to +2.25D.
• 60 years: +2.5D to +3D.
o Basic principles for presbyopic correction:
• Always find out refractive error for distance and first correct it.
• Find out the presbyopic correction needed in each eye separately and add it to the distant correction.
• Near point should be fixed by taking due consideration for profession of the patient.
• The weakest convex lens with which an individual can see clearly at the near point should be
prescribed, since overcorrection will also result in asthenopic symptoms.

08. Posterior capsular opacification. [2017, 2005]

❖ Posterior capsular opacification (PCO), often referred to as secondary cataract or after cataract, is the most common post-
operative complication of extra-capsular lens extraction surgery.
❖ Aetiopathogenesis:
o Risk factors:
• Most important: Young age.
• Others: Diabetes mellitus, uveitis, myotonic dystrophy, retinitis pigmentosa and traumatic cataract.
o Causes:
• Residual opaque lens matter may persist as PCO when it is imprisoned between the remains of anterior
and posterior capsule, surrounded by fibrin (following iritis) or blood (following hyphaema).
• Proliferative PCO may develop from lens epithelial cells (LECs), which can undergo:
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✓ Proliferation towards the posterior capsule.

✓ Migration towards the posterior capsule.
✓ Normal or abnormal differentiation.
❖ Clinical features:
o Symptoms: Reduced visual acuity, impaired contrast sensitivity and monocular diplopia. Occurs usually 9-12
months after surgery.
o Signs on slit-lamp examination:
• Semi-opaque membrane with variable levels of fibrosis on the posterior capsule.
• Capsular wrinkling.
❖ Clinical types:
o Elschnig's pearls:
• Most common type of PCO.
• Formed by proliferation and migration of LECs along the posterior capsule.
• Vacuolated and clustered soap bubble like appearance.
o Soemmering’s ring:
• Formed by capsular fibrosis due to fibrous metaplasia of epithelial cells.
• Appeared as a thick ring behind the iris, enclosed between two layers of capsule.
❖ Treatment:
o Elschnig's pearls: As the central posterior capsule is involved, it is best treated by Nd:YAG-laser capsulotomy. In
absence of Nd:YAG-laser, cystitome or Zeigler's knife is used.
o Sömmering’s ring: As central posterior capsule is clean, no treatment is needed.
o If dense membrane is present, surgical membranotomy is also done.

09. Management of recurrent pterygium. [2017, 2008]

❖ Pterygium is a wing-shaped fold of conjunctiva encroaching upon cornea from either side within the interpalpebral fissure.
❖ Recurrence: After surgical excision of the pterygium, the main problem is the recurrence with a recurrence rate of 30-50%.
❖ Management of recurrence:
o Surgical excision with free conjunctival limbal autograft (CLAU): Latest and most effective technique.
o Surgical excision with amniotic membrane graft (AMG) and mitomycin-C (MMC) (0.02%) application.
o Surgical excision with lamellar keratectomy and lamellar keratoplasty: May be required in deeply infiltrating
recurrent recalcitrant pterygium.
o Old methods: Not used now.
• McRaynold’s operation: Transplantation of pterygium in the lower fornix.
• Postoperative use of ß irradiations: May cause serious ocular complications.
❖ Surgical excision with free conjunctival limbal autograft (CLAU):
o Surgical excision procedure (bare sclera technique):
• After topical anaesthesia, eye is cleansed, draped and exposed using universal eye speculum.
• Head of the pterygium is lifted and dissected off the cornea very meticulously.
• Main mass of pterygium is then separated from the sclera underneath and the conjunctiva superficially.
• Pterygium tissue is then excised taking care not to damage the underlying medial rectus muscle.
• Haemostasis is achieved and the episcleral tissue exposed is cauterised thoroughly.
o Autografting procedure:
• Autograft is usually harvested from the superior paralimbai area of the same eye or the other eye.
• The conjunctival autograft may be retained with the help of:
✓ Suture: Not much in use due to discomfort.
✓ Fibrin glue: Expansive.
✓ Autologous serum: Patient's own serum, now a common practice.

10. Hypopyon corneal ulcer. [2016, 2002, 1998, 1996, 1994]

❖ Aetiopathogenesis:
o Causative organism: Hypopyon corneal ulcer is characteristically caused by Pneumococcus and is also called ulcer
serpens. It is not same as the corneal ulcer with hypopyon, which is caused by the Staphylococcus, Streptococcus,
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Gonococci, Moraxella and Pseudomonas pyocyanae.

o Source of infection: Exogenous, usually from chronic dacryocystitis.
o Predisposing factors: Old debilitated or alcoholic subjects.
o Mechanism of development: Severe iritis → diffusion of bacterial toxins → outpouring of PMNs from vessels into
the anterior chamber → precipitation of PMNs due to gravitation → sterile hypopyon formation with no bacterial
invasion.
❖ Clinical features:
o Symptoms:
• Little pain during initial stage which delays its diagnosis and treatment.
• Foreign body sensation.
• Watering, photophobia, redness of eye and blurred vision is also associated.
o Signs:
• Swelling of lid.
• Blepharospasm.
• Conjunctiva is chemosed and shows conjunctival hyperaemia and ciliary congestion.
• Corneal ulcer:
✓ Greyish white or yellowish disc-shaped ulcer near the centre of cornea.
✓ Ulcer creeps over cornea in a serpiginous fashion with an active end and a healing end.
✓ Active end shows infiltration and can cause perforation.
✓ Healing end shows simultaneous cicatrization, the edges may be covered with fresh epithelium.
• Associated severe iridocyclitis.
• Rapid increase in size of hypopyon can cause secondary glaucoma.
❖ Management:
o Topical antibiotic: Cefazoline (5%) and tobramycin (1.3%) or vancomycin (5%).
o Systemic antibiotic: Usually not required.
o Cycloplegic drugs: Atropine (1%) to reduce pain, prevent the formation of posterior synechiae and to reduce
exudation by decreasing hyperaemia and vascular permeability.
o Systemic analgesics and anti-inflammatory drugs.
o Vitamin: A, C and B complex help in early healing of ulcer.
o Anti-glaucoma drugs: Topical timolol, BID and oral acetazolamide.
o Dacryocystectomy: If dacryocystitis is detected.

11. Retinoblastoma. [2016]

❖ Retinoblastoma is a common malignant tumour arising from neurosensory retina in one or both eyes.
o Most common primary malignant intraocular tumour in children (average age is 18 months).
o Second most common malignant intraocular tumour after uveal melanoma.
o Most common cause of intraocular calcification.
❖ Genetics:
o First cancer to be associated with gene.
o Associated with RB gene, a cancer suppressor or anti-oncogenic gene, located in chromosome 13q.
o Knudson's two hit hypothesis: Deletion or inactivation of both the normal alleles of RB gene by two mutations.
❖ Heredity:
o Heritable (40%): 10% familial and 30% sporadic germline mutation.
• First hit (mutation) occurs in one allele of RB gene before fertilization.
• Second hit (mutation) occurs in late post zygotic phase.
• Bilateral multifocal retinoblastoma.
• Sometimes along with pinealoblastoma (trilateral retinoblastoma).
• Autosomal dominant inheritance, i.e. 50% children will have retinoblastoma.
o Non-heritable (60%): Sporadic somatic mutation.
• Both hits (mutations) occur in same retinal cell in the embryo after fertilization.
• Unilateral unifocal tumour.
• Patient has no predisposition for any non-ocular tumour.
❖ Clinical features:
o Leukocoria is the most common presentation.
o Squint is the second most common presentation.
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o Proptosis, orbital cellulitis, neovascular glaucoma and phthisis bulbi are also associated.
o Pseudohypopyon (tumour cells in anterior chamber) is seen in some cases.
o Spreads to CSF i.e. subarachnoid space via optic nerve.
o Most common site of metastasis is brain (CNS).
❖ Growth pattern:
o Endophytic: Most common, from retina grows into the vitreous.
o Exophytic: From retina grows towards choroid, which leads to serous retinal detachment and diffuse retinal
thickening.
❖ Investigation:
o MRI of orbit and brain is the investigation of choice.
o USG A scan V-V pattern.
o Paracentesis: Aqueous humour has increased LDH.
o FNAB/FNAC is contraindicated.
❖ Treatment:
o Chemotherapy: Treatment of choice.
• CVE regimen: 3 weekly 6 cycles of carboplatin on day 1, vincristine on day 1 and etoposide on day 1 & 2.
• Intra arterial chemotherapy by ophthalmic artery cannulation is done for targeted therapy.
o Focal treatment:
• Laser photocoagulation by diode laser.
• Cryotherapy only for peripheral tumours.
o Radiation:
• Brachytherapy.
• External beam radiation therapy (EBRT).
o Enucleation: Indicated when patient is presented with:
• Neovascular glaucoma.
• Tumour filling more than half of the vitreous.
• Optic nerve involvement.

12. Pterygium. [2015, 2000]

❖ Pterygium is a degenerative and hyperplastic changes of conjunctiva that affects the cornea also.
❖ Aetiopathogenesis:
o Environmental factors: UV rays, dry heat, high wind and abundance of dust.
o Pathology: Elastotic degeneration of subconjunctival tissue → proliferation as vascularized granulation tissue
under the epithelium → degeneration of corneal epithelium, Bowman's layer and superficial stroma.
❖ Clinical features:
o Symptoms:
• Mostly seen in old males doing outdoor work.
• Cosmetic problem is the only issue without any symptoms in most cases.
• Foreign body sensation and irritation.
• Defective vision during involvement of pupillary area.
• Diplopia due to limitation of ocular movement.
o Signs:
• Triangular or wing-shaped fold of conjunctiva encroaching upon the cornea from either side (mostly
nasal) within the interpalpebral fissure. Very rarely both sides are involved (primary double pterygium).
• Stocker line: Due to iron deposition, it is seen in corneal epithelium anterior to advancing head of
pterygium.
❖ Parts of a fully developed pterygium:
o Head: Apical part present on cornea.
o Neck: Constructed part present in the limbal area.
o Body: Scleral part, extending between limbus and the canthus.
o Cap: Semilunar whitish infiltrate just in front of the head.
❖ Types: Based on extent:
o Type I pterygium: Extends less than 2 mm onto the cornea.
o Type II pterygium: Extends upto 4 mm onto the cornea.
o Type III pterygium: Extends more than 4 mm onto the cornea and involves the visual axis.
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Based on progression, pterygium can be classified as progressive or regressive also.

❖ Complications:
o Common: Cystic degeneration and infection.
o Rare: Neoplastic changes like epithelioma, fibrosarcoma or malignant melanoma.
❖ Treatment:
o Medical: Tear substitute and steroids are used along with sunglasses to protect against UV rays.
o Surgical: Excision by bare sclera technique.
o Recurrence: Group D, question no. 09.

13. Epiphora. [2015, 1998]

❖ Watering of eye due to inadequate drainage (outflow) of normally secreted tear is called epiphora.
❖ Causes of epiphora: Group A, question no. 02.
❖ Clinical evaluation:
o Regurgitation on pressure over lacrimal sac (ROPLAS) test: To see any obstruction in the sac or NLD.
o Fluorescein dye disappearance test (FDDT): To evaluate atonia of sac or any mechanical obstruction.
o Lacrimal syringing test: To evaluate obstruction in the punctum, sac or NLD.
o Jones dye test: To rule out the cause if partial obstruction is suspected.
o Dacryocystography: To know the exact site, nature and extent of a mechanical obstruction.
o Radionucleotide dacryocystography (lacrimal scintillography): To assess the functional efficiency of lacrimal
drainage apparatus.

14. Eye banking and keratoplasty. [2015]

❖ Keratoplasty and eye banking: There is a need of around 2 lakh corneas per year for transplantation to clear the backlog
of corneal blindness. Currently we are collecting around 60,000 eyes per year. As keratoplasty operation can restore vision
in a significant number of corneal blinds, an intensive publicity and cooperation of government and nongovernment
agencies is needed to enhance the voluntary eye donations.
Under NPCB, eye donation fortnight is organized from 25th August to 8th September every year to promote eye
donation. Under Vision 2020: Indian initiative emphasis is on hospital retrieval system to get better donor material. Death
certificates should bear one line on eye donations.
❖ Keratoplasty: Group D, question no. 30.
❖ Eye banking: Eye bank is an organization which deals with the collection, storage and distribution of cornea for several
purposes. Functions of an eye bank includes:
o Promotion of eye donation by increasing awareness about eye donation to the general public.
o Registration of the pledger for eye donation.
o Collection of the donated eyes from the deceased.
o Receiving and processing the donor eyes.
o Preservation of the tissue for short, intermediate, long or very long term.
o Distribution of the donor tissues to the corneal surgeons.
o Research activities for improvement of the preservation methodology, corneal substitute and utilisation of the
other components of eye.

15. Anti-glaucoma drugs. [2016]

❖ Miotics or parasympathomimetic drugs: Increases trabecular outflow.

o Direct acting: Pilocarpine.
o Indirect acting or cholinesterase inhibitor: Echothiophate, demecarium bromide, physostigmine.
o Dual acting: Carbachol.
❖ Adrenergic agonists or sympathomimetic drugs:
o Non selective: Epinephrine, dipivefrine:
• Increases trabecular outflow.
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• Increases uveoscleral outflow.

• Decreases aqueous production by stimulating alpha receptors in ciliary processes.
o Selective alpha 2 agonist: Brimonidine, apraclonidine:
• Increases uveoscleral outflow.
• Decreases aqueous production by stimulating alpha receptors in ciliary processes.
❖ Beta blockers: Decreases aqueous production.
o Non selective: Timolol, levobunolol, carteolol, metipranolol.
o Cardio selective: Betaxolol.
❖ Prostaglandin analogues:
o Latanoprost, travoprost, unoprostone, tafluprost: Increases uveoscleral outflow.
o Bimatoprost:
• Increases trabecular outflow.
• Increases uveoscleral outflow.
❖ Carbonic anhydrase inhibitors: Acetazolamide, dorzolamide, brinzolamide: Decreases aqueous production.
❖ Hyperosmotic agents: Glycerol, mannitol, urea, isosorbide: Draw fluid from the eye into the circulation by osmotic effect.
❖ Indications:
Acute congestive glaucoma Chronic simple glaucoma
Osmotic agents: Adrenergic agonists:
✓ Mannitol 20% IV. ✓ Dipivefrine 0.1% topical.
✓ Glycerol 50% oral. ✓ Apraclonidine 1% topical.
Carbonic anhydrase inhibitors:
Carbonic anhydrase inhibitors: ✓ Acetazolamide oral.
✓ Acetazolamide IV or oral. ✓ Dorzolamide topical.
✓ Brinzolamide topical.
Beta blockers:
Beta blockers: ✓ Timolol 0.25% topical.
✓ Timolol 0.5% topical. ✓ Betaxolol 0.25% topical.
✓ Carteolol 1% topical.
Miotics: Miotics:
✓ Pilocarpine 2% topical. ✓ Pilocarpine 0.5% topical.
Prostaglandins: Prostaglandins:
✓ Latanoprost 0.005% topical. ✓ Latanoprost 0.005% topical (DOC).

16. Trabeculectomy. [2014, 2007]

❖ Trabeculectomy, first described by Cairns, is the most frequently performed partial thickness filtering surgery.
❖ Indications:
o PACG with peripheral anterior synechiae (>270°) or where medical therapy is not effective.
o POAG where medical therapy is not effective.
o Congenital and developmental glaucoma where trabeculotomy and goniotomy fail.
o Secondary glaucoma where medical therapy is not effective.
❖ Mechanisms of filtration:
o Aqueous flows from anterior chamber into the subconjunctival space through a fistula, which is created around
the margin of scleral flap.
o If the tissue is dissected posterior to the scleral spur, uveoscleral outflow is increased due to cyclodialysis.
❖ Surgical technique:
o Initial steps: Anaesthesia, cleansing, draping, exposure of eyeball and fixation with superior rectus suture.
o Conjunctival flap: A fornix-based or limbal-based conjunctival flap is fashioned and the underlying sclera is
exposed. The Tenon's capsule is cleared away using a Tooke's knife and haemostasis is achieved with cautery.
o Scleral flap: A partial thickness limbal-based scleral flap (5 mm x 5 mm) is reflected down towards the cornea.
o Excision of trabecular tissue: A narrow strip (4 mm x 2 mm) of the exposed deeper sclera near the cornea
containing the canal of Schlemm and trabecular meshwork is excised.
o Peripheral iridectomy: It is performed at 12 O'clock position with de Wecker's or Vanna's scissors.
o Closure: The scleral flap is replaced and 10-0 nylon sutures are applied. Then the conjunctival flap is reposited and
sutured with two interrupted sutures (fornix based flap) or continuous suture (limbal-based flap).
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o Subconjunctival injections: Dexamethasone and gentamicin are given.

o Patching: Eye is patched with a sterile eye pad and sticking plaster or a bandage.
❖ Complications: Shallow anterior chamber, hyphaema, iritis, cataract due to injury to the lens and endophthalmitis.

17. Use of laser in eye. [2014]

❖ Photoradiation:
o Photodynamic therapy (PDT): Vertiforin is used systematically as photosensitizing agent.
o Corneal collagen linking with riboflavin (C3R or CXR): Riboflavin is used topically as photosensitizing agent.
❖ Photocoagulation:
o Eyelid condition: Haemangioma.
o Corneal condition:
• Reduction of post operative astigmatism from cataract sutures by Argon laser suturotomy.
• Corneal neovascularization.
o Glaucoma:
• Laser iridotomy for narrow angle glaucoma.
• Argon laser trabeculoplasty (ALT) for open angle glaucoma.
• Laser goniopunctures for developmental glaucoma.
• Prophylactic pan-retinal photocoagulation (PRP) for neovascular glaucoma with CRVO.
• Cyclophotocoagulation for absolute or near absolute glaucoma.
• Laser sustainalized in trabeculectomy for enhancing aqueous drainage.
o Iris condition:
• Laser coreoplasty for updrawn pupil.
• Photomydriasis for pathologic miotic pupil.
• Laser sphincterotomy.
• Laser shrinkage of iris cyst.
o Retina and choroidal condition:
• Diabetic retinopathy: Pan-retinal photocoagulation (PRP) is used.
• Peripheral retinal vascular abnormalities: Eales' disease, proliferative sickle cell disease, Coats' disease,
retinopathy of prematurity.
• Intraocular tumours: Retinoblastoma, malignant melanoma, choroidal haemangioma.
• Macular diseases: Central serous retinopathy, age related macular degeneration (ARMD).
• Retinal detachment: For sealing of holes.
❖ Photodisruption:
o Nd:YAG laser:
• Capsulotomy for thickened posterior capsule.
• Membranectomy for pupillary membranes.
• Vitreolysis in anterior chamber during management of vitreous loss secondary to trauma or cataract
surgery.
• Phacolysis in phacoemulsification technique of cataract surgery.
o Femtosecond laser:
• Creation of corneal flap for LASIK.
• Creation of tunnel for intracorneal rings.
• Arcuate incision for corneal astigmatism.
• Keratoplasty incisions.
• Small incision lenticular extraction (SMILE) for myopia.
• Femtosecond laser assisted cataract surgery (FLACS).
❖ Photoablation:
o Photorefractive keratometry (PRK).
o Laser assisted in situ keratomileusis (LASIK) for refractive errors.
o Phototherapeutic keratectomy for bandshaped keratopathy.

18. SICS. [2013]

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❖ Small incision cataract surgery (SICS) is a sutureless technique of extra-capsular cataract extraction (ECCE) surgery with
intra ocular lens (IOL) implantation, which is performed through a self-sealing valvular sclerocorneal tunnel incision.
❖ Surgical steps of manual SICS:
o Superior reclus (bridle) suture: It is done to fix the eye in downward gaze. In against the rule (ATR) astigmatism,
bridle suture is passed through lateral rectus muscle and all the next steps are performed on temporal quadrant.
o Fornix-based conjunctival flap formation: It is made with the help of a sharp tipped scissors along the limbus
from 10 to 2 O'clock positions.
o Exposure of sclera: Conjunctiva and the Tenon's capsule are dissected, separated from the underlying sclera and
retracted to expose about 4 mm strip of sclera along the entire incision length.
o Haemostasis: It is achieved by applying gentle and just adequate wet field cautery.
o Sclerocorneal tunnel incision: Self-healing in nature.
• External scleral incision: 5.5 - 7.5 mm in length, 1.5 - 2 mm behind the limbus.
• Sclerocorneal tunnel: 1 - 1.5 mm in length, made in the clear cornea with the help of a crescent knife.
• Internal corneal incision: Made with the help of a sharp 3.2 mm angled keratome.
o Side-port entry of about 1.5 mm valvular corneal incision is made at 9 O'clock position.
o Anterior capsulotomy: It can be performed by:
• Can Opener technique: An irrigating cystitome is introduced into the anterior chamber and mulliple small
radial cuts are made in the anterior capsule for 360°
• Envelope technique (linear capsulotomy): A straight incision is made in the anterior capsule from 2-10
O'clock position. The rest of the capsulotomy is completed in the end after removal of nucleus and cortex.
• Continuous circular capsulorrhexis CCC: The anterior capsule is torn in a circular fashion either with the
help of an irrigating bent-needle cystitome or with a capsulorrhexis forceps.
o Hydrodissection: It is done to separate corticonuclear mass from the posterior capsule.
o Nuclear management: It consists of following manoeuvres:
• Prolapse of nucleus: Initiated during hydrodissection and completed by rotating the nucleus with
Sinskey's hook.
• Delivery of the nucleus outside: It is done through the sclerocorneal tunnel by:
✓ Irrigating wire vectis method.
✓ Blumenthal's technique.
✓ Phacosandwich technique.
✓ Phacofracture technique.
✓ Fishhook technique.
o Aspiration of cortex: The remaining cortex is aspirated out using a two-way irrigation and aspiration cannula from
the main incision and/or side port entry.
o IOL implantation: A PC-IOL is implanted in the capsular bag after filling the bag with viscoelastic substance.
o Removal of viscoelastic material: It is done with the help of two-way irrigation aspiration cannula.
o Wound closure: The anterior chamber is deepened with RL injected through side port entry. This leads to self-
sealing of the sclerocorneal tunnel incision due to valve effect. The conjunctival flap is reposited back and is
anchored with the help of wet field cautery.

19. Binocular vision. [2013]

❖ Definition: When a normal individual fixes his visual attention on an object of regard by the coordinated use of both eyes,
the image is formed on the fovea of both the eyes separately; but the individual perceives a single image i.e. produces a
single mental impression. This state is called binocular single vision (BSV).
❖ Developmental landmarks of BSV: It is a conditioned reflex, which is acquired after birth as:
o At birth: No central fixation and the eyes move randomly.
o By the first month: Fixation reflex starts developing and becomes established by 4 months.
o By 6 months: The macular stereopsis and accommodation reflex is fully developed.
o By6-7 years: Full visual acuity (6/6) is attained and binocular single vision is well developed.
❖ Prerequisites for development of BSV:
o Motor mechanism: Straight eyes starting from neonatal period with precise coordination for all directions of gaze.
o Sensory mechanism: Clear vision in both eyes so that similar images are presented to each retina.
o Mental process: Ability of visual cortex to promote binocular single vision.
Therefore, pathologic states disturbing any of the above mechanisms during the first few years of life will hinder the
development of BSV and may cause strabismus.

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❖ Grades: Tested with the help of synoptophore.

o Grade I: Simultaneous perception (SP): Perception of visual impulses (similar or dissimilar) simultaneously by the
visual cortex upon transmission from both eyes.
o Grade II: Fusion: Ability of two eyes to produce a single composite image from two similar images, which are
incomplete and different from each other in one small detail.
o Grade III: Stereopsis: Ability to perceive the 3rd dimension (depth perception). It is innate. This is possible by fusion
of signals from the retinal disparate elements.
❖ Anomalies:
o Suppression: Temporary active cortical inhibition of the image of an object formed on retina of the squinting eye.
o Amblyopia: Partial reversible loss of vison in one or both eyes in absence of any organic disease of ocular media,
retina and visual pathway.
o Abnormal retinal correspondence (ARC).
o Diplopia: Simultaneous perception of two images of a single object.
o Confusion.

20. Removal of corneal foreign body. [2013]

❖ A corneal foreign body is an object that is superficially adherent or embedded in the cornea. As the most anterior part of
the globe, the cornea is the most exposed to foreign bodies. Some of the common foreign bodies that may be embedded
in the cornea include glass, metal, sand, plastic, or wood.
❖ Steps of removal:
o Patient position: Patient is lied in supine position on an examination table.
o Anaesthesia: Eye is anaesthetized with topical installation of 2 to 4% xylocaine.
o Exposure of the cornea:
• Lids are separated with universal eye speculum.
• The patient is asked to look straight upward in a fixed object to keep the eye steady.
• Light is focused on the cornea through a slit lamp.
• The cornea is approached at an oblique or tangential angle to avoid corneal perforation.
o Loosening of the foreign body: The foreign body is engaged in the edge of a needle and is loosened. One can use
a subtle flicking motion to complete the procedure.
o Removal: The loosened up foreign body is now removed gently with the help of a forceps from the eye.
o Postoperative care:
• Patching with antibiotic eye ointment is applied for 24 to 48 hours.
• Antibiotic eye drops are instilled 3-4 times a day for about a week.
❖ Removal techniques for special foreign bodies:
o Vegetable matter, long needle like object or a foreign body adherent to the corneal surface can be removed by
jeweler’s forceps.
o Metallic foreign body can be removed with a magnetic spud.
o After removal of a metallic foreign body, there might be a brownish-orange rust ring remaining. It can be lifted
with a needle or jeweler’s forceps. The Alger brush is used in most cases to remove the rust ring.
o Superficial foreign body can be removed by a moist cotton tipped applicator.
o Multiple small particles can be removed by irrigation.
o Deep foreign body should be removed with extra care as it may enter the anterior chamber during removal.

21. Hypermetropia. [2012]

❖ When parallel rays of light coming from infinity are focused behind the retina when accommodation is at rest is called
hypermetropia.
❖ Aetiological classification:
o Axial hypermetropia: Due to decreased axial length of eyeball. It is commonest form of hypermetropia. Seen in:
• Congenital pathological: Microphthalmos, nanophthalmos, microcornea.
• Acquired pathological: Forward displacement of retina due to retinal detachment, central serous
retinopathy and orbital tumours.
• Developmental or physiological hypermetropia: Newborn.
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o Curvatural hypermetropia: Due to decreased curvature of cornea or lens or both. Seen in:
• Congenital pathological: Cornea plana, sclerocornea.
• Acquired pathological: Post traumatic or post inflammatory corneal flattening.
• Developmental or physiological hypermetropia.
o Index hypermetropia: Due to decreased refractive index of lens. Seen in:
• Old age due to cortical sclerosis.
• Diabetic patients under treatment.
o Positional hypermetropia: Due to congenital or acquired posterior subluxation of lens.
o Aphakia: Extreme hypermetropia due to absence of lens. May be congenital acquired.
o Consecutive hypermetropia:
• Overcorrected myopia following refractive surgery.
• Underpowered IOL implantation during cataract surgery and refractive lens exchange (RLE).
❖ Clinical features:
o Symptoms: Defective vision or asthenopia or both.
o Signs:
• Fundus findings: Small optic disc and cup, silk-shot appearance of retina, pseudopapillitis.
• Eye findings: Shallow anterior chamber, narrow angle.
o Complications:
• Recurrent styes, blepharitis or chalazion.
• Accommodative convergent squint.
• Amblyopia.
• Predisposition to development of primary narrow angle glaucoma.
• Anterior ischaemic optic neuropathy.
❖ Treatment:
o Optical treatment: Convex spectacles or contact lenses.
o Surgical treatment:
• Cornea based procedures:
✓ Thermal laser keratoplasty (TLK) by Thallium-Holmium-Chromium (THC):YAG laser.
✓ Conductive keratoplasty (CK).
✓ Hyperopic PRK.
✓ Hyperopic LASIK.
• Lens based procedures:
✓ Phakic refractive lens (PRL) or implantable contact lens (ICL) is used.
✓ Refractive lens exchange (RLE).

22. Bacterial corneal ulcer. [2012]

❖ Aetiopathogenesis:
o Risk factors: Corneal epithelial defect, foreign body, contact lens, dry lens.
o Causative organisms:
• Most common is Staphylococcus (oval, yellowish white, densely opaque ulcer with clear cornea).
• Most common in contact lens users is Pseudomonas (irregular, greenish exudative, semiopaque ulcer
with diffuse liquefactive necrosis and hypopyon).
• Others: Streptococcus (same as Staphylococcus), Enterobacteriaceae (shallow, greyish white, ulcer with
diffuse stromal opalescence), Neisseria.
o Pathology: Depending upon the virulence of the organism and treatment received ulcer may:
• Become localized and heal: Corneal epithelial damage → exogenous bacterial invasion → progressive
infiltration → active ulceration → regression → cicatrisation.
• Penetrate deep leading to corneal perforation.
• Spread fast to involve the whole cornea as sloughing cornea.
❖ Clinical feature:
o Types: Broadly bacterial corneal ulcer may be presented as two forms:
• Purulent corneal ulcer without hypopyon.
• Hypopyon corneal ulcer.
o Symptoms: Pain, foreign body sensation, watering, photophobia, blurred vision and redness.
o Signs:
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• Lid swelling.
• Blepharospasm.
• Conjunctival chemosis with conjunctival hyperaemia and ciliary congestion.
• Corneal ulcer: Features of the ulcer vary with respect to the causative organism.
• Iris is slightly muddy in colour.
• Pupil is small due to toxin induced iritis.
• IOP may be raised.
❖ Treatment: Group D, question no. 10.

23. Diabetic retinopathy. [2011]

❖ Diabetic retinopathy (DR) refers to retinal changes seen in patients with diabetic mellitus (DM).
❖ Risk factors:
o Duration of DM: Most important risk factor.
• After 10 years: 20% type I and 25% type II patients develop DR.
• After 20 years: 90% type I and 60% type II patients develop DR.
• After 30 years: 95% type I and 95% type II patients develop DR.
o Controllable systemic factor: Glycaemic index, BP, lipid level, urea, creatinine.
o Others: Smoking, pregnancy, hereditary.
❖ Pathogenesis and clinical presentations:

Diabetes mellitus (DM): Vascular and haematological changes:

✓ Sorbitol accumulation in cells. ✓ Thickening of capillary basement
✓ Advanced glycogen end-product (AGE) accu- membrane.
mulation in cells. ✓ Capillary endothelial cell damage.
✓ Activation of protein kinase C. → ✓ RBC shape deformation and rouleax
✓ Activation of eicosanoids, nitric oxide and in- formation.
tracellular adhesion molecules. ✓ Increased stickiness of platelets.
✓ Excessive oxidative stress due to excess free ✓ Increased plasma viscosity.
radical accumulation in cells. ✓ Loss of capillary pericytes.

Clinical presentations:
✓ Capillary leakage.
✓ Microaneurysm (1st sign).
✓ Dot-blot haemorrhage.
→ microvascular occlusion → retinal ischemia → ✓ Retinal oedema.
✓ Hard exudate.
✓ Arteriovenous shunts (intraretinal micro-
vascular abnormalities – IRMA).
✓ Neovascularization.

❖ Classification: On the basis of clinical features and progression, DR is classified as:

o Non-proliferative diabetic retinopathy (NPDR): Mild, moderate, severe or very severe.
o Proliferative diabetic retinopathy (PDR): With or without high-risk characteristics (HRCs).
o Diabetic maculopathy: Focal exudative, diffuse exudative, ischaemic or mixed.
o Advanced diabetic eye disease (ADED).
❖ Management:
o Screening:
• First examination: 3 years after diagnosis of DM I and immediately for DM II.
• Every year: Till no DR or in mild NPDR.
• Every 6 months: In moderate NPDR.
• Every 3 months: In severe NPDR.
• Every 2 months: In PDF with no HRCs.
o Strict controlling of the controllable risk factors.
o Anti VEGF drugs: Intravitreal injection of bivacizmzumab, ranibizumab or pegaptanib.
o Intravitreal steroid injection.

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o Laser therapy: Macular photocoagulation, panretinal photocoagulation (PRP, gold standard).

o Surgery: Tractional DME with NPDR or advanced PDR.

24. Capsulotomy in cataract surgery. [2011]

❖ Optimal outcomes of a cataract surgery largely depend on the successful performance of an anterior capsulotomy. It can
be performed by any of the following methods:
❖ Can-opener's technique:
o Technique: A circular opening, 5-6 mm in diameter is created by series of small radial tears in the anterior capsule
with a cystitome, made by bending a 26-gauge needle or using a prefabricated commercially available cystitome.
o Disadvantages: Easy to perform but its radial tears make the capsule unstable. So it creates difficulty in other
surgical steps like phacoemulsification.
❖ Linear capsulotomy or envelope technique:
o Technique: A linear incision is made in upper one-third of anterior capsule from 2-10 o’clock position, followed
by nucleus delivery and intercapsular aspiration of cortical matter. After complete removal of cataract, radial cuts
are made at ends of incision with Vannas scissors and capsular flap is torn off.
o Advantages: Major advantages include minimal trauma to corneal endothelium and a good centration of IOL.
❖ Continuous curvilinear capsulorrhexis (CCC):
o Recently, this is the most commonly performed procedure.
o Technique: A small tear is created in the centre of the anterior capsule and later the resulting capsular flap is
advanced into a circular shape by guiding the leading edge with the cystitome.
Alternatively, the capsular flap can be pulled in a circular fashion by grasping the leading edge with a
forceps and advancing the tear with frequent regrasping.
o Instruments used: Various instruments and devices have been developed to facilitate the creation of a CCC that
include needle capsulorrhexis, forceps capsulorrhexis, bimanual capsulorrhexis and two-staged capsulorrhexis.
o Advantages: CCC provides a more predictable effective lens position (ELP) and optimal refractive outcome. In
addition, it also reduces the occurrence of posterior capsular opacification (PCO).
❖ Capsulotomy of special cataracts:
o Triangular capsulotomy in hyper mature cataract.
o Crossed-swords, capsule-pinch technique in soft cataract.
❖ Advanced capsulotomy techniques:
o Femtosecond laser assisted capsulotomy.
o Plasma blade capsulotomy.
o Precision pulse capsulotomy (PPC) or Zepto.
o Capsulotomy using pulse electron avalanche knife.

25. Red eye. [2010, 2007]

❖ Red eye is formed due to irritated or inflamed blood vessels on the surface of the sclera due to different pathological or
non-pathological reasons.
❖ Non-pathological reasons:
o Rubbing eye.
o Sleep deprivation.
o Prolonged screen time.
o Chlorine or smoke exposure.
❖ Pathological reasons and algorithm for diagnosis:
Patient presented with red eye
↓
History of pain
↓ ↓
Mild or no pain with mild Moderate to severe pain with vision loss,
blurring or normal vison distorted pupil and corneal involvement
↓ ↓

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Hyperaemia
↓ ↓ Vesicular rush (herpetic keratitis), severe mucopurule-
Focal Diffuse nt discharge (hyperacute bacterial conjunctivitis, kera-
↓ ↓ titis, corneal ulcer, acute angle glaucoma, iritis, traum-
Episcleritis History of discharge atic eye injury, chemical burn, scleritis → emergency
↓ ↓ ophthalmological reference
No Yes
↓ ↓
Subconjunctival haemorrhage Frequency of discharge
↓ ↓
Intermittent Contentious
↓ ↓
Dry eye Type of discharge
↓ ↓
Watery or serous Mucopurulent or purulent
↓ ↓
History of itching ● Acute bacterial conjunctivitis
↓ ↓ ● Chlamydial conjunctivitis
Mild to none Moderate to severe
↓ ↓
Viral conjunctivitis Allergic conjunctivitis

26. Side effects of topical steroids. [2010]

❖ Topical corticosteroid drugs are used in uveitis, scleritis, allergic conjunctivitis, allergic keratitis, cystoid oedema and after
intra-ocular surgery. But these drugs, specially on prolonged use, show 4 important side effects:
1. Cataract.
2. Glaucoma.
3. Infection.
4. Delayed wound healing.
❖ Corticosteroid induced cataract:
o Mechanism: Posterior subcapsular opacities are associated with the use of topical steroids. Exact relationship
between dose and duration of corticosteroid therapy with the development of cataract is still unclear.
o Risk factor: Young age.
❖ Steroid induced glaucoma:
o Mechanism: Steroid use → increased expression of ocular extracellular matrix proteins → increased resistance to
the outflow of aqueous from the eye → increase in the IOP.
o Risks factor:
• Pre-existing primary open angle glaucoma.
• A history of increased IOP with previous steroid administration.
• Type I DM.
• Extremity of age.
❖ Activation of infection and delayed wound healing: While local steroid therapy is valuable in infections of the eye along
with antibiotics, owing to their ability to reduce inflammation and scarring, these benefits must be weighed against the
risk of recurrent infection and delayed wound healing. Activation of infection generally occurs in herpetic, bacterial and
fungal keratitis.
❖ Other side effects:
o Dry eye.
o Ptosis.
o Abrupt stoppage of use can cause rebound inflammation.
❖ Prevention:
o All patients with diseases requiring prolonged corticosteroids therapy should be regularly examined for the
complications.
o Intermittent regimes should be preferred over regular therapy.
o Whenever possible steroids should be substituted by nonsteroidal anti-inflammatory drugs (NSAIDs).

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27. DCR. [2009]

❖ Dacryocystorhinostomy (DCR) is the operation of choice to reestablish the lacrimal drainage. DCR can be performed by
following techniques:
❖ Conventional external approach DCR:
o Anaesthesia: General anaesthesia.
o Skin incision: Either a curved incision along the anterior lacrimal crest or a straight incision 8 mm medial to the
medial canthus is made.
o Exposure of medial palpebral ligament and anterior lacrimal crest: Blunt dissection and cut with scissors is made.
o Dissection of lacrimal sac: Periosteum is separated from the anterior lacrimal crest and along with the lacrimal
sac is reflected laterally with blunt dissection exposing the lacrimal fossa.
o Exposure of nasal mucosa: A 15 mm x 10 mm bony ostium is made by removing the anterior lacrimal crest and
the bones forming lacrimal fossa, exposing the thick pinkish while nasal mucosa.
o Preparation of flap of sac: A probe is introduced into sac through lower canaliculus and the sac is incised vertically.
o Fashioning of nasal mucosal flaps: Done by vertical incision converted into H shape.
o Suturing of flaps: Posterior flap of the nasal mucosa is sutured with posterior flap of the sac using 6-0 vicryl or
chromic cat gut sutures. It is followed by suturing of the anterior flaps.
o Closure: MPL is sutured to periosteum, orbicularis muscle is sutured with 6-0 vicryl and skin is closed with 6-0 silk
suture.
❖ Endonasal DCR: More preferred technique.
o Preparation and anaesthesia: Nasal mucosa is prepared with nasal decongestant drops and local anaesthetic
agent. Conjunctival sac is anaesthetised with topically instilled 2% lignocaine. Then 3 mL of lignocaine 2% with 1
in 2 lac adrenaline is injected into the medial parts of upper and lower eyelids and to the lacrimal fossa region.
o Identification of sac area: A 20-gauge light pipe is inserted via the upper canaliculi into the sac and seen via
endoscope. A further injection of lignocaine with adrenaline is made below the nasal mucosa in this area.
o Creation of opening in the nasal mucosa, bones forming the lacrimal fossa and posteromedial wall of sac can be
accomplished by two techniques:
• By cutting the tissues with appropriate instruments.
• By ablating with Holmium YAG laser (laser-assisted DCR).
o Stenting of rhinostomy opening: The outflow system is then stinted using fine silicone tubes passed via the
superior and inferior canaliculi into the rhinostomy and secured with a process of knotting.
o Nasal packing and dressing is done.
o Postoperative care: After 24 hours of operation nasal packs are removed and patient is advised to use
decongestant, antibiotic and steroid nasal drops for 3-4 weeks.
o Removal of silastic lacrimal stents: Removed 8-12 weeks after surgery and the nasal drops are continued.
❖ Endocanalicular laser DCR: In this technique, under general anaesthesia laser probe is passed through a canaliculus up to
the medial wall of sac to form the lacrimal fossa with a Holmium YAG or KTP laser.

28. Keratoplasty indications. [2009]

❖ Keratoplasty, also called corneal grafting or corneal transplantation, is an operation in which the patient’s diseased cornea
is replaced by the healthy clear cornea.
❖ Indications of autokeratoplasty (autografting):
o Rotational keratoplasty: Indicated when pupillary area of the cornea has a small opacity.
o Contralateral keratoplasty: Indicated when cornea of one eye of the patient is opaque and the other eye is blind
due to posterior segment disease (e.g. optic atrophy or retinal detachment) with clear cornea.
❖ Indications of allo-keratoplasty (allografting):
o Penetrating keratoplasty (PK):
• Optical indications i.e. to improve vision: Indicated in corneal opacity, bullous keratopathy, corneal
dystrophies, advanced keratoconus.
• Therapeutic: Indicated when inflamed cornea does not respond to conventional therapy.
• Tectonic graft i.e. to restore integrity of eyeball: Indicated after corneal perforation and in marked
corneal thickening.
• Cosmetic: Indicated to improve the appearance of the eye.
o Anterior lamellar keratoplasty (ALK): Performed when pathology is up to the stroma, and endothelium and
Descemet’s membrane are normal.
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• Superficial ALK (SALK): Indicated in case of superficial stromal haze, indolent corneal ulcer.
• Deep ALK (DALK): Indicated in case of full thickness stromal haze, lattice dystrophy.
o Posterior lamellar keratoplasty (PLK) or endothelial keratoplasty (EK): Performed when only endothelium is
defective.
• Fuchs endothelial dystrophy.
• Bullous keratopathy.
• Pseudophakic corneal oedema.
• Posterior polymorphous dystrophy.
• Aphakic corneal oedema.
• Iridocorneal endothelium (ICE) syndrome.
• Failed corneal graft.
o Small patch graft: Indicated for small defects.
❖ Eye banking and keratoplasty: Group D, question no. 14.

29. Complications of cataract surgery. [2009]

❖ Preoperative complications:
o Anxiety.
o Irritative or allergic conjunctivitis due to pre-operative topical antibiotic drops.
o Complications due to local anaesthesia:
• Retrobulbar haemorrhage.
• Oculocardiac reflex like bradycardia, cardiac arrhythmia.
• Perforation of globe.
• Subconjunctival haemorrhage.
• Spontaneous dislocation of lens.
❖ Operative complications:
o Superior rectus muscle laceration.
o Excessive bleeding.
o Incision related complications:
• In ECCE: Irregular incision leading to defective coaptation of wound.
• In manual SICS and phacoemulsification: Complications can occur during self-sealing tunnel incision.
✓ Button holing of anterior wall of tunnel.
✓ Premature entry into the anterior chamber.
✓ Scleral disinsertion.
o Injury to the cornea, iris with iridocyclitis and lens.
o Complications related to anterior capsulorrhexis:
• Escaping capsulorrhexis: Extension of capsulorrhexis upto equator or posterior capsule.
• Small capsulorrhexis: Can cause posterior capsular tear, nuclear drop and zonular dehiscence.
• Very large capsulorrhexis: Creates problem for in the bag placement of IOL.
• Eccentric capsulorrhexis: Can cause IOL disintegration at later stage.
o Posterior capsular rupture (PCR).
o Vitreous prolapse and loss.
o Nuclear drop into the vitreous cavity.
o Posterior loss of lens fragment.
o Explosive choroidal haemorrhage.
❖ Early post operative complications:
o Hyphaema.
o Iris prolapse.
o Striate keratopathy.
o Flat (shallow or nonformed) anterior chamber:
• Flat anterior chamber with wound leak.
• Ciliochoroidal detachment.
• Pupil block due to vitreous bulge.
o Post operative anterior uveitis.
o Toxic anterior segment syndrome (TASS).
o Bacterial endophthalmitis.
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❖ Late post operative complications:

o Cystoid macular oedema (CME).
o Delayed chronic post operative endophthalmitis.
o Pseudophakic bulbous keratopathy (PBK).
o Retinal detachment.
o Epithelial ingrowth.
o Fibrous downgrowth.
o After cataract or secondary cataract or posterior capsular opacification (PCO).
o Glaucoma in aphakia and pseudophakia.
❖ IOL related complications:
o Uveitis glaucoma hyphaema (UGH) syndrome in rigid anterior chamber IOLs.
o Malposition of IOL:
• Sunset syndrome: Inferior subluxation of IOL.
• Sunrise syndrome: Superior subluxation of IOL.
• Lost lens syndrome: Complete dislocation of IOL into vitreous cavity.
• Windshield wiper syndrome: In case of very small IOL, superior loop moves with movement of head.
o Pupillary capture of IOL following post operative iritis or proliferation of the remains of land fibres.
o TASS.

30. Keratoplasty [2008]

❖ Definition, classification based indication: Group D, question no. 28.

❖ Surgical technique:
o Excision of donor corneal button: The donor corneal button should be cut 0.25 mm larger than the recipient,
taking care not to damage the endothelium. Donor cornea is placed in a tephlon block and the button is cut with
the help of a trephine from the endothelial side.
o Excision of recipient corneal button: With the help of a corneal trephine (7.5 mm to 8 mm in size) a partial
thickness incision is made in the host cornea. Then, anterior chamber is entered with the help of a razor blade
knife and excision is completed using corneoscleral scissors.
o Suturing of corneal graft into the host bed: It is done with either continuous or interrupted 10-0 nylon sutures.
❖ Complications:
o Early complications: Flat anterior chamber, iris prolapse,. infection, secondary glaucoma, epithelial defects and
primary graft failure.
o Late complications: Graft rejection, recurrence of disease and astigmatism.

31. Management of right convergent squint. [2008]

❖ Goal of treatment:
o To achieve good cosmetic correction.
o To improve visual acuity.
o To maintain binocular single vision (BSV).
However, many times it is not possible to achieve all the goals in every case.
❖ Treatment modalities:
o Correction of reflective error: Spectacles with full correction of refractive error should be prescribed. It will
increase the visual acuity. If it is an accommodative squint, correction of visual acuity may correct the squint
partially or completely.
o Occlusion therapy: If the patient is found to have amblyopia, occlusion therapy is indicated. After correcting the
refractive error, the normal eye is occluded and the patient is advices to use the squinting eye. Regular follow-ups
are done in squint clinic. Occlusion helps to improve the vision generally in children below the age of 10 years.
o Pre-operative orthoptic exercises: These are given after the correction of amblyopia to overcome suppression.
o Squint surgery: It should always be instituted after the correction of refractive error, treatment of amblyopia and
orthoptic exercises.
• Principle: Weaken the strong muscle by recession (shifting the insertion posteriorly) and strengthen the
weak muscle by resection (shortening the muscle). Here:

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✓ Weak muscle: Lateral rectus (LR).

✓ Strong muscle: Medial rectus (MR).
• Type and amount of muscle surgery: It depends upon the type and angle of squint, age of patient,
duration of the squint and the visual status. Therefore, degree of correction versus amount of extraocular
muscle manipulation required cannot be mathematically determined. However, roughly:
✓ 1 mm recession of MR: Correct about 2-3 PD.
✓ 1 mm resection of LR: Correct about 2 PD.
✓ Maximum limit allowed for MR recession: 7 mm.
✓ Maximum limit allowed for LR resection: 8 mm.
o Postoperative orthoptlc exercises: These a re required to improve fusional range and maintain binocular single
vision (BSV).

➢ Important to note:
o 1 mm resection of MR: Correct about 2-2.5 PD.
o 1 mm recession of LR: Correct about 2 PD.
o Maximum limit allowed for MR resection: 8 mm.
o Maximum limit allowed for LR recession: 10 mm.

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Note:

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Old questions (before 2006)

01. Anisometropia. [2004]

❖ The optical state with unequal refraction in the two eyes is termed anisometropia.
❖ Aetiology:
o Congenital and developmental anisometropia: Due to differential growth of the two eyeballs.
o Acquired anisometropia: Due to asymmetric age change, uniocular aphakia after removal of cataractous lens or
due to implantation of IOL of wrong power.
❖ Clinical presentation:
o Anisometropia upto 2.5D is well tolerated.
o Anisometropia between 2.5 and 4D can be tolerated depending upon the individual sensitivity.
o Anisometropia more than 4D is not tolerated and is a matter of concern.
❖ Clinical types:
o Simple anisometropia: One eye is normal (emmetropic) and the other eye is either myopic (simple myopic aniso-
metropia) or hypermetropic (simple hypermetropic anisometropia).
o Compound anisometropia: Both eyes are either hypermetropic (compound hypermetropic anisometropia) or
myopic (compound myopic anisometropia), but one eye is having higher refractive error than the other.
o Mixed anisometropia: One eye is myopic and the other is hypermetropic. This is also called antimetropia.
o Simple astigmatic anisometropia: One eye is normal (emmetropic) and the other eye has either simple myopic
or hypermetropic astigmatism.
o Compound astigmatic anisometropia: Both eyes are astigmatic but of unequal degree.
❖ Status of binocular vision in anisometropia: Three possibilities are as follows:
o Binocular single vision: BSV is present in small degree of anisometropia (less than 3D)
o Uniocular vision: When refractive error in one eye is of high degree, that eye is suppressed and develops
anisometropic amblyopia. Thus, the patient has only uniocular vision. Efforts should be made to fully correct the
anisometropia in children to prevent anisometropic amblyopia.
o Alternate vision: In antimetropia, the hypermetropic eye is used for distant vision and myopic for near vision.
❖ Diagnosis: By retinoscopic examination and/or autorefractometry in patients with defective vision.
❖ Treatment:
o Spectacles: Can be tolerated up to a maximum difference of 4D. After that there occurs diplopia.
o Contact lenses: For higher degrees of anisometropia.
o Other:
• Intraocular lens implantation for uniocular aphakia.
• Refractive corneal surgery for unilateral high myopia, astigmatism and hypermetropia.
• Phakic refractive lenses (PRL) and refractive lens exchange(RLE) in very high degree anisometropia.

02. Blepharitis. [2000]

❖ Blepharitis is a subacute or chronic inflammation of the lid margins.

❖ Bacteria blepharitis: Also called chronic anterior, ulcerative or staphylococcal blepharitis.
o Aetiology: Coagulase positive Staphylococci.
o Symptoms: Chronic irritation, itching, mild lacrimation, gluing of cilia and mild photophobia.
o Signs:
• Lid margins are red, thickened and associated with yellow crusts, small ulcers.
• Mild papillary conjunctivitis and conjunctival hyperaemia are also associated.
o Complications:
• Lash abnormalities: Madarosis (absence of cilia), trichiasis (misdirected cilia), poliosis (greying of lashes).
• Tylosis: Thickening and scarring of lid margins.
• Punctal eversion: Eversion of punctum → epiphora → eczema of skin and ectropion.
• Others: Recurrent stye, marginal keratitis, tear film instability and dry eye, secondary inflammatory and
mechanical changes in the conjunctiva and cornea.
o Treatment:
• Lid hygiene: Warm compression, crust removal, lid margin cleaning and avoid rubbing of eyes.
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• Antibiotics: Oral erythromycin or doxycycline if topical antibiotics are unresponsive.

• Topical steroid: Low potency drug like fluoro-metholone is used in blepharitis associated with papillary
conjunctivitis, marginal keratitis etc.
• Ocular lubricants: If there is tear film instability and dry eye.
❖ Seborrheic or squamous blepharitis:
o Aetiology: This primary anterior blepharitis occurs in association with scalp dandruff and excessive lipase activity
of bacterias like Corynebacterium acne.
o Symptoms: Irritation, itching, occasional lacrimation and history of falling of eyelashes.
o Signs: Lid margins are thickened and associated with white dandruff-like scales.
o Complications: Same as bacterial blepharitis.
o Treatment: Removal of dandruff from scalp and scales from lid margins along with topical antibiotic therapy.
❖ Posterior blepharitis (meibomistis):
o Aetiology: Occurs chronically due to chronic meibomian gland dysfunction along with excessive bacterial lipase
activity and acutely due to Staphylococcal infection.
o Symptoms: Irritation, itching, mild lacrimation, burning, grittiness and exacerbations intermittently.
o Signs:
• Prominent openings of meibomian glands with white frothy (foam like) secretions.
• Vertical yellowish streaks shining through conjunctiva.
• Hyperaemia and telangiectasia of posterior lid margin around orifices of meibomian glands.
• Oily and foamy tear film.
o Complications: Papillary conjunctivitis, inferior corneal punctate epithelial erosion.
o Treatment: Same as bacterial blepharitis with compulsory systemic tetracycline antibiotic.
❖ Parasitic blepharitis (lash infection):
o Aetiology: Phthiriasis palpebrum by Phthirus pubis, pediculosis by Pediculus humanus, demodex blepharitis due
to Demodex folliculorum.
o Symptoms: Chronic irritation, itching, mild lacrimation and burning.
o Signs: Red thickened lid margins with lice and nits (eggs).
o Treatment:
• Mechanical removal of lice and nits.
• Antibiotic ointment and yellow mercuric oxide 1% is used.
• Delousing nog patient, family members, clothing and bedding is important to prevent recurrence.

03. Ptosis. [1999]

❖ Abnormal dropping of upper eyelid covering more than 2mm of the cornea is called ptosis.
❖ Clinico-aetiological types:
o Congenital ptosis:
• Simple congenital ptosis: Not associated with any other abnormality.
• Congenital ptosis with associated weakness of superior rectus muscle.
• Blepharophimosis syndrome: Congenital ptosis, blepharophimosis, telecanthus, epicanthus inversus.
• Congenital synkinetic ptosis: Marcus Funny jaw-winking ptosis due to trigemino-oculomotor synkinesis.
o Acquired ptosis:
• Neurogenic ptosis: It is caused by innervation defects such as third nerve palsy, Horner's syndrome, oph-
thalmoplegic migraine, multiple sclerosis.
• Acquired myogenic ptosis: It is caused by acquired disorders of LPS or myoneural junction such as
myasthenia gravis, myotonic dystrophy, ocular myopathy, trauma to LPS, thyrotoxicosis etc.
• Aponeurotic ptosis: It is caused by defects of levator aponeurosis in presence of normal muscle function.
• Mechanical ptosis: It is caused by excessive weight on upper lid such as tumour, chalazion or oedema.
❖ Clinical evaluation:
o Unilateral cases: Difference between vertical height of palpebral fissures of two sides indicates degree of ptosis.
o Bilateral cases: The amount of cornea covered by the upper eye lid indicates degree of ptosis:
• Mild ptosis: 2 mm.
• Moderate ptosis: 3 mm.
• Severe ptosis: 4 mm.
❖ Treatment:
o Congenital ptosis: Almost always needs surgical correction. It is treated by any of the following operations:
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• Tarso-conjunctivo-Mullerectomy (Fasanel-Servat operation): Indicated in mild ptosis with good levator

function and in Horner's syndrome (acquired ptosis).
• Levator resection: Indicated in moderate to severe ptosis.
• Frontalis sling operation (Brow suspension): Indicated in severe ptosis with no levator function and in
neurogenic ptosis of 3rd nerve palsy.
o Acquired ptosis:
• Treatment of the underlying cause.
• Conservative treatment should be carried out and surgery differed at least for 6 months in neurogenic
ptosis.
• Surgical corrections like congenital ptosis.

04. Lagophthalmos. [1996]

❖ The inability to close the eyelids voluntarily is called as lagophthalmos.

❖ Aetiology:
o Pathological: It occurs in patients with:
• Paralysis of orbicularis oculi muscle.
• Cicatricial contraction of the lids.
• Symblepharon, severe ectropion, proptosis.
• Following over-resection of the levator muscle for ptosis.
• In comatosed patients.
o Physiological: Physiologically, some people sleep with their eyes open (nocturnal lagophthaJmos).
❖ Pathogenesis: The main cause of lagophthalmos is:
o Facial nerve palsy.
o Leprosy.
o Myxoedema.
❖ Clinical features: It is characterised by incomplete closure of the palpebral aperture associated with features of the
causative disease.
❖ Complications:
o Conjunctival xerosis.
o Corneal xerosis.
o Exposure keratitis.
❖ Treatment:
o Measures to prevent exposure keratitis:
• Artificial tear drops: This should be instilled frequently.
• Antibiotic: The open palpebral fissure should be filled with an antibiotic eye ointment during sleep and
in comatosed patients.
• Soft bandage contact lens: This may be used to prevent exposure keratitis.
• Tarsorrhaphy: This is a surgical procedure which may be performed to cover the exposed cornea when
indicated. It can be temporary or permanent.
o Measures to treat the cause: Wherever possible should be taken.

05. Bitot's spot. [2001]

❖ Bitot's spot is an ocular manifestation of nutritional deficiency causing xerophthalmia.

❖ Aetiology:
o Dietary deficiency of vitamin A.
o Defective absorption of vitamin A from gut.
o Accompanied by protein-energy-malnutrition (PEM) and infections.
❖ Pathogenesis: Nutritional deficiency causes conjunctival xerosis. Extension of this xerotic process due to continuation of
the nutritional deficiency or absence of proper treatment leads to Bitot's spot formation.
❖ Features:
o Appearance: Silvery white, foamy, triangular patch of keratinized epithelium.
o Location: Situated on the bulbar conjunctiva in the interpalpebral area.
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o Laterality: Usually bilateral and temporal and less frequently nasal.

o In the new WHO xerophthalmia classification, it is classified as X1B.
❖ Treatment:
o Local ocular therapy: Artificial tear should be installed every 3-4 hours.
o Vitamin A therapy:
• All patients above the age of 1 year (except women of reproductive age): 200,000 lU of vitamin A orally
or 100,000 IU by intramuscular injection should be given immediately on diagnosis and repeated the
following day and 4 weeks later.
• Children under the age of 1 year and children of any age who weigh less than 8 kg: They should be
treated with half the doses for patients of more than 1 year of age.
• Women of reproductive age, pregnant or not: Should be treated with a daily dose of 10,000 lU of vitamin
A orally (1 sugar coated tablet) for 2 weeks.
o Treatment of underlying conditions: PEM and other nutritional disorders, diarrhoea, dehydration and electrolyte
imbalance, infections and parasitic conditions should be considered simultaneously.

06. Xerosis of conjunctiva. [2002,1998]

❖ Xerosis of the conjunctiva is a symptomatic condition in which conjunctiva becomes dry and lustreless. Normal conjunctiva
is kept moist by its own secretions, mucin from goblet cells and aqueous solution from accessory lacrimal glands. Therefore,
even if the main lacrimal gland is removed, xerosis does not occur.
❖ Aetiological classification:
o Parenchymatous xerosis: It occurs following cicatricial disorganization of the conjunctiva due to local causes like:
• Destructive interstitial conjunctivitis: Seen in trachoma, diphtheric membranous conjunctivitis, Steven-
Johnsons syndrome, pemphigus or pemphigoid conjunctivitis, thermal, chemical or radiational burns of
conjunctiva.
• Exposure of conjunctiva to air: Seen in marked degree of proptosis, facial palsy, ectropion, lack of
blinking (as in coma) and lagophthalmos due to symblepharon.
o Epithelial xerosis: It occurs due to hypovitaminosis A. In the new WHO classification of xerophthalmia,
conjunctival xerosis is marked as X1A.
❖ Clinical features:
o Parenchymatous xerosis: Marked dryness, thickening, scarring and even keratinization associated with features
and complication of the causative disease.
o Epithelial xerosis:
• Mostly seen in children.
• Appearance: One or more patches of dry, lusterless, nonwettable conjunctiva, which has been well
described as ‘emerging like sand banks at receding tide' when the child ceases to cry.
• Association: It is generally associated with night blindness or as a part and parcel of the xerophthalmia.
• Location: Almost always involve the interpalpebral area of temporal quadrant and often the nasal
quadrant as well. In more advanced cases, the entire bulbar conjunctiva may be affected.
• Other presentations of conjunctiva: Thickening, wrinkling and pigmentation.
❖ Treatment:
o Local ocular therapy: Artificial tear should be installed every 3-4 hours.
o Vitamin A therapy:
• All patients above the age of 1 year (except women of reproductive age): 200,000 lU of vitamin A orally
or 100,000 IU by intramuscular injection should be given immediately on diagnosis and repeated the
following day and 4 weeks later.
• Children under the age of 1 year and children of any age who weigh less than 8 kg: They should be
treated with half the doses for patients of more than 1 year of age.
• Women of reproductive age, pregnant or not: Should be treated with a daily dose of 10,000 lU of vitamin
A orally (1 sugar coated tablet) for 2 weeks.
o Treatment of underlying conditions: PEM and other nutritional disorders, diarrhoea, dehydration and electrolyte
imbalance, infections and parasitic conditions should be considered simultaneously.

07. Subconjunctival haemorrhage. [2000]

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❖ Subconjunctival haemorrhage (SCH) is a common condition of the eye with sharp circumscribed redness of bleeding
underneath the conjunctiva in the absence of discharge and inflammation in contagious areas.
❖ Pathology: SCH can be defined as haemorrhage between the conjunctiva and episclera and the blood elements are found
in the substantia propria of the conjunctiva when a subconjunctival vessel breaks.
❖ Risk factors:
o Systemic vascular diseases: The fragility of conjunctival vessels as a result of arteriosclerosis, systemic hyper-
tension and diabetes mellitus can cause SCH.
o Sudden severe venous congestion: Valsalva manoeuvre, whooping cough, vomiting, sneezing, weight lifting,
crush injuries or spontaneously (without any apparent cause). Compression of the thorax and abdomen as in
accidents or explosions may act in the same way and raised venous pressure can cause severe SCH.
o Haematological dyscrasias: Pathologies of the coagulation system including the disorders associated with
thrombocytopenia and platelet dysfunction, such as thrombocytopenic purpura, anaemia, leukaemia, splenic
disorders, anticoagulant or antiplatelet therapy and uraemia.
o Contact lens use.
❖ Causes:
o The majority of cases are mostly considered to be idiopathic.
o Trauma: Minor trauma originating from a foreign body or eye rubbing to major traumas, such as blunt or
penetrating injuries of the globe, which can cause SCH at all levels.
o Orbital injuries: SCH may develop 12–24 hours after the fracture of orbital bones or base of the skull and results
from influent leakage of blood under the conjunctiva.
o Conjunctival pathologies: Acute haemorrhagic conjunctivitis, conjunctival tumours, amyloid of conjunctiva,
conjunctivochalasis.
o Ocular surgeries: Cataract surgery, filtration surgery, refractive surgery and local anesthesia techniques, such as
sub-Tenon’s anesthetic injection and peribulbar block.
o Ocular adnexal tumours.
❖ Treatment:
o In most of the cases, SCH resolves spontaneously.
o Supportive care is done.
o Treatment of the underlying cause if the aetiology and risk factors are known.

08. Papilloedema. [1999]

❖ Passive swelling of the optic disc is called papilloedema and is not exactly same as disc oedema.
❖ Aetiology:
o Congenital condition: Aqueductal stenosis and craniosynostosis.
o Intracranial space-occupying lesions (ICSOLs): Brain tumours, abscess, tuberculoma, gumma, subdural haema-
toma and aneurysms.
o Intracranial infections: Meningitis, encephalitis.
o Intracranial haemorrhage: Cerebral and subarachnoid haemorrhage.
o Obstruction of CSF absorption: Damaged arachnoid villi.
o Tumours of spinal cord.
o Idiopathic intracranial hypertension (IIH): Also called as pseudotumour cerebri.
o Systemic conditions: Malignant hypertension, pregnancy induced hypertension (PIH), cardiopulmonary insuffi-
ciency, blood dyscrasias and nephritis.
o Diffuse cerebral oedema: Due to blunt head trauma.
o Cerebral venous sinus thrombosis.
❖ Heyreh's theory of pathogenesis: Papilloedema develops as a result of stasis of axoplasm in the prelaminar region of optic
disc, due to an alteration in the pressure gradient across the lamina cribrosa.
❖ Clinical features:
o General features: Headache, nausea, projectile vomiting and diplopia.
o Ocular features:
• Laterality: Usually bilateral.
• Ocular symptom: Transient attack of blurred vision with no pain. Later vison decreased for optic atrophy.
• Pupil and colour vision: Normal.
• Fields: Enlarged blind spot.
• Fluorescence angiography: Vertical oval pool of dye due to leakage.

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o Fundus examination:
• Media: Clear.
• Disc appearance: Red and juicy appearance with blurred margins and swelling of 2-6 diopters.
• Peripapillary oedema: Present.
• Venous engorgement: Marked.
• Retinal haemorrhage with exudates: Marked.
• Macula: Macular star may be present.
❖ Treatment and prognosis: Papilloedema is a neurological emergency and requires immediate hospitalisation. Urgent
neuroimaging (CT scan or preferably MRl with a gadolinium enhancement) may reveal primary pathology. As a rule unless
the causative disease is treatable or cerebral decompression is done, the course of papilloedema is chronic and ultimate
visual prognosis is bad.

09. Pannus. [1995, 1994]

❖ Corneal pannus is a subepithelial fibrovascular tissue ingrowth from the limbus onto the cornea.
❖ Aetiopathogenesis:
o It typically results from inflammation, which may be caused by:
• Chlamydial infection like trachoma.
• Herpetic conjunctivitis.
• Chronic irritation in contact lens users.
• Chronic epithelial oedema in glaucoma.
o In corneal pannus, a fibrous tissue with a significant vascular component is seen between the epithelium and
Bowman's layer, so this is called subepithelial fibrovascular pannus.
❖ Classification:
o Progressive pannus:
• Infiltrative component: It is associated with prominent leukocytic infiltration and includes polymorpho-
nuclear leukocytes and plasma cells in the active stages.
• Vascular component: Corneal infiltration is ahead of vascularization. Frequently, the Bowman's layer is
disrupted and the vessels wander haphazardly through the anterior stroma.
o Regressive pannus (pannus siccus):
• Infiltrative component: It is associated with fewer inflammatory cells.
• Vascular component: The vascular component has never been prominent and is liable to regress, leaving
a hyalinised, relatively acellular layer of fibrous tissue.
• This type of pannus is especially common in conditions that give rise to chronic epithelial oedema, such
as glaucoma.
❖ Treatment: Treatment of the cause.

10. Cycloplegics. [2004]

❖ Group A, question no. 14.

11. Siderosis bulbi. [2001]

❖ Siderosis bulbi refers to the ocular degenerative changes produced by an iron foreign body.
❖ Time of manifestation: It usually occurs after 2 months to 2 years of the injury. However, earliest changes have been
reported after 9 days of trauma.
❖ Mechanism: The iron particle undergoes electrolytic dissociation by the current of rest and its ions are disseminated
throughout the eye. These ions combine with the intracellular proteins and produce degenerative changes. In this
process, the epithelial structures of the eye are most affected.
❖ Clinical manifestations:
o Anterior epithelium and capsule of the lens:
• These structures are involved first of all.

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• Initially: The rusty deposits are arranged radially in a ring like fashion.
• Later stage: The lens becomes cataractous.
o Iris:
• Initially: It is stained greenish.
• Later stage: Turns reddish brown (heterochromia iridis).
o Retina: It develops pigmentary degeneration which resembles retinitis pigmentosa. Electroretinography (ERG)
shows progressive attenuation of the b-wave over time.
o Secondary open angle glaucoma: It may occur due to degenerative changes in the trabecular meshwork.
❖ Treatment: Early detection, localization and removal of the foreign body is essential for good prognosis.

12. Posterior staphyloma. [2004]

❖ Group B, question no. 12.

13. Ring synechiae. [2002]

❖ The adhesions between the iris with any other intraocular structure is called synechiae.
❖ Ring synechiae:
o Also called annular synechiae or 360° posterior synechiae.
o Ring synechiae is a morphological subtype of posterior synechiae.
o The adhesions between the posterior surface of iris and anterior capsule of crystalline lens or any other structure
which may be artificial lens, after cataract, posterior capsule left after extracapsular cataract extraction or
anterior hyaloid face is called posterior synechiae.
o The 360° adhesion of pupillary margin to anterior capsule of lens is called ring synechiae.
❖ Formation: Formed due to organization of the fibrin-rich exudates.
❖ Clinical features and complications:
o Seclusio pupillae: Prevention of circulation of aqueous humour from posterior chamber to anterior chamber.
o Iris bombe formation: Seclusio pupillae → collection of aqueous humour behind the iris → forward bowing of iris
→ iris bombe formtaion.
o Anterior chamber: Funnel shaped or irregular.
o Peripheral anterior synechiae: It is formed due to forward bowing of iris.
o Glaucoma: Peripheral anterior synechiae → decreased trabecular outflow → increased intraocular pressure →
secondary angle closure glaucoma formation.
❖ Treatment:
o Cycloplegic drugs like atropine is used to prevent synechiae formation and to break the preformed synechiae.
o Treatment of the complications are done.

14. Phthisis bulbi. [2002]

❖ Phthisis bulbi is the final stage end result of any form of chronic uveitis in which the eye becomes soft, shrink and atrophic.
❖ Development: Development of phthisis bulbi can be divided into three overlapping stages:
o Stage of atrophic bulbi without shrinkage: It is the initial stage of loss of function of ocular tissues which occurs
due to continued inflammation and loss of nutritional support. In this stage:
• Shape of globe is maintained.
• Vision is completely lose.
• Lens becomes cataractous.
• Retina develops serous detachment and atrophic changes.
• IOP is raised in early stages due co inflammatory glaucoma.
o Stage of atrophic bulbi with shrinkage: It occurs due to continued ciliary body dysfunction. ln this stage:
• IOP is lowered.
• Cornea becomes oedematous and vascularised.
• Anterior chamber is collapsed.
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• Eyeball becomes smaller and square shaped (maintained by four recti).

o Atrophic bulbi with disorganization: It is the final stage known as phthisis bulbi. In this stage due to continued
disorganization of ciliary body:
• IOP is markedly lowered.
• Size of eyeball is markedly decreased.
• Cornea becomes sclera like.
• Histopathological examination reveals:
✓ Disorganization of all the intraocular tissues.
✓ Calcification may occur in Bowman's layer of cornea, lens and retina.
✓ Intraocular ossification (bone formation) may occur due to metaplasia in the retinal pigment
epithelium in the end stage.
✓ Sclera become markedly thickened.

15. Ciliary congestion. [2001]

❖ See bellow: Important to note: Difference between conjunctival and ciliary congestion.

➢ Important to note:
o Difference between conjunctival and corneal congestion:
Features Conjunctival congestion Ciliary congestion
Also known as Conjunctival injection. Ciliary injection / flush, circumcorneal congestion / injection.
Site More marked in fornices. More marked around the limbus.
Colour Bright red. Purple or dull red.
Vessels involved Posterior conjunctival. Anterior ciliary.
Direction of blood flow Centripetal. Centrifugal.
Branching Profusely branched. Limited branching.
Mobility of vessels Movable with conjunctiva. Fixed.
Plane of vessels Superficial on the conjunctiva. Deep below the conjunctiva.
Effect of adrenaline Blanching occurs immediately. No blanching.
Ciliary tenderness Present. Absent.
Aetiology Acute conjunctivitis Acute iridocyclitis, acute glaucoma, keratitis and corneal ulcer.

16. Commotio retinae. [2003]

❖ Also known as Berlin's oedema.

❖ This is a manifestation of a closed-globe injury in the retina.
❖ Aetiology: Blow on the eye.
❖ Clinical manifestation:
o Milky white cloudiness involving a considerable area of the posterior pole.
o Cherry red spot in the foveola.
❖ Fate:
o It may disappear after some days.
o It may be followed by pigmentary changes.

17. Pseudophakia. [2005]

❖ The condition of aphakia when corrected with intraocular lens implant (IOL) is referred to as pseudophakia or artephakia.
❖ Refractive status of a pseudophaldc eye: It depends upon the power of the IOL implanted as follows:

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o Emmetropia: It is produced when the power of the IOL implanted is exact. It is the most ideal situation. Such
patients need plus glasses for near vision only.
o Consecutive myopia: It occurs when the lOL implanted overcorrects the refraction of eye. Such patients require
glasses to correct the myopia for distance vision and may or may not need glasses for near vision depending upon
the degree of myopia.
o Consecutive hypermetropia: It develops when the under power IOL is implanted. Such patients require plus
glasses for distance vision and additional +2 to +3 D for near vision.
o Astigmatism: Varying degree of surgically induced astigmatism is also present in pseudophakia.
❖ Signs of pseudophakia (with posterior chamber IOL):
o Surgical scar: May be seen near the limbus.
o Anterior chamber: Slightly deeper than normal.
o Iris: Mild iridodonesis (tremulousness) of iris may be demonstrated.
o Purkinje image test: Shows four images.
o Pupil: It is blackish in colour but when light is thrown in pupillary area shining reflexes are observed.
o IOL: Presence of IOL is confirmed on slit-lamp examination after dilating the pupil.
o Visual status and refraction: Will vary depending upon the power of lOL implanted.
❖ Management of pseudophakia:
o Optical management: Spectacles for near vision alone (in pseudophakiia with emmetropia) or as bifocal or
progressive glasses for both distance and near vision (in pseudophakiia with consecutive refractive error) are
required.
o Laser management: LASIK or Advanced surface ablation (ASA) may be required in moderate consecutive refractive
error.
o Surgical management: Intraocular lens (IOL) exchange or pigiback IOL is required when the consecutive refractive
error is large.

18. Macula lutea. [2001]

❖ Macula lutea, also called the yellow spot, is comparatively darker than the surrounding fundus and is situated at the
posterior pole temporal to the optic disc.
❖ Measurement: It is about 5.5 mm in diameter.
❖ Parts:
o Fovea centralis:
• It is the central depressed part of the macula.
• Measurement: It is about 5.5 mm in diameter.
• Features:
✓ Most sensitive part of the retina.
✓ Lowest threshold for light.
✓ Highest visual acuity.
✓ It contains only cones.
o Foveola:
• In the centre of the foveola, there is a shining pit called foveola.
• Measurement: It is about 0.35 mm in diameter.
• Location: It is situated about 2 disc diameters (3-4 mm) away from the temporal margin of the disc and
about 1 mm below the horizontal meridian.
o Umbo: The tiny depression in the centre of foveola is called umbo which is seen as shinning foveal reflex on fundus
examination.
o FAZ: An area about 0.8 mm in diameter (including foveola and some surrounding area) does not contain any retinal
capillaries and is called foveal avascular zone (FAZ).
o Surroundings: Surrounding the fovea are the parafoveal and perifoveal areas.

19. IOL. [1999]

❖ Presently intraocular lens (IOL) implantation is the method of choice for correcting aphakia. IOLs can be classified in
different types on the basis of different aspects.

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❖ Based on the method of fixation in the eye:

o Anterior chamber IOL (angle supported IOL): These lenses lie entirely in front of the iris and are supported in the
angle of anterior chamber. Presently, AC-IOL (Kelman multiflex type) are used only in those cases of ICCE or ECCE,
where it is not possible to use the PC-IOL.
o Iris-supported lens: These lenses are fixed on the iris with the help of sutures, loops or claws. These are not used
now due to high incidence of postoperative complications. Example: Singh and Worsts iris claw lens.
o Posterior chamber lens: PC-IOL rest entirely behind the iris. They may be supported and fixed as below:
• In the capsular bag fixation of PC-IOL: This is the most ideal method. Commonly used models of PC-IOLs
are modified C loop and quadri loop.
• In the ciliary sulcus fixation of PC-IOL: It is done in the absence of intact capsular bag but with adequate
capsular support.
• Scleral fixation of PC-IOL: It is done in the absence of capsular support. Broadly, there are two types of
techniques for scleral fixation of PC-IOL:
✓ Trans-scleral suture fixation of PC-IOL.
✓ Trans-scleral sutureless fixation of PC-IOL (glued IOL).
• Retro-iris fixation: It is the technique of implanting iris claw lens in the posterior chamber.
❖ Depending on the material of manufacturing: 3 types of PC-IOLs are available:
o Rigid IOLs: These are made entirely from PMMA.
o Foldable IOLs: These are made of silicone, acrylic, hydrogel and collamer. These are implanted with the help of an
IOL injector.
o Rollable IOLs: These are ultra-thin IOLs and are made of hydrogel.
❖ Based on the focussing ability:
o Unifocal IOL: This is the most commonly used one having unifocal power.
o Multifocal IOL: It has separate optics to focus for distance and near, so also known as simultaneous vision lenses
or pscudoaccommodative IOLs. These are of 2 types, either refractive or diffractive optics types.
o Accommodative IOL:
• Crystalens: It is based on optic shift principle.
• Synchrony lens: It is based on dual optic mechanism.
o Extended-depth-of-Jocus IOL e.g. Tcchnis Symphony: It provides uncorrected distance, intermediate as well as
near vision to some extent due to its elongated focus. However, for fine near work glasses may be required. These
IOLs are rapidly gaining popularity.
❖ Aphakic versus phaklc refractive IOLs: In addition to the aphakic IOLs which are implanted after lens extraction, special
phakic IOLs have been developed to correct the refractive errors. These are also called implantable collamer lenses (ICLs)
and are of three types.
❖ Special function IOLs:
o Toric IOLs: To correct the associated astigmatism.
o Aspheric IOLs: To reduce spherical aberrations.
o Aniridia IOLs: These lenses are devised to cosmetically cover the defects of aniridia or partial iris loss in cases like
trauma. ln these lenses around the central optical part, there is a black diaphragm.

20. Convex lens. [2000]

❖ Convex lens or plus lens is a converging lens. It may be of biconvex, piano-convex or concavo-convex (meniscus) type.
❖ Identification of a convex lens:
o The convex lens is thick in the centre and thin at the periphery.
o An object held close to the lens, appears magnified.
o When a convex lens is moved, the object seen through it moves in the opposite direction to the lens.
❖ Uses of convex lens:
o For correction of hypermetropia, aphakia and presbyopia.
o In oblique illumination (loupe and lens) examination.
o In indirect ophthalmoscopy, as a magnifying lens and in many other equipment.
❖ Image formation:
Position of the object Position of the image Nature and size of the image
At infinity At focus (F2) Real, very small and inverted
Beyond 2F1 Between F2 and 2F2 Real, diminished and inverted
At 2F1 At 2F2 Real, same size and inverted
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Between F1 and 2F1 Beyond 2F2 Real, enlarged and inverted

At focus F1 At infinity Real, very large and inverted
Between F1 and optical centre of lens On the same side of lens Virtual, enlarged and erect

➢ Important to note:
o Concave or minus lens is a diverging lens. It may be of biconcave, piano-concave or convexo-concave (meniscus).
o Identification of a convex lens:
• The concave lens is thin in the centre and thick at the periphery.
• An object held close to the lens, appears minified.
• When a concave lens is moved, the object seen through it moves in the same direction to the lens.
o Uses of convex lens:
• For correction of myopia.
• As Hruby lens for fundus examination with slit-lamp.
o Image formation:
Position of the object Position of the image Nature and size of the image
At infinity At focus Virtual, very small and erect
Between infinity and optical centre Between focus and optical centre Virtual, diminished and erect

21. Contact lens. [2000]

❖ Contact lens is an artificial device whose front surface substitutes the anterior surface of the cornea.
❖ Parts of contact lens:
o Diameters:
• Overall diameter (OD): Linear measurement of the greatest distance across physical boundaries of lens.
• Optic zone diameter (OZ): Dimension of central optic zone of lens which is meant to focus rays on retina.
o Curves:
• Base curve (BC) or central posterior curve (CPC): It is a curve on the back surface of the lens to fit the
front surface of cornea.
• Peripheral curves: These are concentric to base curve and include intermediate posterior curve (IPC) and
peripheral posterior curve (PPC). These are meant to serve as reservoir of tears and to form a ski for lens
movements.
• Central anterior curve(CAC) or front curve (FC): It is a curve on the anterior surface of the optical zone
of the lens. Its curvature determines the power of contact lens.
• Peripheral anterior curve (PAC): It is a slope on the periphery of anterior surface which goes upto the
edge.
• Intermediate anterior curve (TAC): It is fabricated only in the high power minus and plus lenses. It Lies
between the CAC and PAC.
o Edge: lt is the polished and blended union of the peripheral posterior and anterior curves of the lens.
o Power: lt is measured in terms of posterior vertex power in dioptres.
o Thickness: It is usually measured in the centre of the lens and varies depending upon the posterior vertex power.
o Tint: It is the colour of the lens.
❖ Types:
o Hard lens: Hard, oxygen impermeable, made of PMMA (polymethylmethacrylate).
o Rigid gas permeable lens: Hard, oxygen permeable, made of silicone acrylate or cellulose acetate butyrate (CAB).
o Soft lens: Soft, oxygen permeable, made of HEMA (hydroxyethylmethacrylate).
❖ Indications:
o Optical indications:
• In refractive error for cosmetic purposes.
• Absolute indication: Anisometropia, unilateral aphakia, high myopia, keratoconus, irregular astigmatism.
o Therapeutic indications:
• Corneal diseases: Non-healing corneal ulcers, bullous keratopathy, filamentary keratitis and recurrent
corneal erosion syndrome.
• Diseases of iris: Aniridia, coloboma and albinism to avoid glare.
• Glaucoma: As vehicle for drug delivery.
• Amblyopia: Opaque contact lenses are used for occlusion.
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• Bandage soft contact lens: Used following keratoplasty and in microcorneal perforation.
o Preventive indications:
• Prevention of symblepharon and restoration of fornices in chemical bums.
• Exposure keratitis.
• Trichiasis.
o Diagnostic indications: Gonioscopy, ERG, examination of fundus in the presence of irregular corneal astigmatism,
fundus photography, Goldmann's 3 mirror examination.
o Operative indications: Goniotomy operation for congenital glaucoma, vitrectomy, endocular photocoagulation.
o Cosmetic indications: Unsightly corneal scars (colour contact lenses), ptosis (haptic contact lens), cosmetic scleral
lenses in phthisis bulbi.
o Occupational indications: Sportsmen, pilots, actors.
❖ Contraindications: Mental incompetence and poor motivation, chronic dacryocystitis, chronic blepharitis and recurrent
stycs, chronic conjunctivitis, dry eye syndromes, corneal dystrophies and degenerations, recurrent diseases like episcleritis,
scleritis and iridocyclitis.

22. Congenital dacryocystitis. [2005, 2003]

❖ Congenital dacryocystitis is a mild grade chronic inflammation of the lacrimal sac occurring in newborn infants and thus
also known as dacryocystitis neonatorum or infantile dacryocystitis.
❖ Aetiology: It follows stasis of secretions in the lacrimal sac due to congenital blockage in the nasolacrimal duct. It is of very
common occurrence. As many as 30% of newborn infants are believed to have closure of nasolacrimal duct at birth.
o Commonest cause: Membranous occlusion, at its lower end, near the valve of Hasner.
o Other causes: Presence or epithelial debris, membranous occlusion at its upper end near lacrimal sac, complete
noncanalisation and rarely bony occlusion.
o Common bacteria associated: Staphylococci, Pneumococci, Streptococci, Haemophilus influenzae, enterobacter-
iaceae species.
❖ Clinical features:
o Epiphora: Usually developing after seven days of birth.
o Discharge: Epiphora is followed by mucopurulent discharge from the eyes.
o Regurgitation test: Positive.
o Swelling on the sac area may appear eventually.
❖ Differential diagnosis: Congenital dacryocystitis needs to be differentiated from other causes of watering in early
childhood especially ophthalmia neonalorum and congenital glaucoma.
❖ Complications: When not treated in time, there may be recurrent conjunctivitis, lacrimal abscess and fistula formation.
❖ Treatment: It depends upon the age at which the child is brought. The treatment modalities employed are as follows:
o Massage over the lacrimal sac area and topical antibiotics: This is the mainstay of treatment of congenital LD
block. Massage increases the hydrostatic pressure in the sac and helps to open up the membranous occlusions. It
should be carried out at least 4 times a day to be followed by instillation of antibiotic drops. This conservative
treatment coupled with spontaneous recanalization cures obstruction in about 90% of the infants up to 6-9
months.
o Probing of NLD with Bowman's probe: It should be performed in case the condition is not cured by the age of 6
months. Some surgeons prefer to wait till the age of 9-12 months. It is usually performed under general
anaesthesia. While performing probing, care must be taken not to injure the canaliculus. In most instances, a
single probing will relieve the obstruction. In case of failure, it may be repeated after an interval of 3-4 weeks.
o Balloon catheter dilation: It is done with the help of a probe carrying inflatable balloon, may be carried out in
children where repeated probing is failure or directly in cases where the obstruction seems to be due to scarring
or constriction rather than merely by a distal membrane.
o Intubation with silicone tube: It may be performed if repeated probing and balloon catheter dilation fail. The
silicone tube should be kept in the NLD for about six months.
o Dacryocystorhinostomy (DCR) operation: When the child is brought very late or repeated probing, balloon
catheter dilation and intubation are a failure, then conservative treatment by massaging and topical antibiotics as
and when required should be continued till the age of 4 years. After this, DCR operation should be performed.

23. Absolute glaucoma. [2002, 1996]

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❖ Primary angle closure glaucoma, if untreated, gradually passes into the final phase called absolute glaucoma.
❖ Clinical features:
o Painful blind eye: The eye is painful, irritable and completely blind (no light perception).
o Perilimbal reddish blue zone: A slight ciliary flush around the cornea due to dilated anterior ciliary veins.
o Caput medusae: A few prominent and enlarged vessels are seen in long-standing cases.
o Corneal changes: In early cases, cornea is clear but insensitive. Slowly it becomes hazy and may develop epithelial
bullae (bullous keratopathy) or filaments (filamentary keratitis).
o Anterior chamber: Very shallow.
o Iris: Atrophic.
o Pupil: It becomes fixed and dilated and gives a greenish hue.
o Optic disc: Disc shows glaucomatous optic atrophy.
o Intraocular pressure: IOP is high and eyeball becomes stony hard.
❖ Management:
o Retrobulbar alcohol injection: lt may be given to relieve pain. First, 1 mL of 2% xylocaine is injected followed after
about 5-10 minutes by 1 mL of 80% alcohol. It destroys the ciliary ganglion.
o Destruction of secretory ciliary epithelium: It is done to lower the IOP by cyclocryotherapy or cyclodiathermy or
cyclophotocoagulation.
o Enucleation of eyeball: It may be considered when pain is not relieved by conservative methods.
❖ Complications:
o Corneal ulceration: It results from prolonged epithelial oedema and insensitivity.
o Perforation: Sometimes, corneal ulcer may even perforate.
o Staphyloma formation: As a result of continued high IOP, sclera becomes very thin and atrophic and ultimately
bulges out either in the ciliary region (ciliary scaphyloma) or equatorial region (equatorial staphyloma).
o Atrophic bulbi: Ultimately, the ciliary body degenerates, IOP falls and the eyeball shrinks.

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Note:

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Index
Absolute glaucoma 98
Acute angle closure glaucoma,
Clinical features 51
Management 52
Alkali burn eye 67
Angle,
Anatomy 57
Grading 58
Anisometropia 87
Anti-glaucoma drugs 73
Aphakia 54
Difference between aphakia and pseudophakia 54
Management 54
Astigmatism 24
Atropine 22
Aqueous humour,
Circulation 15
Drainage 15
Formation 15
Bacterial corneal ulcer 78
Complications 50
Management 49
Treatment of non-healing 50
Treatment of progressive 51
Binocular vision 76
Biometry 36
Bitot's spot 89
Blepharitis 87
Blunt trauma 60
Buphthalmos 27
Capsulotomy 80
Cataract surgery,
Complications 83
Preoperative work up 45
Prognosis 45
Ciliary congestion 94
Commotio retinae 94
Conjunctiva,
Anatomy 10
Congestion 94
Cornea,
Anatomy 11
Corneal preservation 48
Corneal transparency,
Factors 12
Foreign body 77
Dacryocystitis,
Acute 35
Chronic 37
Congenital 98
DCR 82
Diabetic retinopathy 79
Endophthalmitis 25
Entropion 34
Enucleation 68
Epiphora 73
Esotropia 39
Evisceration 36
Extraocular muscles,
Attachments 8
Functions 8
Name 7
Nerve supply 8
Eye banking 71
Eyelids,
Anatomy 9
Herpes zoster ophthalmicus,
Aetiology 51
Clinical features 51
Complications 51
Treatment 52
Hypermature cataract 40
Hypermetropia b77
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Hyphaema 23
Hypopyon 70
Internal hordeolum 66
IOL 94
IOP 59,
Low IOP conditions 59
Iridocyclitis,
Clinical features 43
Differential diagnosis 44
Management 44
Keratic precipitate 26
Keratoplasty 84
Indications 82
Lacrimal apparatus,
Anatomy 5,7
Lagophthalmos 89
Laser 75
Lens,
Anatomy 13
Concave 97
Contact 97
Convex 96
Lens transparency,
Anatomical factors 15
Physiological factors 13
Physiology 13
Macula lutea 95
Morgagnian cataract 21
Myopia 30
Complications 40
Pathological 33
Treatment 26
Night blindness 66
Nutritional blindness 28
Prevention 49
Pannus 92
Panophthalmitis 23
Papilleodema 91
Paracentesis 30
Phagocytic glaucoma 29
Phlyctenular conjunctivitis 21
Phthisis bulbi 93
POAG,
Diagnosis 56
Follow up 57
Visual field changes 32
Posterior capsular opacification 69
Presbyopia 68
Pseudophakia 94
Pterygium 72
Ptosis 88
Pupil,
Drugs acting on pupil 16
Pupillary light reflex 16
Pupillary reactions 17
Rainbow halos,
Causes 53
Diagnosis 54
Recurrent pterygium,
Management 70
Red eye,
Causes 80
Differential diagnosis 44
Management 55
Retinoblastoma 71
Clinical features 46
Management 47
Right convergent squint,
Management 84
Ring synechiae 93
SICS 75
Siderosis bulbi 92
Staphyloma 29
Subconjunctival haemorrhage 90
Symblepharon 33

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Syringing 65
Tear drainage 6
Topical steroids,
Side effects 81
Trabeculectomy 74
Vernal conjunctivitis 37
Vision 2020 31
Visual acuity determination 38
Vitreous hemorrhage 65
VKC,
Clinical features 35
Watering of eye,
Causes 6
White reflex,
Differential diagnosis 55
Management 56
Xerosis of conjunctiva 90

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