1.

ORBIT

ORBIT AND ITS DISEASES

Size/Volume of Orbit:

Shape:

Attachments:

Boundaries:
Bones: Orbit is made up of seven bones. (MCQ)
1. Medial Wall (Mn: uSMLE)
U S M L E

Sphenoid (Body) Maxillary Lacrimal Ethmoid

2. Inferior wall/Floor
ƒ Palatine
ƒ Zygomatic
ƒ Maxillary (Pa, Ma, Za)
3. Lateral wall
ƒ Zygomatic
ƒ Sphenoid (Greater wing)
4. Superior wall/Roof of Orbit:
ƒ Frontal
ƒ Sphenoid (Lesser wing)
 OPHTHALMOLOGY WORKBOOK 2024 | 3

• Thinnest wall of orbit: Medial wall (Lamina papyracea).

• Thickest & strongest wall of orbit: Lateral wall.
• Weakest point of orbit: Floor (Postero-medial aspect of maxillary bone).
In Blunt Trauma, weakest point is fractured: Inferior wall / Postero- medial aspect of maxillary bone of
the orbit.

Apex of orbit:

1. Optic canal:
Gap in lesser wing of sphenoid
Structures Passing: Optic nerve & Ophthalmic artery.

2. Superior orbital fissure: Gap between Lesser & Greater wing of Sphenoid.

Clinical application

Superior Orbital Fissure Syndrome

I. Proptosis
II. Total External Ophthalmoplegia ( Due to involvement of 3, 4 & 6 Cranial Nerves)
III. Decreased Corneal Sensations (First Branch of 5 Cranial Nerves)

Orbital Apex Syndrome

i. Optic Nerve, Occulomotor Nerve, Trochlear Nerve, Trigeminal Nerve (First division of 5th Cranial
Nerve), Abducent’s Nerve (6th cranial Nerve)

Involvement of Optic Nerve leads to Blindness.

4 | OPHTHALMOLOGY WORKBOOK 2024

Blow out fracture:

Orbital cellulitis and Pre Septal Cellulitis

 OPHTHALMOLOGY WORKBOOK 2024 | 5

CAVERNOUS SINUS THROMBOSIS (MCQ)

▫ Earliest sign: Abduction defect due to 6th cranial nerve palsy
▫ Life threatening condition
▫ CNS Symptoms: Disorientation, Drowsiness, Coma
▫ Treatment : Systemic Antibiotics I.V Heparin, Tissue Plasminogen activator, Steroids.
6 | OPHTHALMOLOGY WORKBOOK 2024

Thyroid eye disease

Etiopathogenesis:
• Most common cause of unilateral or bilateral proptosis in adults.
• Smoking is a major risk factor.
• Female Predisposition is present.
• Thyroxine Levels: Increased, decreased or may even remain normal.

• Thyroid ophthalmopathy involves an organ-specific autoimmune reaction in which an antibody that

reacts against thyroid gland cells and orbital fibroblasts leads to inflammation of extraocular muscles,
interstitial tissues, orbital fat and lacrimal glands characterized by pleomorphic cellular infiltration,
associated with increased secretion of glycosaminoglycans (GAG) and osmotic imbibition of water.
• Increased GAG deposition (absorb water & swell)
• Bellies of Extra Ocular Muscles are involved: First Swelling occurs and, then, Fibrosis

Clinical features:
 OPHTHALMOLOGY WORKBOOK 2024 | 7

Proptosis/Exophthalmos:

Hertel’s Exophthalmometer: Used to assess exophthalmos in adults.

Luedde’s: Used to assess exophthalmos in children.

Proptosis:
Axial Non Axial
1) Thyroid Eye Disease 1) Lacrimal gland tumour: Down & Medial position of eye.
2) Cavernous hemangioma Most common cause is Pleomorphic adenoma Other causes:
3) Optic nerve tumours like optic nerve glioma associated with Adenoid Cystic Ca., Lymphoma
Neurofibromatosis-type 1 and Optic nerve Meningioma

2) Lacrimal sac tumour: Down & out position of eye.

Proptosis
1. Intermittent proptosis
2. Pulsatile proptosis
ƒ Carotid - Cavernous Fistula (Bruit will be typically present)
ƒ Fracture of Roof of Orbit
ƒ Meningocele
ƒ Sphenoid Dysplasia
8 | OPHTHALMOLOGY WORKBOOK 2024

Tumours of orbit:
• Rhabdomyosarcoma

• Dermoid cyst

• Orbital lymphoma

• Cavernous Hemangioma
 OPHTHALMOLOGY WORKBOOK 2024 | 9

Coats of eyeball:
2. LENS AND IT'S DISEASES

Snellens chart:

N=6/6 i.e. A normal person is reading letters from a distance of 6 meters; also the person being
examined is reading it from distance of 6 meters
6/60 i.e a person being examined is reading alphabets from a distance of 6 meter that a normal person
can read from a distance of 60 meters.
So, less is denominator, better is vision

• Snellen’s chart in based on form sense (mcq)

• Other senses
ƒ Colour sense
ƒ Contrast sense
ƒ Light sense

Criteria (mcq)
A. Low vision 6/18 - 6/60
B. Economic blindness 6/60 - 3/60
C. Social blindness 3/60 - 1/60
D. Manifest blindness vision less than 1/60
E. Absolute blindness pl negative.

6/60 to 3/60 to 1/60.

Finger count: counting (or counts) fingers (cf) denotes that the patient is able to tell how many fingers
the examiner is holding up at a specified distance, usually at 1 metre.
Hand movement: hand movements (hm) is the ability to distinguish whether the examiner’s hand is
moving when held just in front of the patient.
Projection of rays (PR) : the patient is able to determine the direction from which the light is being
projected.
Perception of light (PL): the patient can discern only light (e.g. Pen torch), but no shapes or movement.
Pin-hole : A pinhole (PH) aperture compensates for the effect of refractive error, and consists of
an opaque occluder perforated by one or more holes.
Diameter of the hole =1.2 mm
 OPHTHALMOLOGY WORKBOOK 2024 | 11

• It cuts off all peripheral rays & allow only central ray of light to pass through, which doesn’t take part
in refraction.

ƒ Best-corrected Va (BCVA) denotes the level achieved with optimal refractive correction.

SLIT LAMP EXAMINATION

• Structure
12 | OPHTHALMOLOGY WORKBOOK 2024

• Metabolism

Cataract:
• Cataract is the most common cause of blindness / preventive blindness in world. (mcq)
• 2nd most common cause is glaucoma followed by:
Armd> trachoma > onchocerciasis (river blindness)

Etiological classification:

1. Congenital cataract
• Most common congenital cataract is blue dot cataract.
• Most common cataract associated with loss of vision is zonular/ lamellar cataract
 OPHTHALMOLOGY WORKBOOK 2024 | 13

2. Metabolic cataract:
• Diabetes mellitus is a common cause.
Early senile cataract True diabetic/ snow flake cataract

• Age of onset: early forties. • Age of onset: young.

• Non insulin dependent diabetes mellitus (niddm) • Insulin dependent diabetes mellitus. (iddm)
• Chronic onset • Acute onset
• No specific appearance • Snow flake appearance

• Most common cataract associated with diabetes mellitus (overall) : early senile cataract.
• Most common cataract associated with niddm: early senile cataract.
• Most common cataract associated with iddm: snow flake cataract.

• Cataract associated with Myotonic dystrophy: Christmas tree cataract.

• Cataract associated with Fabry’S Disease: Spoke Cataract.
14 | OPHTHALMOLOGY WORKBOOK 2024

Cataract associated with Galactosemia: Oil Drop Cataract.

It is the only reversible cataract and the enzymes that are responsible are: Galactokinase
& Galactose Phosphateuridyl transferase.
 OPHTHALMOLOGY WORKBOOK 2024 | 15

• Cataract associated with Wilson’s Disease: Sunflower Cataract.

Copper deposition in Wilson’s disease is reversible and happens to be in Descemet’s membrane of

Cornea.

3. Traumatic cataract

• Blunt trauma leads to development of posterior cortical cataract and penetrating trauma leads to
development of anterior cortical cataract.

Vossious ring:
16 | OPHTHALMOLOGY WORKBOOK 2024

Siderosis bulbi:

4. Heat & radiation induced cataract

• Posterior subcapsular cataract is most common
• IR Rays/ UV rays, Gamma rays X rays etc.
• True exfoliation cataract.
• Glass blowers industry, steel factory workers.
• Lens is most sensitive to radiation & hence its damaged first.

5. Complicated cataract:
Associated with other disease of eye like:
1. Uveitis
2. Glaucoma
3. High Myopia
4. Retinitis Pigmentosa.

• Complicated cataracts are mostly posterior subcapsular type of cataracts.

• Bread crumb appearance of opacities is present.
• Poly-chromatic lustre is seen.
• The spread is axial i.e. Antero- posteriorly.
 OPHTHALMOLOGY WORKBOOK 2024 | 17

6. Drug induced cataract

ƒ Posterior subcapsular cataract is most common.
ƒ Drugs responsible:
A: amiodarone, Au (gold)
B: busulphan
C: chloroquine, chlorpromazine
D: dexamethasone
E: ecothiophate

7. Senile cataract:
18 | OPHTHALMOLOGY WORKBOOK 2024

1. Stage of Lamellar Separation:

ƒ No signs/ symptoms
2. Incipient/ Intumescent cataract
ƒ Formation of small micro-droplets in lens.
ƒ Loss of Contrast Sensitivity.
ƒ Uniocular diplopia.
3. Immature Cataract (IMSC)
ƒ Half moon shaped shadow is present(diagnostic).
ƒ Loss of vision
ƒ Partially opaque lens
4. Mature cataract
ƒ Pearly white colour of Lens.
ƒ Phacomorphic Glaucoma: Lens swelling will put pressure at base of iris which will narrow down
Irido-Corneal angle leading to angle closure type of Glaucoma.
5. Hypermature Cataract
ƒ Lens is of Milky white colour
ƒ Small & Shrunken Lens with crumpling capsule leading to small ruptures over it.
ƒ Zonules can’t support it & lens may start moving upon its axis: Phacodonesis.
ƒ Also there can be subluxation or dislocation of Lens.
Subluxation of Lens: When part of Lens lies outside normal anatomical position.
Dislocation of Lens: When whole of Lens lies outside normal anatomical position.
▫ Lens normally lies in Patellar Fossa
(i) Morgagnian: Liquification of cortex and nuleus falls into it.
Liquefied cortex is then released into Anterior chamber which settle down at bottom & blocks trabecular
meshwork leading to raised Intraocular pressure (I.O.P) causing Phacolytic Glaucoma.
(ii) Sclerotic:
ƒ Lens shrinks due to leakage of water.
ƒ Anterior capsule gets wrinkled & thick due to proliferation of anterior Cells.
ƒ Anterior Chamber becomes deep.
ƒ It is called Cataracta brunescence if the appearance of the nucleus turns brown in colour. (VMQ)
ƒ Similarly, Cataracta Niagra for black coloured nucleus and Cataracta Rubra for red coloured
Nucleus. (VMQ)

Cortical cataract:
 OPHTHALMOLOGY WORKBOOK 2024 | 19

Nuclear cataract:

Posterior subcapsular cataract:

Signs and symptoms of cataract:

Contrast senstivity- pelli- robson chart
20 | OPHTHALMOLOGY WORKBOOK 2024

Halos:

Xanthopsia:

Cyanopsia:

Nyctalopia:

Hamarlopia:
 OPHTHALMOLOGY WORKBOOK 2024 | 21

Cataract of second sight:

Index myopia:

Index hypermetropia:

Management of cataract:
Calculation of IOL Power in Adults.
The refractive status (normal curvature, axial length, total power of eye, etc.) is different for different
eyes. So, before going on for a cataract surgery, it is important to determine the power of IOL to be
implanted.
The process is known as biometry. It has got two components:
1. Keratometry: Determination of power of cornea by measuring it’s curvatures.
2. A-Scan: Determination of axial length of eye ball.

• A-Scan can be either be Ultrasonographic or Optical like IOL master.

• IOL power calculation: Most commonly used formulae is: SRK II
• Also, if axial length < 22 mm. , Hoffer Q formulae is used.
• If axial length > 26 mm, SRK-T formulae is used.
22 | OPHTHALMOLOGY WORKBOOK 2024

1. ICCE: Intra Capsular Cataract Extraction

• Both Lens and capsule is removed.
• Not done nowadays.
• Indicated in Subluxated & Dislocated Cataracts.
• Aphakic glasses can be prescribed.

Aphakia:
Signs are:
• Deep anterior chamber.
• Jet black pupil.
• Iridodonesis.
• Absent purkinje image IIIrd & IVth .
• Glasses / Spectacles given are of the order of + I0D to + 12D (Biconvex lens).
• Roving Ring Scotoma:
OPHTHALMOLOGY WORKBOOK 2024 | 23
24 | OPHTHALMOLOGY WORKBOOK 2024

The edge of a convex lens acts as a prism and the higher the power of the convex lens the greater is
the prism angle (alpha). The light falling on the prism bends towards its base by an angle alpha/2 ,
therefore, greater the angle alpha the more will be the bending. In aphakic spectacles, the angle alpha
being large, the light falling at the edge of the lens bends towards the center of the lens (base of prism)
and does not reach the pupil and is, therefore, not seen.

The presence of the above scotoma leads to another interesting phenomenon. If an interesting object
appears in the periphery of the patients visual field, it appears blurred (because the light is passing from
the side of the spectacle frame). The person tends to move his head towards the object in order to see it
clearly. But as he turns the head the object comes to lie in the area of scotoma and thus disappears. As
he turns his head further so that the object comes to lie in front of the spectacle in the visible area and
so reappears again clear and sharp. This sudden disappearance and sharp reappearance of the objects
is called jack-in-the-box.
 OPHTHALMOLOGY WORKBOOK 2024 | 25

2. ECCE: Extra Capsular Cataract Extraction.

• Capsular bag is left behind & Intraocular Lens (IOL) is put into Capsular bag.
• Length of Incision is 10-12 mm.

Anterior Capsulotomy: Three main types.

a) Can Opener type: 26-G needle bent at its tip, and is introduced into anterior chamber & multiple
small radial cuts are given in anterior Capsule.
b) Envelope Type: Straight incision is given in anterior capsule from 2 O’ Clock to 10 O’ Clock position.
c) Continuous Curvilinear Capsulorrhexis (CCC): Anterior capsule is removed in a circular fashion
with capsulorrhexis forces.

• Hydrodissection (separation of the cortex from the capsule) is performed by keeping the tip of Cannula
(with BSS) under the peripheral part of anterior capsule.

• Hydrodelineation is performed to break the lens into small pieces which can be removed easily.

Manual Small incision cataract surgery (MSICS)

• Scleral tunnel is made to make the wound self sealing.
• Length of incision- 5 to 6 mm
• External scleral incision is given.
• Sclero corneal tunnel: Crescent knife is used.
• Internal corneal incision: Keratome is used.

3. Phacoemulsification
26 | OPHTHALMOLOGY WORKBOOK 2024

• Length of Incision is 2.8 - 3.2 mm.

• Clear Corneal Incision is given.
• Continuous Curvilinear Capsulorrhexis (CCC): 4-6mm in diameter
• Jack hammer effect of phacoemulsifier: 40,000 times /second.
• Foldable Intra Ocular Lens (IOL) is implanted.

4. Femtosecond laser cataract surgery (FLACS)

Three important Steps are performed with Femtolaser which are:
a) Corneal Incision
b) Capsulorrhexis
c) Lens Fragmentation

• IOL’s:

(i) Non- Foldable:

• Rigid IOLs. : Made up of Polymethyl Methacrylate (PMMA)

(ii) Foldable: material

• Silicone
• Hydragel
• Acrylic
 OPHTHALMOLOGY WORKBOOK 2024 | 27

(iii) Rollable IOL: material

• Ultrathin IOL
• Hydragel

• IOL can be implanted in the bag (Best mode of implantation)

• If there is a lack of a posterior capsule support, other modes of implantation can be:
(i) Anterior Chamber IOL
(ii) Iris Claw
(iii) Scleral Fixed

Complication of cataract surgery:

Pre- Operative Complications:
• Retrobulbar haemorrhage during peribulbar/retrobulbar block.
• Oculocardiac reflex
• Globe perforation
In modern times, the cataract surgery is being done under topical anaesthesia, so there is no
room for Globe perforation/ Retrobulbar block.

Intra Operative Complications:

• Corneal injury
• Iris injury
• Injury to posterior capsule
• Nucleus drop
• Suprachoroidal haemorrhage

Post Operative Complications:

Early post operative Complications (less than 6 weeks)
Incision related
ƒ Wound Leak
ƒ IOP
ƒ Iris Prolapse

Hyphema
Late post operative complications (More than 6 Weeks)
1. After cataract:
28 | OPHTHALMOLOGY WORKBOOK 2024

It is the most common late post op. complication.

a) Elschnig’s pearls (Diffuse):

b) Sommering Ring (Thick, Peripheral):

Treatment: Nd-Yag Laser is used for ablation of after cataract. (Wavelength- 1064Nm).

2. Irwin gass syndrome:

It is the collection of fluid in Henle’s layer of macula within 1-3 months of surgery .
• Nepafenac, Bromofenac (Topical NSAIDS) can be prescribed prophylactically.

3. Endophthalmitis:

Early and Late onset

 OPHTHALMOLOGY WORKBOOK 2024 | 29

Early onset:
• <6 weeks
• Causative organism is Staph. Epidermidis (MCQ) > Staph. Aureus

Late onset:
• After more than 6 weeks of surgery.
• Causative organism is Propionbacterium acnes (MCQ)
• Prevention by 5% Povidone-Iodine on eyelids

Treatment of endophthalmitis:
a. Intravitreal antibiotics: Broad spectrum like inj. Vancomycin, Ceftazidime etc.
b. Pars Plana Vitrectomy (PPV).

Paediatric cataract surgery:

• Phacoemulsification with primary posterior capsulotomy with PCIOL implant is done in pediatric
cataracts.
• Lensectomy with pars plana vitrectomy.
• Leave the eye aphakic & put IOL at a later stage.
• IOL power is under corrected by 10-20%.
ƒ If age is less than 2 years: 20% undercorrection is done.
ƒ If age is 2 to 8 years: 10% undercorrection is done.

           

Lenticonus:
• It is a cone shaped elevation of anterior or posterior pole of lens.

Anterior Lenticonus:

• Alport’s Syndrome (Most common)

Posterior Lenticonus:
• Alport’s syndrome
• Lowe’s syndrome
3. UVEA

UVEA AND IT’S DISEASES

Anatomy of Uvea:
Intermediate

Anterior Posterior

Aqueous Humour formation:

• Non pigmented epithelial cells of Pars plicata produce aqueous humour.
• The Process of formation of aqueous humour involves:
ƒ Secretion: max (70%) (Active mechanism by Na-K pump)
ƒ Diffusion: 20 %
ƒ Ultra filtration: 10%
Rate of formation of aqueous humour is 2.3µl/min.

UVEITIS CLASSIFICATION:
 OPHTHALMOLOGY WORKBOOK 2024 | 31

• Anatomical classification
ƒ Anterior uveitis: Inflammation of iris and pars plicata of ciliary body.
ƒ a.k.a Iritis (iris)/Anterior cyclitis (Pars plicata)/ Iridocyclitis (iris and pars plicata)

ƒ Intermediate uveitis /pars planitis: Inflammation of Pars Plana of ciliary body.

ƒ Posterior uveitis
Inflammation of Choroid of eye.
It is almost always associated with inflammation of retina, hence chorioretinitis.
ƒ Panuveitis: Inflammation of all parts of uvea.

• ANTERIOR UVEITIS

ETIOLOGY:
• Idiopathic is most common.
• HLA B-27 associated Spondyloarthropathies (Mn: PAIR)
P – Psoriasis
A- Ankylosing spondylitis
I – inflammatory bowel disease (Crohn’s disease, Ulcerative colitis)
R- Reiter’s Disease

Other causes:
• Juvenile rheumatoid arthritis (JRA).
• Tuberculosis
• Syphilis
• Leprosy

SYMPTOMS:

• Sudden painful loss of vision

• Circumcorneal congestion
• Lacrimation.
• Bluish red congestion due to underlying inflamed uveal vessels.

SIGNS:
Cells in Anterior Chamber:
32 | OPHTHALMOLOGY WORKBOOK 2024

Proteins & flare:

Hypopyon:
Sterile pus in anterior chamber due to thick and heavy exudates, lymphocytes settling down in lower
part of anterior chamber.

Keratic Precipitates (KPs):

ƒ Cells deposited at back of cornea. (Endothelium)
ƒ Arlts’s line: Deposition of KPs in triangular fashion at centre & inferior part of cornea(Lower 1/3rd)
due to convection currents in aqueous humor.
Mutton fat KP’s: Seen in granulomatous iridocyclitis due to epitheloid cells & macrophages
Small and Medium KP’s: seen in non granulomatous uveitis due to lymphocytes
Fine KP’s - Seen in fuch’s hetrochromatic iridocyclytis.

Iris Nodules:
Iris nodules can occur in both granulomatous and non-granulomatous anterior uveitis
ƒ Koeppe’s nodule – Small in size, present at pupillary border.
ƒ Busacca’s nodule – Large in size, present at base of pupil.
 OPHTHALMOLOGY WORKBOOK 2024 | 33

Festooned Pupil:
Anterior synechiae - Iris touching cornea and this leads to development of Glaucoma due to closure
of angle of anterior chamber.
Posterior synechiae - Iris touching lens and this leads to development of cataract due to disturbance
in the physiology of lens.
Cataract is more common than glaucoma because posterior synechiae are more common than
anterior synechiae.

Synechiae:
Ring synechiae /annular posterior Synechiae: All 360 degree synechiae of pupillary margin to
anterior lens capsule.
34 | OPHTHALMOLOGY WORKBOOK 2024

Iris Bombe:
• Ring Synechiae blocks circulation of aqueous humor from posterior chamber to ant chamber.
Pupil is secluded. (Seclusio pupillae)
This aqueous humor collects behind iris & pushes it anteriorly leading to iris bombe formation.

Occlusio pupillae is pupil which is completely occluded with fibrinous membrane obstructing flow of
aqueous from posterior chamber to anterior chamber.

Total posterior synechiae : It is complete plastering of total posterior surface of Iris to anterior lens
capsule

Band Shaped Keratopathy:

Deposition of calcium and phosphate in bowman’s layer of cornea.
ƒ The treatment is topical EDTA application

Granulomatous uveitis Non granulomatous uveitis

ONSET Insidious Acute

PAIN Minimal Marked

PHOTOPHOBIA Less More

CILIARY CONGESTION Less More

KERATIC PRECIPITATES Mutton Fat Small

FLARE Mild Marked

IRIS NODULE Present Absent

POST SYNECHIAE Thick & Broad Thin and Tenaceous

 OPHTHALMOLOGY WORKBOOK 2024 | 35

Treatment:
1. Topical Steroids is Drug of choice.
2. Cycloplegics are given to give rest to ciliary muscle. (Alleviate pain)
3. Antiglaucoma drug (Timolol is preferred) is given to lower IOP.
4. Systemic steroids can also be prescribed.

Luminate Programme – Volcosprine drug is used in the treatment of Anterior Uveitis under this
programme.

• INTERMEDIATE UVEITIS:
ƒ It is the inflammation of pars plana, peripheral retina, choroid and vitreous base.
ƒ Idiopathic is most common

Clinical features:
• Mostly asymptomatic
• Floaters
• Loss of vision occurs if Intermediate uveitis is associated with cystoid macular edema.
• Pain, photophobia & redness is absent.
Posterior segment involves Snow ball / cotton ball opacities which are collections of inflammatory cells
and exudates in the vitreous seen in anterior quadrant.

Snow banking: It is presence of grey white fibrovascular plaque over Pars plana with /without
association of peripheral retinal periphlebitis.

Management:

• POSTERIOR UVEITIS:
36 | OPHTHALMOLOGY WORKBOOK 2024

CMV retinitis:

Sarcoidosis:

Toxoplasmosis:

MANAGEMENT:

FUCH’S HETEROCHROMIC IRIDOCYCLITIS:

ƒ Chronic non granulomatous type of anterior uveitis.
ƒ Triad: heterochromia + stellate keratic precipitates + cataract
ƒ It is unilateral & occur mostly in middle aged persons which is it’s typical presentation.
ƒ Amsler’s sign is present: The sudden change of pressure in the anterior chamber upon suction
induced by the paracentesis, or during a cataract surgery, causes bursting of the fragile superficial
iris capillaries resulting in micro-bleeding.
ƒ Treatment is topical steroid.
 OPHTHALMOLOGY WORKBOOK 2024 | 37

Glaucomatocyclitis crisis
• HLA BWS4 associated
• Also known as posner-schlossman syndrome.
• There is acute rise of IOP (40-50 mm of hg)
• Fine keratic precipitates and corneal edema
• Pupil is dilated
• Treatment is antiglaucoma drugs and topical steroids.

SYMPATHETIC OPHTHALMITIS:
38 | OPHTHALMOLOGY WORKBOOK 2024

• It is a bilateral granulomatous pan uveitis.

• Related to trauma to eye.
• Two form of trauma can be there:
(i) Penetrating trauma: point of entry but no exit.
(ii) Perforating trauma: point of entry & point of exit.

Metallic foreign body injury is most common: Iron, Copper.

Mechanism:
• Uveal pigment is a sequestered antigen. So, when damage to ciliary body occurs, it leads to breakage
of barriers leading to exposure of uveal pigment to immune system via blood.
• There is incitation of antibody response.
• These very antibodies act upon the uvea of sound eye & damages it.
ƒ Ciliary body – Dangerous area of eye.
ƒ Most dangerous period is 2 weeks to 2 months.
ƒ Dalen- fuch nodules.
ƒ Earliest sign of sympathetic ophthalmitis is retrolental flare.
ƒ Earliest symptom is loss of accommodation.
ƒ Mutton fat keratic precipitates.
ƒ Hypotony: Decrease in IOP (<7 mm of Hg.)

Treatment:
• Enucleation: When vision in injured eye is PL (Light perception) negative and other eye is normal.
• Repairing of the wound: When vision in injured eye is 6/60 and other eye is normal.
• High dose of corticosteroids: When sign & symptoms of sympathetic ophthalmitis starts in the other
eye.

Endophthalmitis:
• Inflammation of inner structures of eye i.e uvea, retina, vitreous cavity, anterior chamber & posterior
chamber.
• The sclera is typically spared. (whereas in panophthalmitis, entire globe is involved with extension of
inflammation into the orbit).
• It can be infectious or non-infectious.
• Acute onset is when it is between 1- 7 days while delayed is between 7- 28 days.

Clinical features:
Symptoms:
ƒ Severe pain
ƒ Redness
ƒ Lacrimation
ƒ Photophobia
ƒ Sudden painful loss of vision
 OPHTHALMOLOGY WORKBOOK 2024 | 39

Signs:
• Swelling of eye lids.
• Conjuctival chemosis
• Hazy cornea
• Hypopyon
• Muddy & oedematous iris
• Leukocoria due to purulent exudation in vitreous.
• Amaurotic cat’s eye reflex due to whitish mass in vitreous cavity seen through dilated pupil. (MCQ)
• IOP is high initially.

Treatment
1. Intravitreal antibiotics:
ƒ Vancomycin + Ceftazidime or Vancomycin + Amikacin
ƒ Gram positive & gram negative cover.
ƒ Pars plana approach is used.
2. Topical fortified antibiotics
3. Systemic antibiotics can be given but not much helpful.
4. Steroids limits tissue damage due to inflammation
ƒ It can be given after 24 -48 hours of control of infection
ƒ Intravitreal, topical, systemic routes can be used.
5. Cycloplegics
6. Antiglaucoma drugs
7. Enucleation

Panophthalmitis:
Purulent inflammation of whole eye ball including tenon’s capsule.

Treatment
1. Anti inflammatory & analgesic drugs.
2. Broad spectrum antibiotics
3. Evisceration
It is the removal of ocular contents leaving sclera behind.
Frill evisceration is a procedure in which about 3 mm of frill of is left around optic nerve head.
4. GLAUCOMA

Definition:
Any 2 out of the following 3 Conditions:
1. Raised Intraocular pressure (IOP): Normal IOP is 10-21 mm Hg.
ƒ IOP is measured by Tonometry
2. Optic nerve head (ONH)/Retinal RNFL changes
3. Visual field defects

Classification:
a) Primary glaucoma
1. Congenital glaucoma:
ƒ Congenital glaucoma- 0 to 3 years
ƒ Juvenile onset glaucoma- 3 to 40 years
2. Adult onset: more than 40 years
(i) Primary open angle glaucoma
(ii) Primary angle closure glaucoma
b) Secondary glaucoma : glaucoma associated with other diseases.

Intraocular pressure measurements:

1. Indentation tonometer:
ƒ Impression tonometry.
ƒ Soft eye is indented more than hard eye.
ƒ Schiotz Tonometer.
2. Applanation tonometer

Goldmann’s tonometer:
ƒ Gold standard
 OPHTHALMOLOGY WORKBOOK 2024 | 41

• Perkin’s tonometer:
Hand held portable GOLDMANN’S Tonometer.

• Non contact pneumo tonometer

Angle of anterior chamber: grading methods

42 | OPHTHALMOLOGY WORKBOOK 2024

• Gonioscopy: direct & indirect

Measures Angle of Anterior Chamber:

1. S –SCHWALBE’S LINE GRADE 1 -100
2. T- TRABECULAR MESHWORK GRADE 2- 200
3. S – SCLERAL SPUR GRADE 3-300
4. C- CILIARY BODY GRADE 4- 400

Optic nerve head changes:

Nasal bending of blood vessels and bayonetting sign:

Laminar dot sign:

           
 OPHTHALMOLOGY WORKBOOK 2024 | 43

Splinter hemorrage:

• Ophthalmoscopy: Direct & Indirect:

  
44 | OPHTHALMOLOGY WORKBOOK 2024

Visual field defects:

• Visual Field is an area of Space Visible to human Eye without moving the Eye from Central target.
• Visual Field defects are due to Optic Nerve Damage
• Normal Visual Field
ƒ Superior Retina controls Inferior Field
ƒ Inferior Retina controls Superior Field
ƒ Temporal Retina controls Nasal Field
Nasal Retina controls Temporal Field.

ƒ Extent of visual field (VMQ)

ƒ SUPERIOR – 50 0
ƒ NASAL – 600
ƒ INFERIOR – 700
ƒ TEMPORAL – 900
Scotoma - It is a focal region of abnormally of decreased sensitivity surrounded by an area of Normal
Sensitivity.
Absolute – Doesn’t see anything
Relative – Decreased Visual Sensitivity
Positive - Patient realises it
Negative – Patient doesn’t realize it
Blind Spot is an example of Absolute - Negative Scotoma

Nerve Fibres:
 OPHTHALMOLOGY WORKBOOK 2024 | 45

Confrontational:
• The Patient is made to sit directly across from the person administering the test.
• Patient is then asked to cover one eye & fix at on a point usually nose of the tester with eye under
test.
• The tester would then move a stimulus, usually a finger or a pen light inwardly from a point outside
the patient‘s visual field until the patient see the stimulus.
• Because of the relative distance between the patient & tester, the tester could compare the patient
response against their own visual acuity.

Kinetic:
• Uses a mobile stimulus moved by an examiner
• Stimulus is moved towards centre of vision from periphery until its first detected by patient

Static:
• Patient places his head in chin rest & fixed his gaze toward a central fixation point in a large, white
hemispherical bowl.
• When patient sees a presented stimulus, he press button on a hand held remote control.
46 | OPHTHALMOLOGY WORKBOOK 2024

Perimetry charting:

Visual field defects:

1. Isopter contraction: earliest visual field defect.
2. Paracentral scotoma: earliest clinically significant visual field defect.
3. Bjerrum’s scotoma: scotoma in bjerrum’s area occurring in the region of 10-25 degree
ƒ There is an extension of blind spot in the form of an arc.
4. Siedel’s scotoma: it is sickle shaped scotoma.
5. Roenne’s nasal step: scotoma consisting of 25 degree - 30 degree of field involvement.
6. Double arcuate scotoma: superior arc and inferior arc of scotoma meet in the midline forming a
double arcuate scotoma.
7. Advanced glaucoma changes: ring scotoma/ tunnel vision
ƒ Involvement of visual field: nasal> central> temporal
ƒ Infero- temporal retina is first to get damaged and hence, supero nasal field is involved first.
ƒ It characteristically follow horizontal meridian i.e it does not cross the midline.
OPHTHALMOLOGY WORKBOOK 2024 | 47
48 | OPHTHALMOLOGY WORKBOOK 2024

1. Congenital glaucoma

Etio-Pathogenesis:
a) Presence of Barkan’s membrane
b) Angle anomaly
c) Plateau iris configuration
d) Trabecular dysgenesis
e) Hereditary: AR inheritance
f) Maternal smoking

ƒ Triad of Congenital Glaucoma

(i) Lacrimation (most common)
(ii) Photophobia
(iii) Blepharospasm

Important Signs:
• Buphthamos: Large eye ball; sclera is elastic & soft, so it expands due to raised intra ocular pressure
(IOP) giving “Bull’s eye” appearance to the eye.
• Raised axial length leading to Myopia.
• Hazy cornea due to Edema of cornea.
• Ground glass appearance of the cornea.
• Bluish White Sclera.
• Haab’s striae: Rupture of Descemet’s Membrane of Cornea due to raised IOP.
• Flat lens due to raised IOP pressing upon it.
• Lens Subluxation/Dislocation and Disc cupping are other features.

Management:
Goniotomy: It is the surgery of choice and involves cutting up of Barkan’s Membrane
Trabeculotomy: Opening up of schlemm’s canal.
Trabeculectomy: Removing of a piece of trabecular meshwork.
 OPHTHALMOLOGY WORKBOOK 2024 | 49

2. Primary angle closure glaucoma:

ƒ ‘Angle closure’ refers to occlusion of the trabecular meshwork by the peripheral iris, obstructing
aqueous outflow.

Etiology:
• Middle aged female
• Small eyes
• Decrease axial length
• Hypermetropia
• Decrease corneal diameter- Small eyes
• Raised lens thickness
• Shallow anterior chamber

Clinical Features:
1. Latent stage /Prodromal stage
ƒ Pre disposing factors are present.
ƒ Patient is asymptomatic but sometimes can complain of Halos around lights & Transient haziness
of vision.
2. Stage of constant instability:
ƒ Some part of angle closes when pupil is mid dilated & then re-opens spontaneously.
ƒ During closure, the patient complains of pain, redness, loss of vision (transient).
ƒ Symptoms are relieved when the angle opens.
3. Acute congestive stage
ƒ Whole 360 degree angle gets closed and fails to re-open spontaneously.
ƒ Severe pain associated with nausea and vomiting.
ƒ Very high IOP = 60 mm Hg
ƒ Coloured Halos due to corneal edema
ƒ Severely congested eye.
ƒ Shallow Anterior Chamber.
ƒ Pupil oval, Mid dilated , not reacting to light and accommodation.
ƒ Field defects are typically absent.
ƒ Retinal nerve fibre layer (RNFL) changes (C:D Ratio) may not be there.
50 | OPHTHALMOLOGY WORKBOOK 2024

4. Chronic angle closure glaucoma

ƒ All feature of Open angle glaucoma i.e raised IOP ,fundus changes, field defects etc.
5. Absolute glaucoma/ Painful blind eye stage
ƒ Painful blind eye.

Stony hard eye.

VOGT’S TRIAD (MCQ)
ƒ Iris atrophy.
ƒ Non reacting pupil due to sphincter damage
ƒ Glaucoma flecken’s: Focal epithelial necrosis of lens capsule leading to anterior subcapsular
lens opacity.

• Pilocarpine 2% eye drops can be given which was earlier Drug of Choice for PACG
Now ,PGF2 analogues i.e Latanoprost, Bimatoprost is preferred(DOC Now)

Surgery
• Laser peripheral iridotomy is management of choice in PACG cases (Nd-Yag laser) but it needs to have
a closer view of anterior chamber to focus laser on iris.
• Next best option is surgical peripheral iridectomy: It is specifically done in acute congestive glaucoma
attacks.
• Prophylactic laser iridotomy is done in contralateral eye.
• Before going on for surgical peripheral iridectomy, it is important to lower IOP by giving intravenous
mannitol to prevent expulsion of eye contents during incision.
3. Primary open angle glaucoma:

Etiology:
• Males
• Myopes
• Age- >65 years
• Trabecular Meshwork fibrosis
• Diabetes mellitus
• Hypertension
• Smoking

Clinical Features:
• ONH changes
• Visual field defects
• Optic Cup: Disc ratio of more than 0.7 is highly suspicious.
• Asymmetry in cups.
• Disc palor.
• Splinter haemorrhages.
 OPHTHALMOLOGY WORKBOOK 2024 | 51

• Nasalisation of vessels.
• Bayoneting sign - Bending of vessels while emerging out of optic cup.
• Laminar dot sign.

Neuro Retinal Rim (NRR) thinning: It follows ISN’T Rule

Inferior> Superior> Nasal> Temporal
i.e Inferior thinning is first to take place and Temporal, last.

Symptoms of open angle glaucoma:

• Frequent changes in presbyopic glasses.
• Raised dark adaptation time.

Frequent changes in Myopic glasses: Cataract in old patients.

Frequent changes in myopic glasses in young adult patients: Keratoconus
Fluctuation of vision in patients: Diabetic mellitus

Management:

Medical management: Anti glaucoma drugs

1) Carbonic anhydrase inhibitors:
Mechanism of Action: Decreases the production of aqueous humour.
Oral: Acetazolamide.
Topical: Brinzolamide, Dorzolamide

Side effects:
Oral administration:
• Sulfa allergy
• Hypokalemia
• Tingling
• Numbness
Topical administration: Corneal decompensation

2. Parasympathomimetics/Cholinergics:
Mechanism of Action: Increases aqueous humour drainage from anterior chamber.
Parasympathomimetics: Pilocapine – It was earlier drug of choice in Primary Angle closure Glaucoma
(PACG).

Side effects:
• Uveitis
• Ciliary spasm- Pain
• Iris cyst
• Pseudomyopia
• Cataract
• Retinal detachment
• Shallow Anterior Chamber
52 | OPHTHALMOLOGY WORKBOOK 2024

3. Alpha agonists:
Mechanism of Action: It decreases the production of Aqueous Humour.
Brimonidine is an Alpha 2 Agnoist. (Selective action)

It’s Side effect profile include:

• Respiratory Apnoea in child
• Drowsiness
• Depression
Apraclonidine: Alpha 1 & Alpha 2 agonist (Non selective action)

Side effects:
• Lid Retraction (due to Alpha 1 action)
• Conjunctival blanching
Brimonidine is a well known Neuro-protective agent.
These are the only drugs which can be given in pregnancy

4. Beta bockers:
Mechanism of Action: Decrease production of Aqueous Humour.
Betaxolol is a selective beta blocker while Timolol is non selective.

Side Effects:
• Blepharo Conjuctivitis
• Asthma
• Naso-Lacrimal Duct blockade
 OPHTHALMOLOGY WORKBOOK 2024 | 53

5. Sympathomimetics:
Dual mechanism of action i.e Decrease production and increased Aqueous Humour outflow.

Side Effects:
• CME in Aphakic patient.
• Black deposits in conjunctiva.

Black conjunctival deposit by epinephrine:

6. prostaglandin analogues:
Mechanism of Action: Increases Aqueous humour outflow.
PGF2 alpha analogue: Latanoprost, Travoprost, Bimatoprost
It acts upon uveoscleral pathway.
Normally aqueous humour outflow is via two main mechanisms:
• Trabecular meshwork outflow which constitutes-90%
• Uveo-scleral pathway-10%
It decreases Intra ocular pressure by 30-35%
PG analogues is drug of choice for Primary Open angle Glaucoma(POAG), Primary Angle Closure
Glaucoma (PACG), Normo Tensive Glaucoma (NTG).

Side effects:
• Uveitis
• Cystoid macular edema
54 | OPHTHALMOLOGY WORKBOOK 2024

• Irreversible iris hyperpigmentation

• Blephroconjuctivitis
• Trichomegaly

7. Hyperosmotic agents:
Mechanism of Action: Acts by decreasing the production of aqueous humour.
Examples: Intravenous mannitol/Oral glycerol
Fastest action: 20 minutes.

Side effects:
• Pulmonary edema
• Right side heart failure.
8. Rho Kinase inhibitors:
Mechanism of Action- Increases aqueous humour outflow by acting upon Trabecular Meshwork.
• It is a new generation of drug: RIPASUDIL
Side effect: Conjuctival hyperemia

 OPHTHALMOLOGY WORKBOOK 2024 | 55

Surgical management
Iridectomy & Iridotomy:

Trabeculoplasty (ALT & SLT):

ALT: Coagulation caused by Argon Green laser burns results in contractures of adjacent tissue leading to
widening of adjacent trabecular pores.
SLT (Frequency doubled Nd-Yag laser) targets only pigmented trabecular cells and cause no structural or
coagulative damage to Trabeular Meshwork and leading to activation of phagocytosis which clears debris
from TBM beams ultimately leading to raised aqueous outflow.

Trabeculectomy/filtration surgery: Fistula made between Ant. chamber & subconjunctival space.
Mitomycin-C 0.02% is applied for 2-3 minutes to prevent post op. fibrosis.
56 | OPHTHALMOLOGY WORKBOOK 2024

Drainage implants:
• Non valved implants: Baerveldt implant

• Valved implants: Ahmed glaucoma Valved implant

Minimally Invasive Glaucoma Surgeries(MIGS):

iStent & Express implant:
• acts by bypassing the TRABECULAR MESHWORK
• Minimum tissue trauma is there.
• iStent: Made up of titanium.
• Express implant: Made up of Stainless steel.
 OPHTHALMOLOGY WORKBOOK 2024 | 57

Secondary Glaucomas:
1. Trauma:
• Ghost cell Glaucoma: Degenerated RBCs, which causes raised IOP & glaucoma.
• Haemolytic Glaucoma: It is different from Ghost cell glaucoma in that there are no ghost cells but
Trabecular meshwork clogging is due to released debris, free haemoglobin and macrophages laden
with haemoglobin.

• Haemosiderotic glaucoma: Toxic effects to Iron on cells of Trabecular Meshwork.

• Lens dislocation / subluxation leading to raised IOP
58 | OPHTHALMOLOGY WORKBOOK 2024

Angle Recession: Separation of Circular muscles from longitudinal muscles of ciliary body.
Iridodialysis: Tearing of Iris from it’s root leading to ‘D’ shaped pupil.
Cyclodialysis: Separation of Ciliary body from Scleral Spur.
2. Lens induced:
• Phacomorphic glaucoma
• Phacolytic glaucoma
• Phaco anaphylactic/ Phaco antigenic glaucoma
 OPHTHALMOLOGY WORKBOOK 2024 | 59

3. Uveitis:

4. Neovascularisation induced:

Mechanism:
• Extensive retinal ischemia leads to neovascularisation
• Neovascularization over Iris & consequent fibrosis leads to zip like adhesions of Iris to the cornea at
the angle leading to raised IOP.

5. Pigmentary glaucoma:
Pigment dispersion syndrome (PDS) is characterized by the liberation of pigment granules from iris
pigment epithelium and their deposition throughout the anterior segment leading to Pigment deposition
in Trabecular Meshwork.
• It is due to constant rubbing of posterior surface of iris over zonules leads to release of pigment in
Anterior Chamber. (Concave anterior configuration of Iris, Convex posteriorly)
• Pigment is deposited on the endothelium in a vertical spindle shape pattern known as Krukenberg
spindle- Non specific
• Increased pigment in Trabecular Meshwork (TBM) is seen in the form of SAMPOLESI LINE on
Gonioscopy.- Characteristic
• Transillumination defects are characteristic.
• It is common in young Males and Myopes.
• Reverse Pupillary block glaucoma
60 | OPHTHALMOLOGY WORKBOOK 2024

6. Pseudoexfoliation glaucoma:
Pseudoexfoliative material is a grey-white fibrillary substance deposited on lens capsule, Zonular fibres,
Iris, Trabeculum and conjunctiva.
• These flakes tend to fall off & get collected at base of anterior chamber obstructing drainage of
aqueous humor.
 OPHTHALMOLOGY WORKBOOK 2024 | 61

7. Aqueous misdirection syndrome/ malignant glaucoma:

• Aqueous flow is blocked at ciliary body lens level leading to misdirection of aqueous humor in to the
vitreous.
• Formation of aqueous humor pockets in vitreous chamber leading to raised IOP which push the lens
forward leading to shallowing of AC.
• Cycloplegic agents are prescribed (Atropine 1% eye drops).

8. Drug induced glaucoma:

9. Elevated episcleral venous pressure:

10. Intraocular tumours:

Malignant melanoma, Retinoblastoma

11. Epidemic Dropsy: Hypersecretory glaucoma

5. RETINA

Retina and it’s diseases

• Ten layers.
• The inner nine layers are collectively called as NSL i.e neuro sensory layer while outermost tenth
layer is retinal pigment epithelium (RPE).
• Retina is thinnest at Ora serrata (0.1mm)
• Optic disc colour is pale pink and 1.5mm in diameter.

Macula lutea (5.5mm diameter) is situated temporal to optic disc

• It corresponds to 15 - 20 degree of visual field.
ƒ Fovea centralis is central depressed area of macula which corresponds to 5® of visual field.
ƒ Foveola – It is central floor of fovea.
ƒ UMBO - It is a tiny depression at very centre of foveola

Blood supply:
 OPHTHALMOLOGY WORKBOOK 2024 | 63

Oct macula:

Fluorescein fundus angiography:

Fluorescein (sodium fluorescein) is an orange water-soluble dye.
Fluorescence is the property of the dye to emit light of a longer wavelength when stimulated by light of
a shorter wavelength.

Amsler grid:
Measures central 20 0 of Visual Field.

Retinal detachment:
• Definition: Detachment of inner Neurosensory Retina (inner nine layers) & outermost Retinal Pigment
epithelium (Tenth layer).
64 | OPHTHALMOLOGY WORKBOOK 2024

• Types: rhegmatogenous, exudative and tractional detachment

1. Rhegmatogenous retinal detachment:

Rhegma means ‘Break’.

Causes of RRD:
• High Myopia
• Trauma
• Aphakia

Patho-Physiology
Anywhere break in retina (most common- Superotemporally) allows liquefied fluid from vitreous to seep
through & raise neurosensory layer from retinal pigment epithelium leading to retinal detachment.

Clinical features:
• Sudden painless loss of vision.
• Photopsia: Flashes of light.
• Tobacco dust / Shaffer’s sign can be seen which is due to pigment dispersion in vitreous cavity.
• Floaters: Release of pigment in vitreous cavity which cast a shadow on retina.
• Curtain falling in front of eyes.
• Convex configuration of detached retina.
 OPHTHALMOLOGY WORKBOOK 2024 | 65

2. Exudative RD:
• Malignant melanoma of choroid
• Gestational hypertension
• Malignant hypertension
• Coat’s Disease
• Central serous retinopathy
• Vogt – Kayanagi Harada Syndrome (VKH Syndrome)
• Sarcoidosis

Patho-Physiology
• Accumulation of Subretinal fluid due to inflammatory mediators or exudation of fluid from mass
lesion.

Clinical Features:
• Sudden painless loss of vision.
• Shifting fluid (Hallmark feature): It is in accordance to head posture.
• Photopsia absent.
• No floaters.
• Convex Configuration.

3. Tractional retinal detachment:

Causes:
• Diabetic Retinopathy
• Sickle cell Anaemia
• Retinopathy of Prematurity
• Ocular Ischaemic syndrome

Patho-Physiology:
Retina Hypoxia- Secretion of VEGF from hypoxic cells- Stimulation of Neovascularisation from around
lying area- Retinal hypoxia of around lying area whose blood supply was divided- Secretion of VEGF
from this new area- Neovascularisation from surrounding area- Cascade of neovascularisation leading
to a formation of Neovascular membrane over retina-Contraction of Neovascular membrane causing pull
over retina leading to a traction- Retinal Detachment.
66 | OPHTHALMOLOGY WORKBOOK 2024

Clinical Features:
• Floaters are absent.
• Photopsia is absent.
• Concave Configuration with smooth surface.
• Neovascularisation

Management:
1. Scleral buckling: Works on principle of focal indentation of sclera to reappose retinal breaks to
underlying RPE.

2. Pneumatic retinopexy: Tamponade is done by gas.

Gases used: Sulphur hexafluoride (SF6) and Perfluoro propane (C3F8)
• Best gas to use is C3F8
• Gas is absorbed spontaneously in vitreous cavity.
 OPHTHALMOLOGY WORKBOOK 2024 | 67

3. Silicone oil implant:

• Tamponade by Silicon oil.
• It doesn’t get reabsorbed, so it has to be removed after 2-3 months since it is maculotoxic.

4. Pars-Plana vitrectomy (PPV):

• Removal of vitreous is done by Pars Plana approach.
• Vitreous traction is reduced & liquefied vitreous gel is removed.

Diabetic retinopathy:
Etiopathogenesis:
• Duration is most important prognostic factor i.e longer the duration, worse is the prognosis.
(irrespective of blood sugar control)
• Type-1 Diabetes mellitus (IDDM): Fundus exam is done after 5 years. (Because this disease is not
silent and it takes a minimum of 5 years for retinopathic changes to set in)
• Type-2 Diabetes mellitus (NIDDM): Immediate Fundus exam is done. (because this disease is silent)

Features:
Loss of pericytes due to high blood sugar.
• Pericyte to endothelial (P:E) cell ratio is 1:1.
• P:E ratio becomes 1:3 due to damage to pericytes because of toxicity due to excess blood glucose
leading to microaneurysms formation(earliest feature), blood retinal barrier breakage & leaking of
vascular contents in surrounding tissues.
68 | OPHTHALMOLOGY WORKBOOK 2024

Classification
1. Non proliferative diabetic retinopathy:
• Microaneurysms
• Dot-Blot Haemorrhages
• Exudates: Hard & Soft exudates
Macular edema/DME/CSME i.e Clinically Significant Macular Edema.

2. Pre Proliferative Diabetic Retinopathy:

• Ischemic Changes super imposed on background diabetic retinopathy leads to this stage.
• There is evidence of Ischemia at multiple regions over retina.
3. Proliferative retinopathy: Neovascularisation is there.
ƒ First arise from Disc (NVD)
ƒ Neovascularisation elsewhere (NVE)
ƒ Neovascularisation Iris (NVI) (Rubeosis Iridis)
 OPHTHALMOLOGY WORKBOOK 2024 | 69

ETDRS: Early Treatment of Diabetic Retinopathy Study classification

• Intraretinal microvascular abnormalities (IRMA)are shunt vessels and appear as abnormal branching
or dilation of existing blood vessels (capillaries) within the retina that act to supply areas of non-
perfusion.
• Represent either new vessel growth within the retina or remodeling of pre-existing vessels through
endothelial cell proliferation stimulated by hypoxia bordering areas of capillary nonperfusion.
IRMAs are slightly larger in caliber with a more broad arrangement and are always contained to the
intraretinal layers.
Neovascularisation tends to be much finer and delicate in caliber, and is sometimes more focal in location
depending on its severity. It tends to grow along the posterior hyaloid interface especially around the
optic nerve (i.e. NVD) and periphery (i.e. NVE).
NV will often show late leakage whereas IRMAs traditionally do not leak.
70 | OPHTHALMOLOGY WORKBOOK 2024

Fundus fluorescein angiography:

Management:
1. General

2. Specific:

Photocoagulation:
• Focal: Burns applied to leaking microaneurysm.
• Grid: Burns applied to macular areas of diffuse retinal thickening.
• Pan Retinal Photocoagulation (PRP): Whole of the retina is photocoagulated except circular area of
radius 2 ½ disc diameter with fovea at its centre which is left untouched.

• Intra vitreal injections: Anti VEGF

• Bevacizumab
• Ranibizumab
• Triamcinolone
 OPHTHALMOLOGY WORKBOOK 2024 | 71

Hypertensive retinopathy
Etiopathogenesis:
• Blood pressure ≥ 140/90 mm Hg.
• A:V ratio becomes 1:3 (N-2:3) due to narrowing of lumen of arteries.

Features:
Classification: Modified Scheie’s grading.
Grade 0: No Changes.
Grade 1: Barely detectable arterial narrowing.
Grade 2: Arterial narrowing with focal irregularities.
• Gunn’s Sign: Tapering of veins on either side of crossing.
• Bonnet’s sign: Banking of vein proximal to A-V crossing.
• Salus Sign: Sudden deflection of vein.
• Humping Sign: Vein forms hump while crossing artery.
Grade 3: Grade 2 + Retinal haemorrhage/exudates.
• Flame shaped haemorrhage are present on nerve fibre layer of retina.
• Soft Exudates / cotton Wool spots.
• Copper wiring of Arterioles.
Grade 4: Grade 3 + Disc swelling & Silver wiring of arterioles.
72 | OPHTHALMOLOGY WORKBOOK 2024

Macular star is seen due to collection of hard exudates.

• Management: Control blood pressure

Central retinal vein occlusion

Etiopathogenesis:
• Uncontrolled hypertension, Diabetes mellitus.
• Age more than 65 years.
• Oral contraceptive pills.
• Smoking.

Features:
 OPHTHALMOLOGY WORKBOOK 2024 | 73

Branched retinal vein occlusion

• Management

Central retinal artery occlusion

74 | OPHTHALMOLOGY WORKBOOK 2024

Etiopathogenesis:
• Old age
• Uncontrolled Hypertension
• Uncontrolled Diabetes Mellitus
Pathogenesis: Embolus (Cholesterol plaque known as Hollenhorst plaque is most common cause);
Posterior to Lamina Cribrosa.

Features:
• Sudden painless loss of vision.
• Relative afferent pupillary defect (RAPD).
• Cattle track appearance due to discontinuity in blood column.
• Pale (milky white) fundus.
• Cherry red spot is present at Fovea centralis.

• Management:

Steps of treatment:
1. Ocular massage
ƒ To dislodge the clot.
2. I.V Mannitol
ƒ To lower Intra Ocular Pressure (I.O.P)
3. Paracentesis
ƒ Aspiration of aqueous humor through limbus to lower I.O.P
4. Carbogen (5% CO2 + 95% O2) inhalation
 OPHTHALMOLOGY WORKBOOK 2024 | 75

ƒ To dilate blood vessels

5. Intra venous tPA (tissue plasminogen activator) or Heparin.

Cystoid macular edema

• Etiopathogenesis

• Features

Central serous retinopathy

Exudative form of Retinal Detachment.
76 | OPHTHALMOLOGY WORKBOOK 2024

Etiopathogenesis:
• Outer blood retinal barrier is broken.
• Common in young anxious males (Type A personalities).
• Fluid collects between neurosensory layer (NSL) & retinal pigment epithelium (RPE)

Features:
• Seen in type A personalities.
• Metamorphopsia (Distortion of shape of objects) is present.
• Fluorescein angiography appearance:
Smoke stack pattern is characteristic (but seen in 15-20% of patients).
Ink blot pattern is more common but is not specific to CSR. (seen in 80% of patients).

• Management

Age related macular degeneration

Etiopathogenesis:
• Males, white, smoking, Alcohol, non- vegetarian food intake
• Features:
Drusens are present in centre or macula.

Types:
 OPHTHALMOLOGY WORKBOOK 2024 | 77

DRY (Drusens) WET (RPE Detachment)

90% 10%

10% Go blind 90% Go blind

Drussens Choroidal NEO Vascularisation (CNVM)

Slow painless loss of vision (Sub Retinal Neo Vascularisation)

With Metamorphopsia Treatment

Teatment: 1.Photodynamic Phototherapy (PDT

Self Limited Antioxidants {Diode Laser}

(AREDS i.e. Age related Eye 2 Thermotherapy {Diode Thermal effect}

Disease Study) 3 Intra vitreal Anti – VEGF Agents

Beta Carotene; Vitamin C & E: Zinc, Copper

PDT: Verteporfin dye is injected which is able to go in choroidal circulation but not in retinal circulation as
a result of which when diode laser is exposed, it leads to sclerosis of only CNVM, not of retinal vessels.
78 | OPHTHALMOLOGY WORKBOOK 2024

Myopic Degeneration
Myopic power of more than – 6D
• Presence of Peripapillary atrophy and temporal crescent
• Macular atrophy
• Foster- fuch’s spots / Fuch’s fleck’s (pigment clumps)
• Lacquer cracks (breaks in bruch’s membrane due to stretching)
• Lattice degeneration.
• Increased risk of Rhegmatogenous Retinal detachment
• Chorioretinal atrophic patches are present.
• Tigroid / Tesselated Fundus.
Posterior staphyloma formation is common.

Retinopathy of prematurity
Etiopathogenesis:
• Prematurity (34 weeks)
• Low birth weight (< 200 gram)
• High supplemental oxygen
• Hypoxemia
• Hypercarbia
• Septicaemia

Features:
Retinal vessels extend upto nasal edge of retina by 8th month of gestation while temporal part of retina
is vascularised after 3-4 weeks of birth.
In case of premature birth(<32 weeks), the part of retina remains avascularised, which leads to increase
in VEGF (Vascular Endothelial Growth Factor) Secretion leading to neovascularisation and eventually,
Tractional Retinal Detachment and Vitreous Haemorrrhage.

Staging of ROP:
• Stage
i – Demarcation line
• Stage
ii – Ridge formation
• Stage
iii – Fibro vascular proliferation
• Stage
iv – Subtotal retinal detachment
a – Not involving fovea
b – Involving fovea
• Stage v – Total retinal detachment

Management:
• Screening is done with Indirect ophthalmoscope.
• If age at birth < 28 weeks, the screening is undertaken after 2-3 weeks
• If age at birth >28 weeks, the screening is undertaken after 4 weeks.
 OPHTHALMOLOGY WORKBOOK 2024 | 79

Treatment:
• Laser photocoagulation of hypoxic retina- Diode Laser
• Intra- vitreal Anti-VEGF injections.

Retinitis pigmentosa
Etiopathogenesis:
• Important risk factor is consanguineous marriages.
• Types: Sporadic(most common) & Hereditary
Heritable: Autosomal dominant (most common), Autosomal recessive & X linked recessive (Worst
prognosis)
• Pathogenesis involves apoptosis of Rods> Cones
• Features:

1. Earliest symptom is nyctalopia.

2. Ring scotoma.
3. Triad of retinitis pigmentosa.
 Arteriolar attenuation.
 Pale waxy optic disc.
 Bony spicule pigmentation at mid periphery

4. Glaucoma

5. Cataract

• Management:

Gold Standard: Electro Retinogram (ERG)

Treatment:
• No treatment is helpful as such.
• 15000 International Units (I.U)/ Day vitamin A palmitate can delay blindness to 40 years
of age.
80 | OPHTHALMOLOGY WORKBOOK 2024

Retinoblastoma
Etiopathogenesis:
ƒ Most common Intra ocular tumour of childhood.
ƒ Most common age of presentation is 18 months.
ƒ Hereditary is 6% and non hereditary is 94%.
ƒ 30% are of the tumours are bilateral while 70% are unilateral.

Genetics:
ƒ Rb1 gene is involved.
ƒ 13q14 Chromosomal.
ƒ Knudson 2 hit hypothesis

Features:
• Leukocoria is seen in 60% of cases.
• Squint is seen in 20% of cases.
• Uveitis
• Pseudohypopyon.
• Heterochormia
• Hyphema

Differential diagnosis of Leukocoria:

1. Retinoblastoma
2. Congenital Cataract
3. Coat’s disease.
4. Persistent Hyperplastic Primary Vitreous (PHPV)
5. Retinopathy of Prematurity (ROP)
6. Toxocariasis
7. Endophthalmitis
8. Retinal Detachment
9. Coloboma
 OPHTHALMOLOGY WORKBOOK 2024 | 81

Diagnosis:
Clinical Diagnosis is made:
• Intra Ocular Calcification on CT Scan / X-ray/ USG or Eye
• Flexer wintersteiner Rosette: Hallmark of Retinoblastoma.

International Classification of Retinoblastoma:

Stages of retinoblastoma
A Size of tumour ≤ 3mm.
B Size of tumour > 3mm.
C Localised seeding, within 3mm.
D Diffuse seed, more than 3mm.
E Distant metstasis

Management:
Chemotherapy:
1. Intravenous: 6 Cycles of Vincristine/ Etoposide/ Carboplatin (VEC regimen).
2. Intravitreal: Intravitreal injection of Melphalan.
3. Intra-arterial: The drug is delivered in ophthalmic artery: Melphalan/Topotecan/Carboplatin.
4. Enucleation
6. NEUROPHTHALMOLOGY

Pupil:

Marcus gunn pupil:

Relative afferent pupillary defect (RAPD) is observed during the swinging-flashlight test whereupon the
patient›s pupils dilate when a bright light is swung from the unaffected eye to the affected eye.
 OPHTHALMOLOGY WORKBOOK 2024 | 83

Argyl robertson pupil:

• Bilateral Constricted Pupil.
• Accommodation reflex is present and light reflex absent.
• Neurosyphilis.
• Defect lies in pretectum region.
• Also called as prostitute Pupil.
84 | OPHTHALMOLOGY WORKBOOK 2024

Holmes adie’s pupil:

• Unilateral dilated pupil
• Accommodation reflex is present and light reflex is absent
• ciliary ganglionitis.
Pilocarpine 0.125% instilled in both eyes- Normal Pupil Constrict Slowly while adie’s pupil constricts
immediately due to denervation hypersensitivity.

Hutchinson pupil
• seen after trauma.

Three phases:
1. Initial constriction phase
2. Dilatation of pupil phase
3. Dilated & fixed pupil phase

Optic neuritis
• Etiology:
1. Retrobulbar neuritis: Inflammation of retrobulbar part of optic nerve.
• Disc margins normal
2. Papillitis: Inflammation of intraocular portion of optic nerve.
• Disc margins are blurred.
3. Neuroretinitis:
• Inflammation of Neuroretinal rim.
• Disc margin is blurred
• Macular star appearance is seen.

Features:
• Pain: On ocular movements.
• Sudden painful/painless loss of vision
• Dyschromatopsia
• Uhthoff’s symptom: Increase of symptoms on increase in temperature.
• RAPD: Relative afferent pupillary defect
Treatment: Intra venous methyl Prednisolone. (IVMP)
 OPHTHALMOLOGY WORKBOOK 2024 | 85

Papilledema
• Bilateral disc edema with raise Intra Cranial Tension (ICT)

Etiopathogenesis:
• Pathogenesis involves stasis of axoplasm of optic nerve due to its compression.

Clinical features:
• Headache: occipital
• Projectile vomiting is present.
• Amaurosis fugax: Transient visual loss
• Disc edema: Champagne cork appearance of disc.
• Peripapillary h’ges
• 6th cranial nerve palsy (it is a false localising sign)
• Visual acuity: it is not affected till late in the disease.
• Colour vision is normal.
• Pupillary reaction is normal.
• Disc edema is present.
• Paton’s folds are there.
• Loss of venous pulsation (earliest sign of papilledema).
• Dilated & tortuous vessels.
• Enlargement of blind spot.
86 | OPHTHALMOLOGY WORKBOOK 2024

Management:

Horner’s syndrome: Oculo-sympathetic paralysis

Etiopathogenesis:

1. Central (first-order neuron)

ƒ Brainstem disease: commonly stroke
ƒ Cervical spinal cord lesion
2. Preganglionic (second-order neuron)
ƒ Pancoast tumour
ƒ Carotid and aortic aneurysm and dissection
3. Postganglionic (third-order neuron)
ƒ Internal carotid artery dissection
ƒ Nasopharyngeal tumour
ƒ Cavernous sinus mass
 OPHTHALMOLOGY WORKBOOK 2024 | 87

Features:
• Ptosis
• Miosis
• Anhydrosis
• Enophthalmos
Enophthalmos is not true, hence, Pseudoenophthalmos.

Visual pathway and its lesions

Features:

• Field infront of left eye of doctor: Left Visual Field

• Field infront of right eye of doctor: Right Visual Field
88 | OPHTHALMOLOGY WORKBOOK 2024

Right Optic Nerve Lesion

Right Anopia / Right Monocular Blindness

2. Optic Chiasma Lesion:

Bitemporal Hemianopia
Most common cause is Pituitary Adenoma. (Macroadenoma ie >1cm)

First Defect

Supero-Temporal Involvement
3. Right Side Optic Tract Lesion:

Left Homonymous Heminopia (associated with Wernicke Hemianopic Pupil)

Proximal part of optic tract lesion: Normal pupillary reaction.
4. Right Lateral Geniculate Ganglion Lesion:

Left Homonymous Key Hole Visual Field Defect

5. Right Temporal Lobe Lesion:
 OPHTHALMOLOGY WORKBOOK 2024 | 89

Left Homonymous Superior Quadrantopia

• Typical Pie In sky Appearance (MCQ)
• When Temporal Lobe is Involved: Formed Hallucination are Seen (MCQ)
6. Right Parietal Lobe:

Left Homonymous Inferior Quadrantopia

• Pie On Floor Appearance

Other important associated features are:

• Agaraphia
• Agnosia
7. Right Occipital Lobe Lesion:

Left Homonymous Hemianopia with Macular Sparing

(Because of Additional Blood Supply from Middle Cerebral Artery)
‘Key Hole Vision’ is typically seen in Right occipital lobe lesions. (MCQ)
• Congruous visual field defects are symmeterical defects and are seen in
occipital lobe lesions while incongruous defects are asymmetrical ones and are seen in optic chiasma &
optic tract lesions.
7. SQUINT

Extraocular muscles:
 OPHTHALMOLOGY WORKBOOK 2024 | 91

Muscle movements:
92 | OPHTHALMOLOGY WORKBOOK 2024

Vergences:
 OPHTHALMOLOGY WORKBOOK 2024 | 93

• Nerve Supply – S04; LR-6; Rest 3.

• Superior Oblique Muscle is supplied by FOURTH Caranial Nerve( Trochlear).
• Lateral Rectus Muscle is supplied by SIXTH Cranial Nerve ie Abducens.
• other four Extra ocular Muscles are supplied by THIRD Cranial Nerve.

Angle between optical Axis & Orbital axis (Muscle plain) is 230

• Superior Rectus- Maximum Elevator in Abducted Position

• Inferior Rectus- Maximum Depression in Abducted Position
• Inferior Oblique- Maximum Elevator in Adducted Position
• Superior Oblique- Maximum Depressor in Adducted Position

Gaze positions:

Laws in extraocular muscle movements:

1. Sherrington’s law of reciprocal innervation
During ocular motility, an increased flow of innervations to the contracting agonist muscle is accompanied
by a decreasing flow to the medial rectus of same eye.
2. Herrings law of equal innervation
It states that equal & simultaneous innervation flows from the brain to a pair of muscles of both eyes
(yoke muscle) which contract simultaneously in different binocular movements.
Corresponding points & normal retinal correspondence
• Those elements of two retinae the stimulation of which in binocular vision gives rise to localisation in
one & the same visual direction
• Image falling on corresponding points give rise to a single impression to visual direction.
• Both fovea corresponds to each other.
• Example: the receptor 50 temporal to fovea in one eye corresponds to a receptor 50 nasal to fovea
in other eye.
• Two foveae no longer have a common visual direction, & fovea of one eye & peripheral retinal element
of other eye acquire common visual direction.
94 | OPHTHALMOLOGY WORKBOOK 2024

Classification:

Pseudosquint:

Latent squint: Squint which is not present all the time.

Known as Phorias-
Esophoria
Exophoria
Hyperphoria
Hypophoria
Manifest squint: Present all the time
Tropias-
 OPHTHALMOLOGY WORKBOOK 2024 | 95

Types of tropias:
1. Concomitant squint
2. Incomitant squint: Paralytic & Restrictive squint

Tests done in squint

Hirschberg test:

Cover test for tropias:

• The patient fixates on a straight-ahead target.
• If a right deviation is suspected, the examiner covers the fixing left eye and notes any movement of
the right eye to take up fixation.
• No movement indicates orthotropia or left heterotropia
• Adduction of the right eye to take up fixation indicates right exotropia and abduction, right esotropia
• Downward movement indicates right hypertropia and upward movement right hypotropia.
• The test is repeated on the opposite eye.
96 | OPHTHALMOLOGY WORKBOOK 2024

Cover-Uncover test for phorias/latent squint:

• The patient fixates a straight-ahead distant target.
• The examiner covers the right eye and, after 2–3 seconds, removes the cover.
• No movement indicates orthophoria. A keen observer will frequently detect a very slight latent
deviation in most normal individuals, as few individuals are truly orthophoric, particularly on near
fixation.
• If the right eye had deviated while under cover, a refixation movement (recovery to BSV) is observed
on being uncovered.
• Adduction (nasal recovery) of the right eye indicates exophoria and abduction esophoria.
• Upward or downward movement indicates a vertical phoria.
• After the cover is removed, the examiner notes the speed and smoothness of recovery as evidence
of the strength of motor fusion.
• The test is repeated for the opposite eye.

Prism Bar cover test:

• Prisms of increasing strength with apex towards deviation are placed in front of one eye & patient is
asked to fixate an object with other eye.
• Cover test is performed till there is no recovery movement
• This will tell amount of deviation in Prism Dioptres.
 OPHTHALMOLOGY WORKBOOK 2024 | 97

Worth four dot test:

Interpretation:
1. Normal binocular single vision: A- 1 red, 2 green, 1 orange (red- green)
2. Abnormal retinal correspondence:B - 1 red, 2 green, 1 orange
3. Left suppression: C- 2 red lights
4. Right suppression:D- 3 green lights
5. Altering suppression:E1- 3 green & 2 red lights alternatively
6. Diplopia (in the pic: crossed diplopia seen in exotropia): E-2 5 lights i.e. 2 red & 3 green

Maddox rod test

98 | OPHTHALMOLOGY WORKBOOK 2024

Accommodative esotropia

• Normal AC/A ratio is ≈ 5 Prism dioptre(PD) ≈ 2.500

• Accommodative convergence per unit accommodation is, convergence of eye per unit accommodation
= PD/D
• Most common type of squint in children.

(1) Refractive accommodative estropia

ƒ Associated with high hypermetropia (+4 to + 7d)
ƒ Due to high hypermetropia , eye will over accommodate leading to excessive convergence.
ƒ Normal AC/A ratio.
ƒ Correction of hypermetropia done.

(2) Non refractive accommodative:-

ƒ Abnormally high AC/ A ratio.
ƒ Esotropia is greater for near than that for distance
ƒ No refractory error
ƒ Bifocal glasses with extra ‘plus’ sphere for near vision. (+3D)
ƒ Miotics in very young children

(3) Mixed accommodative esotropia

ƒ Refractive + non refractive component (vmq)
ƒ Combination of hypermetropia & high ac/a ratio
ƒ Correction of hypermetropia (esotropia for distance) + addition of +3D sphere lens (Residual
esotropia)

Hess Chart: Paralytic Squint

Two Charts are compared:

Small Chart- Paretic Eye
Larger Chart- Overacting Eye
 OPHTHALMOLOGY WORKBOOK 2024 | 99

Features:
PARALYTIC NON PARALYTIC
ONSET SUDDEN SLOW
DIPLOPIA PRESENT ABSENT
OCULAR MOVEMENT LIMITED FULL
FALSE PROJECTION PRESENT ABSENT
HEAD POSTURE PRESENT ABSENT
(COMPENSATORY)
NAUSEA / VERTIGO PRESENT ABSENT
SECONDARY DEVIATION MORE THAN PRIMARY EQUAL TO PRIMARY
PATHOLOGICAL SEQUECAE IN EOM PRESENT ABSENT

1) primary deviation
ƒ Deviation of affected eye

2) secondary deviation
ƒ Deviation of normal eye seen under cover when patient is made
to fix with squinting eye
ƒ Greater than primary deviation
Strong impulse of innervation is required to enable paralysed eye to fix
& this impulse is also transmitted to yoke muscle of sound eye leading
to greater amount of deviation.

Restrictive squint:
• Movement of extra ocular muscle is restricted mechanically.
• Positive forced duction test
• Smaller ocular deviation in primary position in proportion to limitation
of movement.

Causes:
• Incarceration of extra ocular muscle in blow out fracture of orbit.
• Dysthyroid ophthalmopathy

Management of squint:

1. Non-surgical management

• Refraction

• Occlusion
100 | OPHTHALMOLOGY WORKBOOK 2024

• Orthoptics: Excercises

• Prisms

• Botulinum toxin

• 2. Surgical management
• Recession
 OPHTHALMOLOGY WORKBOOK 2024 | 101

• Resection
8. CORNEA

Shape:
Diameter:
Thickness:
Refractive index:
Layers of cornea:

1. Bacterial corneal ulcer

Etiopathogenesis:
Most common bact: Staph Epidermidis

Bacteria Penetrating intact corneal Epithelium:

• Corynebacterium
• Gonococcus
• Meningococcus
 OPHTHALMOLOGY WORKBOOK 2024 | 103

• Shigella
• Listeria
• H. Influenza

Perforated corneal ulcer:

• When ulcerative process is deepened & reaches upto descemet’s membrane leading to its bulging, it
is then known as descematocele.
• Any straining in the form of sneezing & coughing will perforate corneal ulcer leading to escape of
aqueous humor & lowering of intraocular pressure (IOP).

Anterior staphyloma:
• Perforation of cornea is followed by plugging of the perforation by iris.
• Epithelisation of plugged iris takes place by palisades of vogt present at limbus leading to formation
of pseudocornea.
• Pseudocornea is thin & cannot withstand Intraocular pressure (I.O.P), so it bulges forward along with
Iris plastered posteriorly (Ectatic cicatrix) leading to Anterior staphyloma.

Clinical Features:
• Pain
• Foreign Body Sensation
• Redness / Congestion
• Watering
• Photophobia

Signs:
• Eyelid swelling
• Conjunctival chemosis
• Blepharospasm
• Hypopyon
• Muddy iris
• Small pupil (due to release of toxins in anterior chamber).
104 | OPHTHALMOLOGY WORKBOOK 2024

• Topical Antibiotics: Moxifloxacin, Gatifloxacin

Fortified antibiotics viz Tobramycin, Cefazoline & Vancomycin etc.

• Systemic Antibiotics can be given in severe cases.

• Cycloplegics like homatropine, atropine etc.
• Systemic NSAIDS
• Bandage contact lens, Amniotic membrane grafting, keratoplasty.
2. Fungal corneal ulcer

Etiopathogenesis:
Most common Fungus causing Mycotic corneal ulcer: Aspergillus Fumigatus
Other fungus: Rhizopus, Mucor, candida etc.
• Vegetative Matter injury, Animal tail injury etc.
• Excessive use of Steroids or Antibiotics.
 OPHTHALMOLOGY WORKBOOK 2024 | 105

Features: Signs are more prominent than symptoms

• Dry Looking ulcer
• Non defined/fluffy margins
• Satellite Lesions
• Wesley’s Immune ring (Line of demarcation where fungal antigen & host antibody meet)

Hypopyon is characteristically fixed & non sterile.

Treatment:
• Natamycin: Filamentous Fungi
• Nystatin: Non-Filamentous Fungi
• Voriconazole: New generation antifungal.
• Systemic Drugs: Fluconazole, Ketoconazole etc.
• Intracameral & Intracorneal injections of antifungal drugs like Voriconazole.
• Fortified antifungals
• Therapeutic penetrating keratoplasty (tpk) is done in non-responsive cases.

3. Herpetic eye disease:

• Herpetic simplex keratitis & herpes zoster ophthalmicus
• Type-1 HSV: Above Waist infections
• Type-2 HSV: Below Waist infections
• NEONATES: Ocular Infection is by Type-2: Normal Vaginal Delivery

Etiopathogenesis:
• Primary Ocular Herpes / Primary Infection or first attack occurs in a Non-immune person by getting
in direct contact of Secretions of an infected person.
• Virus is dormant in Trigeminal ganglion which reactivates, replicates & travel along Trigeminal nerve
to cause recurrent infection.

Features:
1. Punctate epithelial keratitis consists of epithelial lesions resembling those of primary herpes.
2. Dendritic ulcer consists of irregular, zig-zag linear branched lesions which are knobbed at ends.
ƒ Stained with fluorescein dye(orange coloured) & seen in cobalt blue light: green fluorescence is
present.
3. Geographical ulcer is formed by coalition of dendritic ulcer leading to a large ulcer resembling ‘map’
of a country.
4. Discifrom keratitis / endothelitis:
ƒ Due to delayed Hypersensitivity reaction of endothelial antigen to antibodies formed against HSV
antigen leading to corneal edema.
106 | OPHTHALMOLOGY WORKBOOK 2024

Herpes Zoster Ophthalmicus:

1. Pseudodendritic keratitis: Epithelial lesions which are ‘Dendrite’ Like Lesions but Peripheral bulbs are
lacking & hence called Pseudo Dendrites.
2. Nummular keratitis: Anterior stromal infiltrates forming ‘cone shaped lesions’.
3. Disciform keratitis: similar to herpes simplex keratitis.
ƒ Most common nerve involved is frontal nerve.
 OPHTHALMOLOGY WORKBOOK 2024 | 107

Hutchinson rule- If the side or tip of nose is involved, ocular involvement will be there, it is due to
common nerve supply to the cornea as well as to the side/tip of nose.

Management: Topical antivirals, cycloplegics, antibiotics.

4. Acanthamoeba keratitis:
ƒ Most common cause of infection in contact lens wearers washing contact lenses with tap water,
history of swimming in pond water with contact lens ‘on’.

Features:
• Symptoms are more than Signs.
• Pseudo dendrites
• Ring ulcer
• Radial keratoneuritis
• Cultured on Non- nutrient agar enriched with Ecoli.
• Treatment: Poly hexa methylene biguanide (PHMB).
5. Trophic corneal ulcers
A) Neurotrophic keratopathy
ƒ Corneal sensations are hampered due to damage to sensory nerves.
B) Exposure keratopathy
ƒ When eyes are covered insufficiently by the lids & there is loss of protective mechanism of blinking.
6. Peripheral ulcerative keratopathies
ƒ Peripheral corneal thinning is seen
ƒ Ulceration & infiltrates are present
Examples: mooren’s ulcer, peripheral ulcerative keratitis due to connective tissue disorders.
7. Photo-ophthalmia
ƒ Multiple epithelial erosions due to exposure to ultra violet light rays from 290 µm-311µm
ƒ Bright light exposure from short circuit welding arcs & cinema halls.
ƒ Snow reflections is another important cause, hence also known as snow blindness.
ƒ Desquamation of corneal epithelium occurs after 4-6 hours of exposure.
108 | OPHTHALMOLOGY WORKBOOK 2024

Clinical features:
• Redness, burning pain, lacrimation, photo phobia, blepharospasm
• Crook’s glass is used as a shield to prevent ultra violet ray exposure during welding.

Treatment:
• Cold compresses.
• Patch the eye for 24 hours.
• Oral NSAIDS

Corneal degeneration:
1. Arcus Senilis: Age related due to lipid infiltration at periphery.
ƒ Starts in superior & inferior quadrants, & progress circumferentially to form ring which is approx.
1 mm wide.

2. Band shaped Keratopathy – Deposition of calcium phosphate in Bowman’s membrane of cornea.

Keratoconus:
• It is a non inflammatory bilateral ectatic condition of cornea in its axial region.

Signs:
• Distorted window reflex
• Irregularity of circles on placido disc exam
• Scissor Reflex on Retinoscopy
 OPHTHALMOLOGY WORKBOOK 2024 | 109

Vogt’s Striae

Fleischer Ring

Placido Disc exam

Munson sign

Prominent corneal nerves

110 | OPHTHALMOLOGY WORKBOOK 2024

Oil drop reflex on Distant Direct Ophthalmoscopy

Management:

1. Refraction

2. Rigid gas permeable contact lenses

3. Corneal collagen crosslinking with riboflavin(C3R)

 OPHTHALMOLOGY WORKBOOK 2024 | 111

4. INTACS:

5. Keratoplasty

Corneal transplantation: Keratoplasty

Types: Penetrating & Lamellar

• Penetrating keratoplasty: Full thickness corneal tissue grafting

112 | OPHTHALMOLOGY WORKBOOK 2024

• Lamellar keratoplasty: partial thickness corneal tissue grafting

Anterior lamellar keratoplasty :

Posterior lamellar keratoplasty:

Corneal preservation techniques
1. Short term: upto 48 hours; Moist chamber technique
2. Intermediate term: 3-5 days; Mc carney –Kaufman (MK) medium
3. Long term: upto 30 days; Organ culture method
 OPHTHALMOLOGY WORKBOOK 2024 | 113

Cryopreservation- upto 1 year

Refractory procedures on cornea

Principle:
Myopia: Flattening of Cornea is done.
Hypermetropia: Cornea Steepening is done.
Astigmatism: Both Flattening and steepening is undertaken.

1. Radial keratotomy:
ƒ Upto -3D can be corrected
ƒ Radial cuts are given on corneal surface leading to flattening
114 | OPHTHALMOLOGY WORKBOOK 2024

2. Photorefractive keratectomy: Upto -5D can be corrected

ƒ Excimer laser is used.
3. LASIK:
ƒ Gold Standard treatment.
ƒ Myopia correction upto –12D can be done.
ƒ Hypermetropia correction Upto +4D can be done.
ƒ Astigmatic correction upto ± 3D can be done.

Procedure:
ƒ Corneal Flap of Thickness 160 µm is raised (conventional LASIK) with the help of a Keratome.
ƒ Corneal Stroma bed is exposed & it is ablated with the Excimer laser
ƒ After ablation, Corneal flap is replaced over the stromal bed.
ƒ Golden Rule: Residual Stromal thickness should not be less than 250µm.
 9. CONJUNCTIVA

Any insult to conjunctiva:

• Papillae
116 | OPHTHALMOLOGY WORKBOOK 2024

• Follicles

Conjunctivitis
1. Bacterial:
Staph Aureus is most common cause.
• Others: Staph Epidermidis, Strept Pneumoniae, Strept. Pyogenes, Pseudomonas, Neisseria etc.

Features:
• Discomfort
• Foreign Body Sensation
• Grittiness
• Congestion
• Photophobia
• Mucopurulent Discharge
• Matting of Eyelids
• Coloured Halos (Due to Prismatic Effect of Mucus present of Cornea)
• Mucopus Flakes are present in the fornices.
• Chemosis
• Lid edema
 OPHTHALMOLOGY WORKBOOK 2024 | 117

Treatment:
Topical antibiotics: Moxifloxacin, Gatifloxacin, Tobramycin
Dark glasses: Photophobia.

Angular bacterial conjunctivits

• Inflammation confined to conjunctiva & lid margins near angles.
• Moraxella axenfeld (most common)

2. Viral:
1. Epidemic keratoconjunctivitis : Adenovirus (m/c)
• Redness, watering, foreign body sensation, photophobia
• Pre auricular lymphadenopathy can be seen

Treatment:
• Supportive- cold compresses
• Topical antibiotics, antivirals

2. Acute Hemorrhagic Conjunctivitis

• Subconjunctival haemorrhage
• PicoRNA Virus: Enterovirus 70 & Coxsackie A24
• C/F same as EKC.

Treatment:
• Same as epidemic keratoconjunctivitis

3. Ophthalmia neonatorum:

Etiopathogenesis & features described alongwith:

Ophthalmia neonatorum: cause with respect to the timing of signs/symptoms:

Chemical conjunctivitis:
• 1% silver nitrate has been used as prophylaxis on gonococcal conjunctivitis (crede’ method)
• No more used now
118 | OPHTHALMOLOGY WORKBOOK 2024

Gonococcal conunctivitis:
• Hyper Acute Conjunctivitis
• Moderate to Severe Pain
• Lid swelling
• Thick Copious Purulent Discharge
• Pre auricle lymph node swelling & tenderness

Treatment:
1. Systemic therapy: 3rd gen cephalosporin
2. Topical antibiotics erythromycin eye ointment
3. Irrigation of eyes

Trachoma:
OPHTHALMOLOGY WORKBOOK 2024 | 119
120 | OPHTHALMOLOGY WORKBOOK 2024

Management

4. Vernal keratoconjunctivitis:

ƒ Also known as Spring catarrh

ƒ Type 1 & Type 4 Hypersenstivity reaction
ƒ Age: 4-20 Years, More common in boys
ƒ More common in summers
ƒ Cobblestone Papillae.
ƒ Horner Tranta spots are raised whitish dots.
 OPHTHALMOLOGY WORKBOOK 2024 | 121

Treatment:
• Antihistaminics- Olopatidine
• Mast cell stabilizers: sodium chromoglycolate
5. Phlyctenular conjunctivitis:
ƒ Allergic response of Conjunctival & Corneal Epithelium to Endogenous allergen.
ƒ Type –IV Hypersensitivity reaction- unilateral condition m/c.
ƒ Most common bacteria is: Staph Aureus > Mycobacterium TB
ƒ Age- 3-15 Years, Girls > Boys, Low socio economic Status
ƒ Limbal nodule
ƒ Fascicular ulcer
122 | OPHTHALMOLOGY WORKBOOK 2024

Treatment: Topical steroids

Pterygium:
• Wing Shaped Fold of Conjunctiva encroaching upon Cornea.
• Etiology: U.V Rays Dust, Heat, Wind
• Elastotic degeneration of conjunctiva and involvement of Epithelium, Bowman’s Layer & Superficial
Stroma

Features:
• More common in males > females
• Can be unilateral or bilateral: usually nasal side

Symptoms
• Foreign body sensation
• Diplopia
• Defective vision

STOCKER’S LINE: It is due to deposition of iron on epithelium of cornea and is located at the leading
edge of pterygium.

Management:

Treatment: Surgical Excision but it is only undertaken when the following is present:
• Cosmetic concerns
• Visual Impairment
• Diplopia – due to astigmatism and ocular movement restriction

Bare Sclera Technique - 70-90% Recurrence

• PERFECT Surgery
• Amniotic Membrane Graft & Mitomycin – C
 OPHTHALMOLOGY WORKBOOK 2024 | 123

Pinguecula:

Episcleritis and Scleritis:

Phenylephrine test:
124 | OPHTHALMOLOGY WORKBOOK 2024

Dry Eye:

Lissamine green stain:

Dermoid:
• Benign congenital tumors that contain choristomatous tissue (tissue not found normally at that site).
• Most frequently at the inferior temporal quadrant of the corneal limbus.
OPHTHALMOLOGY WORKBOOK 2024 | 125
10. OCULAR ADENEXA

Ptosis
Etiopathogenesis
1. Mechanical ptosis

2.myogenic ptosis

3. Neurological ptosis

4. Involutional
 OPHTHALMOLOGY WORKBOOK 2024 | 127

5. Congenital ptosis

Features
128 | OPHTHALMOLOGY WORKBOOK 2024

Management
 OPHTHALMOLOGY WORKBOOK 2024 | 129

Entropion
1. Involutional/senile entropion

2. Cicatricial

3. Spastic
130 | OPHTHALMOLOGY WORKBOOK 2024

4. Congenital

Management:
Jone’s operation:

Bick’s procedure:
 OPHTHALMOLOGY WORKBOOK 2024 | 131

Quickert procedure:

Weiss operation:

Byron smith(Kuhntz) Operation:

132 | OPHTHALMOLOGY WORKBOOK 2024

Ectropion

1. Involutional/senile

2. Cicatricial

3. Paralytic
 OPHTHALMOLOGY WORKBOOK 2024 | 133

4. Mechanical

5. Congenital

Management:
V-y operation:

Z plasty:
134 | OPHTHALMOLOGY WORKBOOK 2024

Medial Conjunctivoplasty:

Stye:
• Also known as (a.k.a) Hordeolum Externum
• It is an infection of Hair Follicle > Gland of Zeis.
• It is associated with refractory error in children as child tends to rub eye & introduce infection through
dirty fingers.
• Most common organism Staphylococcus aureus.
• The swelling is very tender with mild watering.

TREATMENT:
• Hot Compresses
• Epilation of Cilia to Evacuate pus to relieve pain when Pus point is formed. Antibiotic eye drop/
ointment is prescribed
• Systemic NSAIDS decreases Pain & Inflammation
• Systemic Antibiotics can also be prescribed

Chalazion:
• It is a chronic non infective / Non Suppurative Lipogranulomatous inflammation of Meibomian Gland.
 OPHTHALMOLOGY WORKBOOK 2024 | 135

CLINICAL FEATURES:
1. It is a Painless Swelling
2. Mild heaviness on Eyelid is present
3. There is a presence of reddish Purple area where Chalazion Visually points.
ƒ In some cases, there is a malignant change into Sebacious cell Carcinoma / Meibomian Gland
Adenocarcinoma which may occur in elderly.

TREATMENT:
1) Hot Fomentation, Topical antibiotic & oral NSAID form conservative treatment strategy.
2) Intra lesional injection of long acting steroid (Triamcinolone) is given
3) Incision & Curettag

Lacrimal apparatus of eye

Jones dye test 1

136 | OPHTHALMOLOGY WORKBOOK 2024

Jones dye test 2

Dacryocystitis

Congenital Dacryocystitis:
Etiology-
• Stasis of secretions in lacrimal sac due to congenital blockade of nasolacrimal duct.
• Membranous occlusion near value of hasner (most common cause)
• Non canalisation, membranous occlusion at its upper end.

Clincial features:-
1. Epiphora i.e. Watering due to inadequate drainage of tears.
2. Sac swelling due to back flow / collection of tears.
3. Regurgitation test is positive i.e. When pressure is applied over lacrimal sac area, there is regurgitation
of purulent discharge from lower puncta.
 OPHTHALMOLOGY WORKBOOK 2024 | 137

Treatment:
a) Lacrimal sac massage- criggler’s massage
b) Topical antibiotics.
c) Lacrimal syringing is done if condition is not cured by age of 3 months ( trying above 2 methods).
d) Probing: naso-lacrimal probing is done with bowman’s probe if it is not cured by age of 6 months.
e) Balcon catheter dilation & silicon tube intubation are other methods which can be tried.
f) Dacryocystorhinostomy (DCR)
ƒ Done after the age of 4 years, it is done if other methods fail.

Tear film abnormalities:

1. Mucus Layer
ƒ Innermost layer; 0.2 µm thick.
ƒ It is secreted by conjunctival goblet cells & glands of manz.
ƒ It’s function is to convert hydrophobic corneal surface to a hydrophilic one.
2. Aqueous Layer
ƒ It is the middle layer
ƒ It is approximately 7µm thick
ƒ It forms the bulk of tear film.
ƒ It is secreted by main and accessory lacrimal glands
ƒ Water, sodium chloride, sugar proteins, urea
ƒ Lactoferrin, betalysin & lysozyme
3. Lipid Layer
• It is the outermost layer
• Approximately ≈ 0.1µm and is thinnest of all.
• Secreted by Gland of zeis, meibomian & moll.
• Retards evaporation & lubrication.
11. OPTICS

Emmetropia: State of refraction when parallel rays of light are focused upon retina when coming from
infinity with accommodation at rest.

Ametropia: State of refraction when parallel light rays coming from infinity are focused in front or behind
in one or both meridians with accommodation at rest ex: Myopia, Hypermetropia & Astigmatism.

1. MYOPIA: Parallel light rays are focused in front of Retina while accommodation at rest
ƒ Low Myopia= ≤ -3D
ƒ Moderate Myopia= -3D to -6D
ƒ High Myopia= ≥ -6D

ƒ Uncorrected myopes don’t need accommodation, hence tend to develop convergence insufficiency
overtime resulting in exodeviation.

2. HYPERMETROPIA: Parallel rays of light coming from infinity are focussed behind retina while
accommodation at rest.
 OPHTHALMOLOGY WORKBOOK 2024 | 139

3. ASTIGMATISM: Refraction varies in different meridian.

Regular- refractive power changes uniformly from one meridian to other.

ƒ Corneal- due to abnormal curvature.
ƒ Lenticular- due to abnormal curvature, position {tilting / oblique placement} or variable refractive
index.
ƒ Retinal- oblique placement of macula.
1) With the rule- Two meridia are placed at right angle to one another & the vertical meridian is more
curved than horizontal.
2) Against the rule- Two meridia are at 900 and vertical meridian is less curved than horizontal.
3) Oblique- Two meridia is at right angle to one another but they are not horizontal & vertical.
4) Bi-oblique- Two meridia are not at right angle to each other.

Irregular astigmatism- Irregular change of refractive power in different meridia.

• Corneal- Keratoconus, scars.
• Lenticular- Variable refractive index due to different stages of cataract formation
• Retinal- Distortion of macular area due to scarring or tumors
140 | OPHTHALMOLOGY WORKBOOK 2024

Types of astigmatism based on point of focus:

Simple myopic astigmatism

Simple hypermetropic astigmatism

Compound myopic astigmatism

Compound hypermetropic astigmatism

Mixed astigmatism:
 OPHTHALMOLOGY WORKBOOK 2024 | 141

Colour vision
It is a function of cone cells.

Screening of colour blindness is done by ishihara chart.

ƒ The ishihara test is designed to screen for congenital protan (red) and deuteron (green) defects.

Retinoscopy

Priestley Smith Retinoscope

142 | OPHTHALMOLOGY WORKBOOK 2024

• If the movement of reflex is in opposite direction, patient is myopic by more than 1 D.

• If the reflex doesn’t move, Patient is myopic by 1 D

• If the reflex moves in the same direction, Patient is Myopic by less than 1D, Emmetropic or
hypermetropic.