OPHTHALMOLOGY

INTRODUCTION FROM THE AUTHOR

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OPHTHALMOLOGY

ORBIT:
• Pyramid shaped, 30 ml volume, eyeball
volume 6 ml
• Rule of 7 7 bones, 7 muscles, 7 nerves
in orbit, 7 attachments of eyeball
• Contents  eye ball, muscles, fascia,
fat pads, blood vessels and nerves
• 6 muscles of eyeball, 1 of eyelid
• 6 movements – elevation, depression, abduction, adduction,
intorsion, extorsion
LR6, SO4 R3
• Eyelid elevators  LPS, Muller’s muscle, Frontalis
• Only one eyelid closure muscle-orbicularis oculi

Eyelid Position:

upper eyelid covers 2mm of (N) cornea

Lower eyelid is at limbus

Ptosis: Drooping of upper eyelid

Droops > 2 mm

Congenital Acquired

Birth to 1 year of age > 1 year of age

Types:

Aponeurotic / Involutional-m/c - senile

Neurogenic -3rd CN palsy, Horner ‘s S

Myogenic – myasthenia gravis, Myotonic

dystrophy

Mechanical – Chalazion, lid tumour

Treatment Surgical – based on LPS action

(LPS affected in 80% cases)

 

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OPHTHALMOLOGY
 Good LPS action - LPS resection

Moderate LPS – FASANELLA SERVAT

Poor LPS – Frontalis Sling / Suspension

ORBITAL BLOWOUT FRACTURES

• M/C fracture of orbit

• Fracture of orbit without
including rim
• Size of impact > size of orbital aperture
• M/c wall to facture – inferior wall / floor
• S/S: Diplopia, Infraorbital anaesthesia, Enophthalmos (DIE)
Tear drop sign in CT scan diagnostic

Proptosis /Exophthalmos – protrusion of eyeball

• Causes – Thyroid Eye disease, Tumors, Orbital cellulitis, Metastasis

• MCC Thyroid eye disease / Graves’ Ophthalmology
• D/to deposition of MPS on muscle belly leading to its
enlargement, with sparing of tendon.

Thyroid Eye Disease

Females>> Males- 40-60 years

MC presentation – Lid retraction

Lid lag

U/L or B/L proptosis

Restriction of EOMIMSL- Inferior rectus first

Muscle is replaced by fatty tissue

Muscle involvement IRMRSRLR (I M So Lucky)

Enophthalmos Retraction of eye ball

Causes: Blow out facture/

Ca breast metastasis

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OPHTHALMOLOGY
Orbital tumors

MC primary tumour of the orbit in children  Dermoid cyst

MC malignancy of the orbit in children  Rhabdomyosarcoma

MC secondaries to the orbit in children  Metastasis from Neuroblastoma

MC primary tumor of orbit in adults  Cavernous hemangioma /

lymphoma

MC secondary tumor of orbit in adult’s  Ca breast/ Lungs / Prostate

Enucleation Evisceration
Removal of whole eye leaving Removal of intraocular contents of eye
all other contents of orbit leaving sclera
intact
Removal of middle and inner layers

Ocular Prosthesis

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OPHTHALMOLOGY

BASICS OF OPHTHALMOLOGY
Human Eye

Three concentric layers

• Cornea /sclera (outer)

• Uvea (middle layer)
• Retina (innermost layer)

Cornea/Sclera:

• Eyewall  Cornea/ sclera

• Anterior 1/6 cornea  Transparent posterior 5/6  sclera]
• Function  Protection of intraocular contents
• Made up of collagen, GAG [Glycosaminoglycans]
• Regular arrangement of collagen with equal spacing gives cornea its
clarity
• Cornea contributes 70% of power of eye – 43 D/60 D

Refractive Index – speed of light in a particular media compared to speed

of light in air

Amount of light that can be bent by a particular media.

RI  bending of light

Highest RI  Centre of lens / nucleus of lens

Cornea = 1.376

Aqueous humor and vitreous = 1.33

Air = 1/Glass = 1.5/ Water = 1.3

Lens = Centre (1.40)

Periphery (1.38)

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OPHTHALMOLOGY
UVEA = Grape (Middle layer)

Iris Ciliary body Choroid

(Anterior uvea) (Intermediate uvea) (Posterior Uvea)

IRIS:

• Named after Greek goddess of rainbow

• Pupil – contracts and dilates to control
entry of light
• Iris pattern – different for everyone,
used in biometrics of Aadhar card
• Pupil can contract to 1mm and dilate
to 9mm-sphincter pupillae / dilator pupillae
• Normal pupil diameter varies from 3-4 mm

Ciliary Body:

Pars plicata – folds, Pars plana – plane, Ciliary muscle

anterior CB posterior CB

Function

1. Aqueous humor production

2. Accommodation (ciliary m/s)

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OPHTHALMOLOGY
IRIDODIALYSIS – D-Shaped pupil:

Iridodialysis  Separation of Iris

from root (ciliary body)

CHOROID:

• Named from chorion of placenta

• Intra ocular structure with highest
blood flow
• Thermoregulation
• Drained by vortex veins

RETINA

Inner most layer of eye (Fovea to Ora serrata)

Peripheral retina- Ora serrata Central Retina

 Attached to junction of ciliary

body and choroid 3 structure

 Thinnest part of retina i. Macula (centre of retina)

yellow color

ii. Fovea (centre of Macula)

(a) Most sensitive to light,
clearest and sharpest image
(b) 80% -90% of light focuses
on fovea

iii. Optic disc

• Beginning of optic nerve
• Only part of optic nerve visible
• Optic disc diameter (ODD) =
foveal diameter = 1.5 mm
• 1 DD = 1.5, 2DD= 3 mm, 3 DD=
4.5 mm
• Light rays  fovea  optic
disc /optic nerve  occipital
lobe of brain

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OPHTHALMOLOGY

MICROSCOPIC STRUCTURE OF RETINA

2 types of cells

Neurons Neuroglia

5 Different types • Support neurons

• 3 types

1. Rods and cones – photoreceptors

First order Neurons
2. Bipolar cells – seconds order neurons
3. Ganglion cells - Third order neurons
• Axons of RGC’s collect as optic nerve
4. Horizontal cells
5. Amacrine cells

Rods Cones

Location -Periphery Centre

Number -120 million 6 million

3 types [R  Red, G Green,
1. 1 type of rods B  Blue]
2. Black and white vision Central vision(reading)
3. Peripheral vision(walking, driving)
4. Night (scotopic)
Colour vision

. Daylight vision (photopic)

ANTERIOR CHAMBER (AC)

• Average depth = 3mm

• Shallow in WEC- women , elderly , children
• Deep in young males
• Contains aqueous humor
Provides nutrition to all structures

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OPHTHALMOLOGY
particularly to 2 avascular structures
a)
b)

CORNEA

Glucose Oxygen

Aqueous humor 1. Atmospheric air

2. Aqueous humor

3.

LENS

Glucose Oxygen

Aqueous humor

Lens:
• Crystalline lens
• Proteins (35%)  90% crystallins); Water (65%)
• Biconvex shape
• Transparent, avascular

Power of lens = 19D/60D of eye

Functions

• Transmits and focus light on retina

• Accommodation

Cataract – Opacification of

lens /capsule or both

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OPHTHALMOLOGY
Zonules :

• Suspensory ligaments
• Very fragile, delicate filaments, rupture easily
• Suspend lens in the eye from ciliary body-lens capsule equator

• Lens – Iris - Complex  Move together back and froth

(IRIS/ CB/Zonules/lens)

Vitreous humor – single largest structure in eye – occupies 70% –

80% volume , lies between lens and retina

Clear, transparent gel

98% water, Hyaluronic acid, and collagen

Attached to optic disc margin, macula ,blood vessels of retina and

vitreous base

Strongest attachment to vitreous base

Aqueous Humor Vitreous Humor

• Name derived from H2O Name derived from Glass
(clear)
• Solution (flows) • Gel (doesn’t flow)
• Function- Nutrition of • Function
eyeball o shock absorber to retina
o Optical media
o Maintains shape
• Rate of production  2.5 • Produced only once at birth
/ min

• Composition:
Similar to blood plasma Composition:

98% water

Hyaluronic acid

Type II collagen.

Enter AC through limbus Enter vitreous humor through Pars

plana

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OPHTHALMOLOGY
Angle structures:

Aqueous humour:

Produced from Pars Plicata

Post chamber

through pupil

Anterior chamber

Angle of eye (Junction between irs and cornea)

  If iris shifts forward and blocks the angle –results in angle

closure glaucoma(ACG)

Trabecular meshwork

 System of collagen sheets piled over each other, perforated c

series of holes

Commonest structure to get blocked in OAG

Schlemm’s canal

Episcleral veins

OPTICS OF EYE

Total power of the eye + 60 D (Diopters)

43 D cornea + 19 D (lens) = 60

(70%) (30%)

Maximum bending of light at anterior surface of cornea/ maximum

refraction at air /cornea interface

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OPHTHALMOLOGY
Vasculature of the Eye

1. Principal artery of eye  Ophthalmic artery -10 branches

(OA is 1st branch of ICA)

2. Most critical  Central retinal Artery (CRA)

3. Principal Veins  Central Retinal vein / vortex vein

Nerve Supply of Eye

• 6 cranial nerves - II, III, IV, V, VI, VII

• Autonomic nervous system
o Parasympathetic –through 3rd CN – miosis and ciliary muscle
contraction - accommodation
o Sympathetic –through 5th CN – Mydriasis , Muller’s muscle ,
Inferior tarsal muscle , sweat glands of eye , aqueous humor
secretion

Vision / Visual Acuity:

• Standard normal vision is 6/6 or 20/20

• 6m/6m = distance between patient and the testing chart/distance
between normal person and same chart

Testing:

1. Snellen’s Chart

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OPHTHALMOLOGY
2. ETDRS/ Log mar chart

3. Landolt’s Rings

4. Picture charts for preschool children Allen , Animal charts , HOTV

charts
5. Optokinetic nystagmus for pre verbal children , uncooperative
patients

Near Vision – Triple reflex / Near response / Accommodation reflex

Accommodation

Convergence

Miosis

Accommodation – change in the shape of lens to increase the power of

lens for near vision

Ability of eye to change its focus from distance to

near and vice versa

Controlled by ciliary muscle –CM contracts in blurred

vision –Zonules relax, shape of lens more convex

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OPHTHALMOLOGY
Good vision- CM relaxes, zonules contract, lens
becomes elongated

Convergence – the movements of the two eyes inwards towards each

other

Controlled by Medial rectus muscles

Miosis – pupillary constriction

Near vision chart – Roman charts, Jaegar charts – N6 optimum near

vision

Concave lens Convex lens

• Center – thin, periphery thick Center – thick, periphery thin

• Divergence of rays Convergence of rays
• Minification Magnification
• 1D = 2% 1D = 2%

• Glasses causes highest amount of magnification/minification.

Binocular Singular Vision: (BSV)

• Fusion of two images occurs in

occipital cortex
• Fusion requires -Bifoveal images
Both images similar
• No fusion leads to diplopia

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OPHTHALMOLOGY
Colour Vision:

Daltonism:

• Most common x linked recessive disorder

• 8% males are color blind
• Colour blind people NOT blind, they CONFUSE colors
• Can’t pick up ripe fruits
• Can’t make out if meat is cooked
• Wear mismatched clothing

Classification:

Trichromatism – all 3 types of cones present

Anomalous trichromatism – one colour reduced

sensitivity

Protanomaly - red color weakness

Deuteranomaly - green colour weakness

Tritanomaly -blue color weakness

Dichromatism - 2 cones present

Protanopia – Red cones absent-Red col blindness

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OPHTHALMOLOGY
Deuteranopia - Green cones absent-Green color blindness

Tritanopia - Blue cones absent-Blue color blindness

Monochromatism

Normal Monochromats

Tests for color blindness:

1. Ishihara Chart

2. FM 100 Hue Test

3. NAGEL’S ANOMALOSCOPE

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OPHTHALMOLOGY

CATARACT

(from waterfall ,with a large, vertical drop of water)

Definition: Opacification of lens/Capsule or both.

MCC of blindness in world  Cataract -50 % approximately

Second commonest cause of blindness - Glaucoma

MCC of blindness in India  Cataract (66%)

MC Infectious cause of blindness in world  Trachoma

MCC of blindness in children – Vitamin A deficiency

MCC of visual impairment - Refractive error

Ocular morbidity  conditions causing both visual impairment and non-

visual pathology

Blindness according to NPCB/WHO : <3 / 60

: With best possible correction

: Better eye

Absolute blindness : PL negative

No PL/No light perception

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OPHTHALMOLOGY
Causes of cataract

1. Age related / senile cataract > 55 -60 years Based on

Morphology
• Most common type of cataract-80% 1. Nuclear cataract
Exposure to UV light 2. Cortical (Anterior
/ Posterior)
Damages lens proteins 3. Posterior
subscapular cataract
Prevention  Sun glasses

Smoking -earlier cataracts

Antioxidants: A, C, E; protects against cataract

Exposure to heat, dust, pollution

Chronic long-standing diarrhoea

Women > Males

2. Congenital/ Developmental
3. Traumatic
4. Complicated
5. Metabolic
6. Heat
7. Radiation
8. Drug induced

A. Nuclear cataract:
• Hemeralopia: Day blindness
• Decreased distant vision > Near vision
• due to Index myopia

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OPHTHALMOLOGY

B. Cortical cataract
• Nyctalopia  Night blindness
• Cuneiform cataract  Wedge shaped

C. Posterior subcapsular cataract (PSC)

• Maximum loss of vision
• Maximum glare  Closest to nodal point of eye

Nodal point lies close to posterior capsule
• More posterior the cataract  More loss of vision
• Cupuliform [Cup shaped] Cataract
• Loss of near vision >> Distant vision , due to
pupillary constriction of near vision

Congenital / Developmental cataract

• Critical period for development of foveal fixation – 2-4 months of age

• Cataract can lead to loss of foveal fixation
• MC type of cataract causing loss of vision in child  Zonular /
Lamellar / Rider’s cataract
• TORCH Infections cause cataracts

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OPHTHALMOLOGY
Zonular Cataract

Traumatic Cataract

Blunt trauma

Vossius ring –ring of pigment on lens capsule

Rosette Cataract –flower shaped

Complicated Cataract

Secondary to intraocular disease–Uveitis (MC)

Glaucoma

Retinitis Pigmentosa

High Myopia

Characteristics: PSC
Bread crumb appearance

Polychromatic lustre (Multiple colours)

Metabolic Cataract  Due to Systemic disease

1. Diabetics

Early Senile True Diabetics/Snowflake

Early 40’s Younger age

NIDDM (Type II) IDDM (Type I)

Slow, gradually progressive Acute loss of vision

Only cataract with acute loss of vision

PSC Snowflake / snowstorm cataract

Diabetic/Snowflake Cataract

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OPHTHALMOLOGY
2. Wilson’s Disease – Sunflower cataract
KF Ring

3. Galactosemia- Oil droplet cataract

4. Myotonic Dystrophy – Christmas tree cataract

Heat Cataract:

• True exfoliation cataract

• Glass blower’s cataract
• Iron- worker Cataract

Radiation Cataract:

• Ionizing radiation (MC – Xray)

Non ionizing do not cause cataracts – microwave, radio frequency as
in phone radiation
• PSC
• Earliest structure to be damaged in eyes – lens [Most sensitive to
radiation]

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OPHTHALMOLOGY
Drug Induced Cataract:
Steroid induced
Amiodarone

Busulphan PSC Complicated cataract

Chlorpromazine
Radiation Induced
Chloroquine

Dexamethasone (Steroids) Systemic

Echothiopate MCC

PSC

Stages of Cataract:

1. Incipient
2. Immature
3. Mature
4. Hypermature

I. Incipient
i. Earliest stage
ii. Mild blurring of vision
iii. Glare
iv. Loss of contrast sensitivity:
Measured by Pelli Robson chart

II. Immature
i. Partially opaque
ii. Moderate blurring of vision
iii. Yellowish grey/ iris shadow

III. Mature
iv. Completely opaque
v. Severe loss of vision
vi. White
vii. Intumescent
viii. May lead to glaucoma

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OPHTHALMOLOGY

iv. Hypermature
i. Loss of volume– Lens shrinks
ii. Loss of zonular
support  Phacodonesis


Subluxation / dislocation
iii. Types:

Types

Morgagnian (Cortical) Sclerotic (Nuclear)

 
• Cortex liquifies • Cataract Brunescent, brown
• Nucleus falls into it • Cataract Nigra, black, hardest

Symptoms:

1. Blurred vision
2. Diplopia / Polyopia
3. Coloured halos
4. Glare
5. Change in color perception - more reds and browns , less blues
and greens visible

Slit lamp examination:

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OPHTHALMOLOGY

Treatment Glasses

Surgery

Indication of surgery:

• Visual handicap
• Advanced cataract – Mature / Hypermature
• Avoidable in young patients – as it leads to

loss of
accommodation

Surgery:

1. ICCE
2. ECCE with IDL
3. Phacoemulsification
4. FLACS

I. ICCE:
• Remove cataract + Capsule
• Aphakia
• Corrected by glasses
• Diplopia

• Only indication for ICCE

Subluxated / Dislocated Cataract

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OPHTHALMOLOGY

Aphakia:

Signs / Symptoms:

• Diplopia
• Jack in the box scotoma / roving ring scotoma
• Pincushion defect
• Problems of alignment and orientation
• Deep AC
• Jet black pupil

II. ECCE (With PCIOL)

Cataract removed, capsule left in situ.
PCIOL implanted
Pseudophakia
PMMA IOL –poly methyl methacrylate

III. Phacoemulsification:
Stitch less
3mm incision
Valvular / Multiplanar incision
Self-sealing
Foldable IOL
Silicone / Acrylic IOL

FLACS – Femto laser assisted cataract surgery

Advantages – a perfectly, circular, centered capsulorhexis

Phacoemulsification steps

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OPHTHALMOLOGY
1. Anterior Capsulotomy

• Continuous Curvilinear Capsulorhexis

• Creates a central 5-6mm capsulotomy which is large enough to
remove a cataract
• Trypan blue dye injected in the absence of red reflex as in mature/
hypermature cataract

Hydrodissection

• Injection of Balanced Salt Solution (BSS) under anterior capsule to

separate cortex from the capsule

3. Hydrodelineation

• Separate epinucleus from endonucleus by injecting BSS

Post–Op Complications

1. Posterior capsular opacification/Secondary cataract/After cataract

2. Cystoid Macular oedema (CME)

3. Endophthalmitis

SECONDARY CATARACT/POSTERIOR CAPSULAR OPACIFICATION

Most common complication of cataract surgery (50%)

Risk factors:

Younger age

Pathology:

During cataract surgery

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OPHTHALMOLOGY


Trauma to the LEC in the anterior capsule

Stimulates proliferation of LEC

Migration of Lens Epithelial Cells (LEC) from the anterior capsule

to the posterior capsule

Symptoms:

Slow painless blurring of vision , loss of contrast

Types:

1. Elschnig’s pearls

2. Soemmering’s rings

Management:

Nd – YAG Laser capsulotomy ( 1064nm)

CYSTOID MACULAR EDEMA (CME)

Slow, painless loss of vision

Metamorphopsia

 Contrast sensitivity

Predisposing Factors: Diabetes, uveitis, posterior capsule rupture

Irvine-Gass syndrome: Cystoid Macular Oedema after cataract surgery,

peaks at 4-6 weeks

Management: Topical NSAIDs / topical steroids

POSTOPERATIVE ENDOPHTHALMITIS

Serious intraocular infection  infection of the vitreous cavity - of 2

types:

1. Early onset < 6 weeks

Most commonly within 3 days

Most common Staph epidermidis, Staph aureus

2. Late-onset > 6 weeks

Most common Propionibacterium acnes

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OPHTHALMOLOGY

Symptoms:

Pain, redness, loss of vision

Lid oedema/hazy cornea/hypopyon/hazy media

Treatment:

DOC: Intravitreal antibiotics -Vancomycin(Gram positive), Ceftazidime/

Amikacin(Gram negative)

Intracameral antibiotics

Most important prophylaxis: Clean the eyelid/eyelashes with Povidone-

iodine

AMBLYOPIA (LAZY EYE)

Most common cause visual loss in children

Loss of vision in a child due to prolonged visual deprivation

 VA is not attributable to structural abnormality of eye

Definition:

BCVA (Best Corrected Visual Acuity) less than 6/12 one eye

Critical period – 8 years  Amblyopia develops during this period

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OPHTHALMOLOGY
Types

Strabismic – most common

Anisometropic

Stimulus deprivation- cataract, ptosis, corneal opacity

Symptoms:

 VA, despite correcting the underlying disorder

Crowding phenomena – patient reads better with single optotypes.

Management:

Critical period of visual improvement – 8 years

Occlusion – close the good eye

• Patch 6 hours a day

• Penalization – use Atropine eye drops to blur vision of good eye

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OPHTHALMOLOGY

UVEITIS:
Classification:

1. Anterior Uveitis: MC
• Iritis
• Iridocyclitis (only pars plicata)
2. Intermediate
• Pars planitis
• Vitritis
3. Posterior Uveitis
• Choroiditis
4. Panuveitis
• Sympathetic Ophthalmitis

Anterior Uveitis:

Causes:

• Idiopathic
• HLA-B27 Spondyloarthropathies
• Ankylosing spondylitis
• Inflammatory Bowel disease-Crohn’s
disease /Ulcerative colitis
• Psoriatic arthritis
• Reactive arthritis (Reiter’s Syndrome)
• Conjunctivitis, Urethritis, Arthritis (CUR)
• JRA (Juvenile Idiopathic Arthritis)
o Pauciarticular, ANA positive,
RF Negative
o IOLs contraindicated

Symptoms: Redness, pain, Blurring of vision

Signs:

1. Circumciliary/Circumcorneal congestion.
• Reddish-violet color

2. Cells-WBC in AC
• Sign of activity

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OPHTHALMOLOGY
3. Flare–Protein deposition in aqueous humor
• Earliest sign of uveitis

4. KPs -Keratic precipitates –

• Neutrophils and lymphocytes on corneal endothelium
• Arlt’s triangle
• Mutton-fat KP’s

5. Iris Nodules -
• Koeppe’s –on pupillary margin
• Busaca’s- on iris surface

6. Synechiae – adhesions of iris to surrounding structures

• Anterior- cornea, Glaucoma
• Posterior- lens, Cataract

7. Miosis
8. Low IOP

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OPHTHALMOLOGY

9. Festooned Pupil –irregular pupil due to posterior synechiae

10. Hypopyon- collection of cells at the bottom of AC

Intermediate Uveitis:

• Pars planitis with vitritis

• Idiopathic
• Sarcoidosis
• Floater’s/Muscae volitantes
• CME- MCC of loss of vision
• Signs -Snow balls and Snowbanks

Posterior Uveitis:

Infections Non-infectious

Toxoplasmosis Sarcoidosis

Tuberculosis

Toxocariasis

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OPHTHALMOLOGY
Choroiditis

O/E Choroiditis

Chorioretinitis/ Retinochoroiditis

Vitritis

“Head light in fog”

Treatment

A. Anterior Uveitis
• Topical steroids (DOC)

MC S/E of topical steriodGlaucoma

MC S/E of systemic steroids Cataract

• Cycloplegics – Atropine 14 days

Homatropine 3 days

Cyclopentolate 1 days

Tropicamide 6 hours

Mechanism of action- Relax ciliary spasm

Dilate pupil, break posterior synechiae

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OPHTHALMOLOGY

In children–Atropine cycloplegic of choice

Powerful ciliary tone

Atropine drops NOT used, only ointments

Systemic absorption through nasolacrimal duct-80%

B. Intermediate Uveitis
• Steroid injections
o Triamcinolone
o Subconjunctival
o Subtenon’s

Cycloplegics not required

C. Posterior Uveitis
• Antimicrobials for infections
• Spiramycin DOC for Toxoplasmosis in pregnancy, Pyrimethamine
and Sulphadiazine in non-pregnancy
• ATT for tuberculosis, HAART for HIV, Albendazole in Toxocariasis
• Systemic steroids for non-infections causes

Watch out for side effects !

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OPHTHALMOLOGY

ANTERIOR UVEITIS INTERMEDIATE UVEITIS POSTERIOR UVEITIS

Iridocyclitis Pars planitis & vitritis Chorioretinitis
Idiopathic Idiopathic Toxoplasmosis
Pain + Pain -NO Pain –NO

Redness + Redness-NO Redness - NO

Loss of vision+ Loss of vision –CME Loss of vision major

Muscae/floaters
Cells Snowballs & snowbanks Toxoplasmosis –

Headlight in fog

Vitritis,vasculitis

Chorioretinitis
Topicals steroids Inj Triamcinolone/ Systemic steroids
Steroid

No cycloplegics
Cycloplegics Antimicrobials

Sympathetic Ophthalmitis:

• B/L granulomatous uveitis following trauma to one eye

• Traumatized eye – Exciting
• Other eye – Sympathizing
• Penetrating/Perforating injury
• Metallic foreign body
• Injury to ciliary body – maximum SO
• Surgical repair>48 hour after injury
• Highest frequency 2 weeks-3months.

Dalen Fuch’s Nodules

• Dalen Fuchs’ Nodules on choroid
M/c seen in children
• Earliest symptom-Photophobia
Accommodation failure

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OPHTHALMOLOGY

• Earliest sign-Retrolental flare

• Mutton fat KP s

• Treatment-Enucleation
Repair the injury

PHTHISIS: -end stage ocular response to severe injury

Shrunken , non functional , disorganised

7 S mnemonic

Soft Shrunken Shapeless structureless

Sightless Squared Sore

OCULAR HIV:

Commonest ocular manifestation-Cotton wool spots/soft exudates

(retinal microangiopathy)

MC infection ocular infection-CMV retinitis

Blurring , floaters

Pizza pie/scrambled eggs and ketchup

appearance

DOC – Oral Valgancyclovir

MC tumour-Kaposi Sarcoma

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OPHTHALMOLOGY

GLAUCOMA

1. Increased 10P
At least 2/3
2. Visual field defects
for diagnosis
3. Optic disc damage

Congenital Glaucoma:
 aka Buphthalmos
 Barkan’s membrane – congenital anomaly
 Autosomal recessive
 Consanguineous marriage

Classic Triad:
Lacrimation
Photophobia
Blepharospasm

Hazy Cornea-Corneal oedema

Enlarged eyeball
Myopia
Haab’s striae
Descemet’s membrane ruptures

ARISE MEDICAL ACADEMY 37

OPHTHALMOLOGY
Treatment
1.Goniotomy:
Safer but rare
Hazy cornea-Gonioscopy difficult

2. Trabeculotomy:
Can be done in hazy cornea

Aqueous Humor Dynamics:

Primary Angle Closure Glaucoma:

Risk factors – Middle aged women
Hypermetropia
Asian
Mid dilated pupil leads to pupillary block
Entrapment of aqueous – pushes iris
forward – blocks angle

ARISE MEDICAL ACADEMY 38

OPHTHALMOLOGY
Mid – dilated pupil  Pupillary Block

Normal Angle Angle Closure

Acute ACG–Late night attacks

Mid dilated pupil
Pupillary block- entrapment of aqueous
Angle closure
Sudden rise in IOP
Commonly seen in cinema theatre

Symptoms: Severe pain

Vomiting
Redness
Colored haloes– Corneal edema
Sudden drop in vision

Signs:
 Stony hard eye
 Shallow AC
 Steamy Cornea- corneal edema
 Vertically oval pupil, mid–dilated, non–reacting to light

ARISE MEDICAL ACADEMY 39

OPHTHALMOLOGY
Fincham’s Test- to differentiate between colored halos of cataract and
ACG

Open Angle Glaucoma:

 Colored races
 Myopia
 Middle aged
 Thin CCT
 Pathology – Trabecular meshwork fibrosis
 Slowly rising IOP –progressive visual field loss finally leading to-
1.Tunnel/Tubular vision

2.Progression of Glaucoma

3 Frequent change of presbyopic glasses  Only symptom of OAG

Frequent change of distant vision glasses in old patient Cataract
Frequent change of glasses in a young patient  Keratoconus

ARISE MEDICAL ACADEMY 40

OPHTHALMOLOGY
PACG POAG
Female No gender predisposition
Middle aged Middle aged
Hypermetropic Myopic
Colored haloes/pain No symptoms
 Visual acuity Trabecular fibrosis
Pupillary block

Retina & Visual Field Relationship:

The rays from the visual field focuses on opposite retina
 Superior visual field is viewed by inferior retina
 Inferior visual field is viewed by superior retina
 Nasal visual field is viewed by temporal retina
 Temporal visual filed is viewed by nasal retina
Blind Spot: lies in temporal field
Optic Disc: located in the nasal retina

Perimetry
Visual field changes in Glaucoma:
1. Paracentral Scotoma

2. Bjerrum’s Scotoma

3. Nasal step

ARISE MEDICAL ACADEMY 41

OPHTHALMOLOGY
4. Arcuate scotoma

5. Optic Disc – composed of central pale cup occupying 30 %,

Neuroretinal rim NRR -70%
Cup allows passage of blood vessels , NRR houses all the 1.2 million
neurons of optic nerve
Glaucoma damages the NRR , shrinking the NRR and allowing increase
in cup disc ratio
 Normal optic disc – CDR - .3 -.6
 In glaucoma Cup disc ratio > 0.7

Optic Disc Normal optic disc Cup Disc Ratio > .7

 Changes in glaucoma:

o Increased CDR

ARISE MEDICAL ACADEMY 42

OPHTHALMOLOGY
o Disc Pallor

o Splinter hemorrhage

o Sign of nasalization

Advanced Glaucoma:
Glaucomatous Optic Atrophy–CDR =1

ARISE MEDICAL ACADEMY 43

OPHTHALMOLOGY
Instrument for visualization of optic disc
Direct Ophthalmoscope:
Distance very close
Disc , fovea , macula seen
Real, inverted, magnified image
Magnification 15 times

Treatment of Glaucoma-only lower IOP , rest changes are irreversible

OAG treatment:

1. Medical

2. Argon laser Trabeculoplasty

ARISE MEDICAL ACADEMY 44
OPHTHALMOLOGY
3. Trabeculectomy

Medical:

• Cholinergic Agonists

1. Pilocarpine/ Carbacol – Increases outflow through TM

S/E  Uveitis

Ciliary spasm

Myopia

Retinal detachment

2 .B-blockers

Decreases production of aqueous

Non – selective  Timolol, Levobunolol

Selective – Betaxolol

S/E –

C/I in bronchial asthma

C/I in Arrythmias

C/I in COPD

Dry eyes

Depression

3 Adrenergic drugs –Epinephrine/Adrenaline

Dual mechanism – Increases outflow

Decreases production

• S/E –
Systemic: Palpitations, sweating, tachycardia.
Nervousness, tremors, hypertension
Ocular: CME in aphakia, pupil dilation
• C/I – ACG & Hypertension.

ARISE MEDICAL ACADEMY 45

OPHTHALMOLOGY
Dipivefrine:

• Prodrug of epinephrine
• Only intraocular side effects
• C/I in ACG

4 Carbonic Anhydrase Inhibitors

Decrease production of aqueous

Systemic: Acetazolamide

Topical: Dorzolamide, Brinzolamide

Acetazolamide

S/E: Sulfa allergy

Hypokalemia

Acidosis

Kidney stones

CRF

Hepatic failure

5 Dorzolamide/Brinzolamide

Topical

Safest

DOC in children

S/E: Corneal decompensation

α2 – agonist

• Brimonidine and Apraclonidine

• C/I in children
• S/E: drowsiness, depression
• Neuroprotection

ARISE MEDICAL ACADEMY 46

OPHTHALMOLOGY
Apraclonidine – Not used commonly

Tachyphylaxis

Maximum blepharoconjunctivitis

6 PG analogue (PGA):

• Latanoprost/Bimatoprost/Tafluprost
• Increases outflow – uveoscleral pathway
• DOC for POAG and Normal tension glaucoma
• Most potent anti-glaucoma drugs- 35% lowering IOP

S/E – Uveitis

Cystoid macular oedema

Iris hyperchromia

Blepharoconjunctivitis

Trichomegaly

Hyperosmotic Agents:

Mannitol –IV drug

Fastest anti glaucoma drug – DOC of Acute angle closure glaucoma

S/E – Decompensation in case of CHF

Glycerol / Isosorbide - oral drugs

Glycerol – C/I: DM

ARISE MEDICAL ACADEMY 47

OPHTHALMOLOGY

Surgical Management:

1. ALT (Argon Laser Trabeculoplasty) – increases size of holes of TM

2. Trabeculectomy

ACG – Treatment

• Peripheral Iridectomy PI /Laser Iridotomy LI

• Prophylactic Nd:YAG Laser Iridotomy other eye

Secondary glaucomas

Lens induced glaucomas

ARISE MEDICAL ACADEMY 48

OPHTHALMOLOGY
Phacomorphic Glaucoma:

• ACG caused by mature cataract

• Intumescent cataract pushes iris,
causes angle closure
• Shallow AC
• IOP rises
• Cataract surgery definitive treatment

Phacolytic glaucoma:

• Open angle glaucoma

• Hypermature cataract
• Deep AC
• HMW lens matter leaks out through
old fragile capsule, blocks TM
• IOP rises
• Definitive treatment – Cataract extraction

Neovascular Glaucoma

Retina maximum consumer of oxygen in eye

Retina- hypoxia –VEGF –Neovascularization - NVI/NVA-

neovascularization of angle

Fibrovascular proliferation on iris- closes angle – secondary ACG

Causes: Diabetes

CRVO

Ocular Ischemic disease

• Rubeosis Iridis

• NVI

ARISE MEDICAL ACADEMY 49

OPHTHALMOLOGY
Neovascular Glaucoma:
Secondary angle closure glaucoma

Mx:

2. Reduce IOP

- Drugs contraindicated in NVG-Pilocarpine / PGA

Trabeculectomy

ARISE MEDICAL ACADEMY 50

OPHTHALMOLOGY

OPTICS AND REFRACTION

Emmetropia:

Condition in which the rays of light focus on the retina.

Ametropia:

Condition in which the rays of light do not focus on the retina

If the rays of light,

• Focus in front of the retina: Myopia

• Focus behind the retina: Hypermetropia
• Have two different foci: Astigmatism

Conditions on which Refractive Errors Depend

1. Axial length

2. Corneal curvature: Most important

3. Lens thickness

4. AC depth

MYOPIA/NEAR-SIGHTEDNESS/SHORT-SIGHTEDNESS:

• The rays of light focus in front of the retina

• Blurring of distance vision
• Near vision is normal
• Myopic Look: Patients of myopia tend to keep their eyes half closed
• Myopics wear glasses closer to the eye

ARISE MEDICAL ACADEMY 51

OPHTHALMOLOGY

Causes of Myopia:

1. Axial Myopia:

Most common cause of myopia

Eyeball is longer than normal (Normal axial

length = 24 mm)

Each 1 mm elongation contributes 3 Diopters of myopia

2. Curvature Myopia:

Due to increased curvature of the cornea

The axial length is normal, but the curvature

is increased

E.g. Keratoconus

Treatment of Myopia

Divergent/Concave/Minus lens

Limitation: Minification (1D minifies by 2%)

Myopics are under corrected

Hypermetropia/Long-Sightedness:

Rays of light focus behind the retina

Causes of Hyperopia:

1. Axial Hypermetropia:

• Most common cause of hypermetropia

• Axial length is smaller than normal (Normal Axial Length = 24mm)
• Each 1 mm shortening contributes 3 D of hyperopia

ARISE MEDICAL ACADEMY 52

OPHTHALMOLOGY

Symptoms:

• Blurred vision for both distance and near, more for near

• Asthenopia/ headache/eye strain

• Early onset presbyopia
• Uncorrected hypermetropics have more chances of amblyopia
• Uncorrected hypermetropia develops convergent squint

Treatment:

By Convex/Plus power lenses

Limitation: Magnification (1 D magnifies by 2%)

Detected by cycloplegic refraction

Indications for cycloplegic refraction

• Hypermetropia
• Children – atropine for children < 7 years, homatropine 7-12,
Cyclopentolate 12 -15 years
• Esotropia / Convergent squint

ASTIGMATISM

• Most common refractive error

• Image formed by two different foci
• Highest asthenopia
• Principal reason – corneal curvature is not uniform, cornea shaped
like a prolate spheroid
• Astigmatism correction: Cylindrical/Toric Lenses

ARISE MEDICAL ACADEMY 53

OPHTHALMOLOGY

CLASSIFICATION OF ASTIGMATISM

1. Regular Astigmatism (Most common)

• Two principal meridians separated by 90°

• Correctible by sphero-cylinder lens

2. Irregular Astigmatism

• Principal meridians are not symmetric due to irregular surface of

cornea
• Do not lie 90° apart
• Not correctable by a sphero-cylindrical lens, only by contact lens –
keratoconus ,pterygium, scarred cornea

Symptoms:

Asthenopia

Monocular diplopia

Distortion

Headaches

Ocular fatigue

Halo around lights

Distortion and blurring of images

Classification:

Types of Astigmatism:

1. Simple myopic

Two focal points: One on the retina, the other in front of the retina

E.g.: -2DC x 10o

2. Simple hyperopic

One focal point on the retina, one behind the retina

E.g.: +2DC x 10o

3. Compound myopic

Both focal points are in front of the retina

E.g.: -2DS/-3DC x 180

4. Compound hypermetropic

Both focal points are behind the retina

ARISE MEDICAL ACADEMY 54

OPHTHALMOLOGY
E.g.: +2DS/+3 DC x 180o

5. Mixed

One focal point in front of the retina, one behind the retina

E.g.: -2DS/+3 DC x 143(opposite signs, cylindrical power > spherical

power)

PRESBYOPIA:

• Loss of accommodation with age

• Only ocular condition with a prevalence of 100% in patients older
than 50

• With increasing age:

1. Lens becomes harder due to calcification

2. Capsule becomes fibrous

3. Ciliary muscles become weaker

As a result, the patient cannot accommodate, presbyopia starts at 40

years of age.

Symptoms:

• Normal distance vision

• Difficulty in seeing near objects

Age Expected Presbyopia Correction:

Age in years Addition

40 +1.00 D
45 +1.50 D
50 +2.00 D
55 +2.50 D
60 +3.00 D

ARISE MEDICAL ACADEMY 55

OPHTHALMOLOGY

Treatment Options:

1. Glasses – Bifocals- two separate lenses

Progressives- single lens, but 3 different zones for
distance, intermediate and near vision

2. Presbyopia eye drops

Only FDA approved treatment

Pilocarpine HCl – 1.25%

CM contraction

Miosis

Darkroom Procedures:

• Retinoscopy – Instrument: Retinoscope

• Distant Direct Ophthalmoscopy: Direct Ophthalmoscope
• Direct Ophthalmoscopy: Direct Ophthalmoscope
• Indirect Ophthalmoscopy: Indirect Ophthalmoscope

Pinhole test:

Pinhole: Opaque plastic disc with a central hole (Pin size: approx. 1mm)
To know if it is an optical error or an organic error: Place the pinhole in
front of the eye:

1. If the vision improves: Optical error

2. If the vision does not improve: Organic error. Pinhole allows only a
single ray of light which passes through the nodal point of the eye,
focuses on retina

ARISE MEDICAL ACADEMY 56

OPHTHALMOLOGY
Trial set:

Retinoscopy/Skiascopy:

• Technique to objectively measure the refraction of the eye

• Dilate/Fixate on a distant target
• Distance 1 meter away from patient
• Retinoscopy streak moved from side to side  check the movement
of light reflex in the patient’s pupil
• Differentiates between the types of refractive errors

SPAM –

Same Plus Against Minus

Example:

• The patient is placed at 1m

• The retinoscope is turned on, and the streak of light is observed with
horizontal and vertical movement of the retinoscope
• Assume that the movement of the streak is observed in opposite
direction of the Retinoscope- against the movement
• Indicates minus lens ( against minus (SPAM)
• The same procedure is repeated with retinoscope at horizontal
movement
• Both values are plotted on the power cross

ARISE MEDICAL ACADEMY 57

OPHTHALMOLOGY

Direct Ophthalmoscopy:

Close to patient – within anterior principle focus – 15 cm roughly

Structures visualized

• Disc
• Fovea
• Macula
• Venous pulsations
• Virtual, erect, magnified
• Magnification 15X

Indirect Ophthalmoscopy:

• Lying down position

• Real, inverted, magnified image
• Magnification: 3-5X
• Wide field of view: 30°-45°up to ora serrata upon indentation

ARISE MEDICAL ACADEMY 58

OPHTHALMOLOGY

RETINA AND VITREOUS

RETINA:
• Retina is colourless
• 10 layers: 9 neurosensory layers(NSL) and 1 Retinal pigment
Epithelium (RPE)
o Inner 2/3 blood supply: Central retinal artery (CRA)
o Outer 1/3 blood supply: Posterior ciliary artery (PCA) also
choroid

Retinal Detachment:

• Separation of NSL from RPE

• Floaters (Muscae)
• Flashes (Photopsiae)
• Curtain descending in front of eyes
• O/E  Normal red glow replaced by grey glow

• Schaffer’s sign – tobacco dusting of the vitreous

Types:

Rhegmatogenous

Tractional

Exudative

Rhegmatogenous RD:

Rhegma: Break/Tear/defect in Retina

Risk factors: Myopia

After cataract Surgery

Trauma

ARISE MEDICAL ACADEMY 59

OPHTHALMOLOGY
• Myopic retina  thin, because of increased axial length of the eye
• High Myopia > -6.0 D
• Retinal holes
• Lattices
• Horse shoe tears

Retinal holes Lattices Horse shoe tear

• Aphakia Lens support to vitreous missing  Excessive movement

of vitreous RD.
• Dialysis –separation of retina from ora serrata

• Break in retina allow the vitreous to flow in between the two retina
layers and separate them

Tractional RD:

• Membrane/Band/fibrous tissue pulling off NSL from RPE

• Commonest cause of loss of vision in premature child
• Causes: Diabetes (MC)
ROP (Retinopathy of prematurity)

Tractional RD Diabetic Traction ROP

• All detachments are sudden except tractional RD which is slow, takes

years to pull off.

ARISE MEDICAL ACADEMY 60

OPHTHALMOLOGY
Exudative RD:

• No holes, breaks or tears, no traction on the retina

• Fluid produced by various lesions exudes in between the two retinal
layers and separates them
• Characterized by shifting fluid
• Sudden painless loss of vision
• Causes  Choroidal Melanoma
PIH- pregnancy induced hypertension

Exudative RD Choroidal Melanoma PIH

Management for RD:

Reattach the two layers of retina

1. Buckling- silicone buckle on sclera, for rhegmatogenous RD

2. Exudative RD – treat the underlying cause – the fluid absorbs, retina

falls into position

3. Tractional RD – Vitrectomy to peel off the membranes and bands

Diabetic Retinopathy

WHO  Diabetic capital of the world  INDIA

Duration – most important prognostic factor

Control of blood glucose

Associated Hypertension

Hyperlipidemia

Pregnancy

• Screening guidelines:
Type 1/IDDM – 5 years
Type 2/NIDDM – at time of diagnosis
Subsequently annual exam:
• Symptom characteristic of DR -fluctuating vision – hyperglycemia –
myopia
• Pathology

ARISE MEDICAL ACADEMY 61

OPHTHALMOLOGY
Earliest ocular manifestation – Microaneurysm
Occlusion – hypoxia – VEGF– Neovascularization
Pericyte necrosis leads to leakage of blood on retina

Classification:

1. Non Proliferative Diabetic Retinopathy (NPDR)

• Microaneurysms
• Dot and blot haemorrhages- on inner nuclear layer/Flame shaped
haemorhages – on nerve fibre layer

• Hard exudates
• Soft exudates

2. Proliferative Diabetic Retinopathy (PDR)

• NVD – neovascularization of the disc

• NVE – neovascularization elsewhere

Visual Loss in DR:

NPDR: Macular edema

PDR: Vitreous hemorrhage

Tractional RD

Neovascular glaucoma

ARISE MEDICAL ACADEMY 62

OPHTHALMOLOGY

VITREOUS HEMORRHAGE:

Sudden painless loss of vision, floaters

Red tinted vision

Causes

• M/c Diabetic retinopathy (PDR)

• PVD – posterior vitreous detachment
• Young patients – Trauma MCC
• Eales’ Disease – spontaneous, recurrent, vitreous
hemorrhage in young males
• Tuberculosis most well-known association
• ATT -9 months with systemic steroids

Management of Vitreous hemorrhage –

 Bed rest with head -end elevated for 3 months

 Treat underlying cause – DM/trauma/Eales‘ Disease
 Vitrectomy, if it doesn’t absorb

Viterous Hemorrhage Post vitrectomy

Diabetic Macular edema –

•
• MCC of loss of vision in Diabetes
• Swelling around macula within 500 microns of fovea – Clinically
significant macular edema
• Slow, painless blurring of vision
• Metamorphopsia

DIABETIC MACULAR EDEMA Metamorphopsia

ARISE MEDICAL ACADEMY 63
OPHTHALMOLOGY

Management:

1. Diabetic macular edema (DME)- Anti VEGF Drugs: Ranibizumab/

Bevacizumab through pars plana

2. PDR – Pan Retinal Photocoagulation (PRP)

Best treatment of retinal ischemia – PRP

No ischemia, no further production of VEGF , no further NV

Laser – Double Frequency Nd -YAG laser, (Green laser) wavelength –

532 nm

PRP for retinal ischemia

Central Retinal Vein Occlusion

Age > 65 year

Hypertension

Diabetes

Hyperlipidemia

Young ladies – OC

Sudden, painless blurring of vision

O/E – 1. Blood and thunder fundus – retina full of hemorrhages –flame

shaped , dot and blot

2. Splash tomato/Tomato ketchup fundus

3. 90- day Glaucoma – NVG after CRVO

CRVO – M/c /c loss of vision - Macular edema

Neovascular glaucoma

ARISE MEDICAL ACADEMY 64

OPHTHALMOLOGY

Treatment

1. Anti VEGF drugs (Intravitreal)

Bevacizumab

Ranibizumab

Route of administration –

Intravitreal through pars plana

Central Retinal Artery Occlusion CRAO

central retinal artery gets blocked resulting in sudden vision loss in

affected eye.

• Major ocular emergency  equivalent cerebral stroke

• Risk factors
• Advanced age
• Diabetes
• Hypertension
• Smoking
• Mc/c Embolism – cholesterol – Hollenhorst plaque

• Cherry red spot

S/S: Cattle truck / Box car appearance – segmentation of blood column

RIT: 90 min

Partial recovery by 240 minutes

Irreversible after 4 hours

Treatment : Ocular massage

Immediate lowering of I0P- Mannitol / Acetazolamide

Paracentesis – aspiration of the aqueous humour

Carbogen inhalation – mixture of oxygen and CO2

IV heparin/ TPA- tissue plasminogen activator

Cystoid Macular Edema CME

Fluid in NSL – outer plexiform layer -OPL

Causes – Diabetes

Retinitis pigmentosa

Irvine-Gass syndrome

ARISE MEDICAL ACADEMY 65

OPHTHALMOLOGY
CRVO

Signs and symptoms – Slow painless blurring of vision

Metamorphopsia – distortion of shape –straight lines become wavy

Detected by Amsler’s grid

Fundus exam - +90D lens / Direct Ophthalmoscope

Investigations - Fluorescein Angiography

Dye – Na fluorescein

Injected in ante -cubital vein

Photographed by Fundus camera

Petalloid/Flower petal appearance

Optical Coherence Tomography (OCT )

Cross sectional photo of all layers of retina

Treatment – Irvine Gass Syndrome

1. Topical NSAID’s – Bromfenac/ Nepafenac

2. Topical steroids – Prednisolone/Dexamethasone

3. Sub-tenon’s injection – Triamcinolone

Retinitis Pigmentosa –

 Apoptosis of rods – programmed cell death of rods

 AR/AD/X-linked

 Consanguinity

 Clinical features

 Nyctalopia
Nyctalopia
Nyctalopi Ring
Ringscotomas
Scotoma
 Ring scotomas

 Constriction of visual field

 Tunnel/Tubular vision

Triad: Pale waxy disc

Arteriolar attenuation

Bone spicule pigmentation

ARISE MEDICAL ACADEMY 66

OPHTHALMOLOGY
Investigation of choice: ERG- measures potential difference of retina

Normal ERG – a, b c waves

RP Flat RGR

Treatment –

No proven therapy

 15,000 IU/day of vitamin A in palmitate form with 12mg lutein every

day

 Usually become blind by 40 years but 7 year of vision can be retained

by vitamin-A

 Argus II Implant – Bionic Eye

Retinoblastoma

Commonest ocular tumor of childhood

B/L in 30%: U/L 70%

40% - Heritable

60% - Non inheritable

Genetics: Rb1 gene (Rb1): located on 13q 14

Tumour suppressor gene – prevents tumors

First human cancer suppressor gene to be charted

Clinical features : Leucocoria (Amaurotic cat’s eye pupil)

Strabismus-squint

Glaucoma – NVG

Loss of vision

D/D of Leucocoria – Retinoblastoma

Congenital cataract

Coat’s disease

Hallmark -Flexner Wintersteiner rosettes

Retinoblastoma -commonest cause of

ARISE MEDICAL ACADEMY 67

OPHTHALMOLOGY
Intraocular calcification, detected by

CT scan/ MRI / Ultrasound

Treatment - Primary : Save life

Secondary: Save eye

Tertiary: Save vision

Internation classifcation of Retinoblastoma:

A ≤ 3mm

B > 3 mm

C Localized seeds (< 3mm from tumor)

D Diffuse seeds (> 3mm)

E Massive retinoblastoma > than 50% of eyeball

Treatment

Laser photocoagulation
Cryotherapy – cold probe freezes tumor

Chemotherapy – Intravenous,

intravitreal, intra-arterial

M/c regimen – VEC – 6 cycles

Vincristine, Etoposide, Carboplatin

Enucleation:

 Delaying enucleation may be risky

 Sacrifice 15mm of optic nerve

 Hydroxyapatite orbital implant

Causes of death:

 Metastasis – M/c via optic nerve

 Intracranial tumors associated with RB- pinealoblastoma

 Pinealoblastoma with bilateral retinoblastoma -Trilateral

retinoblastoma

 Secondary tumors associated with RB – Osteosarcoma of femur.

ARISE MEDICAL ACADEMY 68

OPHTHALMOLOGY

NEURO PHTHALMOLOGY

Optic Neuritis:

also called Papillitis-40 %

• Inflammation of optic nerve

• Optic disc also called Papilla

Retrobulbar neuritis: 60%

• MCC : Multiple Sclerosis (Young ladies 20-45)

Investigation of choice: MRI

• Sudden painful loss of vision

• Pain with ocular movements
• Color vision desaturation –“washing out of colors”
• Abnormal pupillary reaction –RAPD (Relative afferent pupillary
defect)/ Marcus Gunn pupil
• Hallmark: Disc Edema

(RBN) Retrobulbar Neuritis:

Inflammation behind the optic disc

“Patient sees nothing &

Doctor sees nothing”

Treatment: Intravenous methyl prednisone (IVMP)

• Commonest visual field defect: Central/ Centrocecal scotoma

ARISE MEDICAL ACADEMY 69

OPHTHALMOLOGY
COMMON NEUROPHTHALMIC FIELD DEFECTS

Central/Centrocecal scotomas Optic neuritis/Retrobulbar neuritis

Enlargement of blind spot Papilledema

Altitudinal hemianopia Anterior Ischemic Optic Neuropathy

Central/Centrocecal scotomas Toxic/Nutritional optic neuropathy

Toxic Amblyopia

Optic Neuropathy

Ingestion of toxic drugs

• MCC: Tobacco (10-15years)

Alcohol (10-15years)

Ethambutol (ATT)

Amiodarone

• Rx : Hydroxycobalamin , VitaminB12

Pupillary Light Reflex: Assesses brain stem functions.

Abnormal PLR will be found in optic nerve lesions, oculomotor nerve

injury and brain stem lesions

1. Direct

2. Consensual

Both will react the same way, either constrict together, or dilate

together

Swinging Torchlight Test:

A modification of the PLR , used to detect RAPD/ Marcus Gunn pupil.
Torchlight is shone into one eye for a few seconds, then swung into the
other eye, and back and forth a few times. In a normal test, the pupils
of both eyes constrict equally regardless of which eye is stimulated by
light. RAPD is present if the affected eye dilates, or constricts briefly
followed by dilation.
RAPD /relative afferent pupillary defect / Marcus Gunn pupil – A
critically important sign that defines a defect in the afferent pathway of
pupil.

ARISE MEDICAL ACADEMY 70

OPHTHALMOLOGY
Seen in asymmetric optic nerve damage / major retinal pathology
Elicited by swinging torchlight test
When light is shone on a normal eye for 3 seconds – both pupils
constrict equally
If both pupils dilate – RAPD
Seen in optic neuritis/ Retrobulbar neuritis
Anterior Ischemic optic neuropathy
Large retinal detachment
CRAO

Argyll Robertson Pupil :


• seen in: Neurosyphilis
• Bilaterally, constricted, irregular pupils
To differentiate from festooned pupil – AR pupil exhibits LND – light near
dissociation
LND – A pupillary sign that occurs when pupillary light reaction is
impaired (negative -pupil does not constrict to light) but near reaction
remains intact (positive -constricts to near vision)
Known as “Prostitute’s Pupil”

Adie’s Pupil:
Unilateral dilation of pupil, usually in young females
Causes- Idiopathic, viral
Damages ciliary ganglion and the parasympathetic fibers responsible for
pupil constriction, which pass through 3rd CN, sparing the unopposed
sympathetic fibers, which dilate the pupil
LND – light near dissociation (light reaction negative, near reaction
positive )
Similar to AR, but different reason
Confirmed by Pilocarpine .125 % test

Diluted pilocarpine unable to constrict normal pupil but is able to

constrict Adie’s pupil because of denervation super sensitivity

ARISE MEDICAL ACADEMY 71

OPHTHALMOLOGY
Horner ‘s Syndrome –
Due to Oculo-Sympathetic Paralysis –OSP
Ptosis – due to Muller’s paralysis
Miosis
Anhydrosis
Causes – Pancoast tumor, Internal carotid
artery dissection
Congenital Horner’s – additional heterochromia
Causes – Birth trauma
• Cocaine test: normal eye dilates, abnormal eye will not dilate pupil
Apraclonidine test - Horner's eye dilates

Papilledema:
Disc edema with raised ICT
Normal ICT = 50 -180 mm of H2O
• Adults > 250 mm
• Children > 200 mm

Causes of raised ICT

• TBI: Traumatic Brain Injury
• ICSOLS: Intra Cranial Space Occupying Lesion
• Pseudotumor Cerebri /Idiopathic Intracranial Hypertension (IIH)
• Meningitis
• Subarachnoid/Intracerebral hemorrhage

Clinical features:
1. Headache: occipital, pulsating/throbbing, change of posture, worsens
with coughing, sneezing
2. Projectile Vomiting
3. Amaurosis fugax (sudden temporary, transient loss of vision)
4.Pulsatile tinnitus
Vision usually normal till last stage, pupils react normally, no loss of
color vision
Disc edema – only sign
6th nerve palsy (false localizing sign)
Papilledema VS Optic neuritis
 
• B/L disc edema • U/L
• Excessive disc edema • little
• Paton’s lines present absent
• Loss of CRV pulsations • Normal CRV pulsations

MC Field defect = Enlargement of Blind Spot

Idiopathic Intracranial Hypertension/PTC :

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OPHTHALMOLOGY
Pseudo Tumor Cerebri
Raised ICT in young, fat, females of child bearing age
• Cause unknown
Symptoms - Severe headaches, transient visual obscurations (TVO)
,pulsatile tinnitus
• Drugs causing IIH Vitamin A
Tetracycline
Oral contraceptives
Lithium
Amiodarone
Signs - Disc edema present

• Treatment - : Weight loss (most important)


• DOC of IIH: Acetazolamide

• Ventrico - Peritoneal Shunt

Visual Pathways

Following components

Optic disc – beginning of optic nerve, called the optic nerve head
(ONH)

Optic nerve – axons of retinal ganglion cells form optic nerve

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OPHTHALMOLOGY
Optic Chiasma - X shaped structure where the optic nerves cross over

Optic Tract - continuation of the optic nerve, carrying information from

chiasma to LGB

Lateral Geniculate Body – pyramidal structure, great relay center of the

retinal ganglion cells where 90% of visual fibers end

Optic radiations -fibers carry information from the LGB to the visual
cortex, pass through internal capsule- two components –

Meyer’s loop – passing through temporal lobe

Baum’s loop – passing through parietal lobe

Occipital lobe - Primary visual cortex, around the calcarine sulcus, V1

Summary Visual field defects :

Site of lesion VF defect

1. Optic Nerve: Same sided, monocular blindness

2. Optic Chiasma: Bitemporal hemianopia

3. Optic tract: Opposite sided Homonymous hemianopia

4. LGB: Rarely seen

5. Optic Radiations:

Meyer’s loop: Pie in the Sky

6. Occipital lobe: Macular Sparing

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OPHTHALMOLOGY

SQUINT/STRABISMUS

• Orthophoria: Parallel eyes

• Heterophoria: Squint/Strabismus –
eyes not parallel

Tropia Phoria
↓ ↓
Manifest Latent

Tropia: Exotropia  Outward deviation of eye

Esotropia  Inward deviation

Hypertropia  upward deviation

Hypotropia  downward deviation

Phoria: exophoria  Outward

Esophoria  Inward

Hyperphoria  Upward

Hypophoria  Downward

(Hidden, not obvious)

9 gazes of humans – 1 primary, 4 secondary, 4 tertiary

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OPHTHALMOLOGY
Tropia:

detected by

Hirschberg test- - flash torchlight on center of forehead, ask patient to

look at light.

If the reflex (reflection of light) is visible on center of pupil -

orthophoria. If not, then tropia

Each 1mm of decentration of light reflex = 7 degrees of squint =14 prism

diopters

(1 degree = 2 prism diopters)

Phoria:


Cover-Uncover Test-

Cover one eye, uncover the eye and look at

the UNCOVERED eye.

No movement in a normal eye, if any movement,

then there is phoria

Usually not clinically significant, may

have asthenopia due to strain of fusion

Tropia

Comitant Paralytic –paralysis of

of
↓
Nerves Neuromuscular
Angle between ↓ junction(NMJ)
two eyes 3 CN Myasthenia gravis
remains the 4 CN
same in all 9 6 CN
gazes.

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OPHTHALMOLOGY

Comitant squint – no functional problem, only cosmetic

Paralytic – the angle between 2 eyes changes in every gaze

Symptoms of Paralytic squint

• Diplopia
• Abnormal Head Position -AHP
Vertigo
Disorientation

Diplopia: double vision

Horizontal diplopia – LR/ MR paralyzed Vertical diplopia- SR/IR

paralyzed Oblique –SO/IO paralyzed

Causes of Diplopia:

Monocular Binocular Diplopia

Diplopia


Squint
 Cataract

 Astigmatism

 Dry eyes

 Keratoconus

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OPHTHALMOLOGY

AHP: Abnormal Head Posture

1. Face Turn = MR/LR paralyzed
2. Chin lift / depression = SR/IR paralyzed
3. Head Tilt = SO/IO paralyzed

Comitant Squint:

Accommodative Non-Accommodative

Idiopathic , post traumatic

Uncorrected Refractive Error Treatment - Surgery

Treatment: Glasses weaken one EOM

Uncorrected Myopia: Divergent squint strengthen opposite EOM

Uncorrected Hypermetropia:
Convergent squint

Recession/ to go back: for weakening EOM

Resection/ to cut : for strengthening EOM

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OPHTHALMOLOGY

Paralytic Squint:

Management – Treat underlying condition –
DM/Hypertension
Wait and watch × 6 months for recovery
Correct diplopia

For treating diplopia- Patching
Prisms – Conventional / Fresnel (Disposable)
Botulinum toxin

Paralytic

Nerve Neuromuscular junction ( NMJ)

 
3 CN Myasthenia Gravis
4 CN
6 CN

3th CN Palsy:
3rd CN supplies all muscles except LR and SO.


• Down and out eye with ptosis
• Outer parasympathetic fibers supplying sphincter pupillae & Ciliary
muscle
• Inner somatic fibers supply SR, IR, MR, IO, LPS,
Causes- Vasculopathic-DM , Hypertension

Pupil Sparing – normal pupil size: Medical 3rd CN palsy :

DM/BP

Pupil involving – pupil dilated: Surgical 3rd CN palsy:

Aneurysms/Tumor

4th nerve Palsy: Trochlear


• Longest intracranial CN
• Least number of axons
• Thinnest cranial CN
• M/C nerve to be involved in head trauma
• Only CN to cross over
• Only nerve to exit dorsally
• Traumatic, Congenital, vasculopathic
• Symptoms: Vertical diplopia on down gaze, as in reading/ walking
downstairs
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OPHTHALMOLOGY
• Position of eyes: up, with head till on opposite shoulder.

6th nerve Palsy:


• Longest subarachnoid nerve
• m/c ocular motor palsy
• m/c CN to be affected in
lumbar puncture
• M/c CN to be affected in raised ICT
Cause: Vasculopathic
Children: Neoplasms –pontine glioma
Symptoms: Horizontal diplopia
Esotropia
Face turn towards affected side

NMJ disorder -Myasthenia Gravis:

Autoimmune disorder, antibodies are produced against post synaptic
acetylcholine receptors, leading to a reduction in number of ACh
receptors .This causes defective nerve impulse transmission leading
loss of muscle contractility and fatigue
M/c disorder of NMJ
Skeletal muscle weakness and rapid muscle fatigue

Affects young ladies and old men

LPS first ocular muscle to be affected
Fluctuating ptosis and diplopia hallmarks of ocular myasthenia gravis
Sleep test – 30 minutes of sleep improves ptosis
Ice pack test improves ptosis
Tensilon test (Injection Edrophonium) diagnostic test
DOC Pyridostigmine and oral steroids

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OPHTHALMOLOGY

CONJUNCTIVA

• Layers of Tear film: 3 layered sandwich

Lipid layer o Secreted by Meibomian glands

o Prevents Evaporation
Aqueous o Secreted by lacrimal glands
o For nutrition –Glucose, O2, lysozyme
Mucin o Goblet cells , stabilizes tear film

Absence of any of these layer cause Dry eyes

(Keratoconjunctivitis sicca)

Deficiency of: Lipid, Aqueous Mucin

Deficiency of lipid – MGD (Meibomian Gland Disease)

• Deficiency of: Aqueous


o Age > 50 y/o, particularly females
o Sjogren’s Syndrome dry eyes/ dry mouth / rheumatoid arthritis
o Prolonged Contact Lenses
o Refractive Surgery – post LASIK
o Drugs:
Anti-cholinergic
Anti-histaminic
Anti-depressants

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OPHTHALMOLOGY

• Deficiency of: Mucin


o Vit A
oTrachoma
o Chemical injuries- Acid and alkali burns
Symptoms of Dry eyes (Keratoconjunctivitis sicca)
1. Foreign Body Sensation – burning of eyes
2. Redness
3. Uncomfortable under fans and AC’s
4. Worsening in evening
5. Computer Vision Syndrome
6. Blurring of vision
7. Ocular fatigue and heaviness
(n) Blink: 20 times/min

Investigations:
1. Rose Bengal/ Lissamine green dye: positive
staining of conjunctiva - Dry Eyes
2. Fluorescein staining positive on cornea

3. Schirmer’s test: <10 mm wetting in 5 min

TBUT: Tear break-up time< 10 seconds in KCS
DOC –Methyl cellulose eye drops,
Cyclosporine eye drops

Lacrimal drainage pathway

Lacrimal gland – upper/lower punctum – upper /lower canaliculi /
common canaliculus – lacrimal sac – nasolacrimal duct - finally into
inferior meatus
Congenital Nasolacrimal Duct Obstruction
Hasner’s valve not patent in 5-10%
Tears stagnate in lacrimal sac – gets infected
Epiphora , discharge , crusting present

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OPHTHALMOLOGY
Differential diagnosis from congenital glaucoma
Differentiated by photophobia and blepharospasm in Buphthalmos
Management
Criggler massage and topical antibiotics – up to 6 months of age
Probing – earlier the better
DCR (Dacryocystorhinostomy) – after 3 years of age

Table: World Health Organization Re-classification of

Xerophthalmia signs:

Classification Ocular Signs

XN Night blindness
X1A Conjunctival xerosis
X1B Bitot’s spots
X2 Corneal xerosis
X3A Corneal ulceration-keratomalacia
involving one-third or less of the cornea
X3B Corneal ulceration-keratomalacia
involving one-half or more of the cornea
XS Corneal scar
XF Xerophthalmic fundus

Vit A dosage
 > 1yr : 200,000 IU: 0, 1, 14 day

Conjunctival Degeneration:
Pterygium: conjunctival overgrowth over cornea
 
Bird’s wing(meaning )
Loss of vision – astigmatism, pupillary obstruction
Excision with conjunctival autograft

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OPHTHALMOLOGY

Conjunctival reactions
 Viral
Chlamydia Follicles
1. Follicles: Collection of lymphocytes
Trachoma

2.Papillae: flat-topped elevations on conjunctiva containing blood

vessels, seen in allergic conjunctivitis

Conjunctivitis:
Bright Red
Painless
Discharge  Purulent (bacterial)
 Serous (viral)
 Mucoid (allergic)
M/c : Viral Conjunctivitis

1. Adenovirus

EKC : Epidemic Keratoconjunctivitis/Pink Eye/ Madras eye

Highly infectious; spreads very fast.

2. Acute Hemorrhagic Conjunctivitis- EV-70 , enterovirus


Apollo Virus/ Apollo disease.

TRACHOMA: mc infectious cause of blindness


 Egyptian Ophthalmia
 Chlamydia trachomatis  A, B, Ba, C
North Africa: Egypt, Sudan, Morocco, Algeria
South Asia : India, Bangladesh, Nepal, Pakistan
Middle East: Yemen, Iraq

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OPHTHALMOLOGY
6 main states of Trachoma in India
1. Punjab
2. Haryana
3. Rajasthan
4. UP
5. Uttarakhand
6. Gujarat

Children: First victim of trachoma, followed by women

Redness

Watering Photophobia
Clinical features
1. Sago grain follicles
2. Herbert’s pits
3. Arlt’s line (Arlt’s tringle: Uveitis)

SAFE Strategy:
Surgery – Trichiasis
Antibiotics: Azithromycin
Facial hygiene- wash with water
Environmental sanitation
Blanket/ Mass therapy: 1% Tetracycline ointment 0D × 10 days in a
month × 6 months
or
1 % tetracycline ointment BD × 5 days in a month for 6 months

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OPHTHALMOLOGY

Delayed clinical features:

 Trichiasis
 Tylosis – thickening of eyelid margins
 Madarosis
 Entropion – inward rolling of eyelid margin

 Corneal Opacities:
1. Nebula: superficial opacity, maximum discomfort
2. Macula- half thickness opacity
3. Leucoma: full thickness opacity maximum loss of vision

WHO Grading of Trachoma

1. Follicles : > 5 on upper tarsal conjunctiva
2. Intense inflammation
3. Scarring: Arlt’s line
4. Trichiasis
5. Opacities

VISION 2020:
Everyone to be 20/20 by 2020, by eliminating
1. Cataract: Surgery

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OPHTHALMOLOGY
2. Trachoma: SAFE; GET 2020
3. Childhood blindness: Vit-A
4. Refractive Error: Glasses
5. Oncocerciasis: Ivermectin

Ophthalmia Neonatorum:
Conjunctivitis in first month of birth

M/c : Chlamydia trachomatis : 14 days
Most severe: Neisseria gonorrhea: 3 – 5 days- hyperacute conjunctivitis

Crede’s method: 1% Silver Nitrate for prophylaxis  cause chemical
conjunctivitis.

Erythromycin ointment used nowadays

Spring Catarrh/ Vernal catarrh / VKC:

 Inflammation of conjunctiva in hot summers in children
 Allergic condition
 Itching most common symptom
 Morning Misery – discomfort, blepharospasm, photophobia, burning
Cobblestone Papillae
Ropy discharge
Horner Trantas spots: eosinophils
Shield ulcer

Treatment:
 Na cromoglycate (mast cell stabilizers)
 Topical steroids: Loteprednol, Prednisolone
 Immuno modulating drugs Cyclosporine, Tacrolimus

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OPHTHALMOLOGY

CORNEA
5 layers
1. Epithelium – guards the cornea
2. Bowman’s membrane: Can’t regenerate – scar formation
3. Stroma- thickest layer
4. Pre-Descemet’s layer (PDL)/Dua’s layer
5. Descemet’s Membrane: Strongest membrane, only fungus can penetrate
6. Endothelium: most important
Maintains transparency of cornea
Have endothelial pumps – Na K ATPase pumps
Endothelium irreparable: Cause irreversible corneal edema.
Layers of the cornea

Corneal endothelium:
Average count:
3000 cells /mm2 (average)
0.5% cells are lost/ year.
Critical density: < 500 cells /mm2.
For corneal donation: > 2000 cell/ mm2.
 (Specular microscopy required )
Treatment for irreversible
corneal edema: Corneal Transplant – Keratoplasty
Optical – for vision
Therapeutic - for saving eye

Optical Keratoplasty

Penetrating Keratoplasty (PK) Lamellar Keratoplasty (LK)

Full thickness – all 6 layers Partial thickness


Outermost 3 layers -donor
Innermost 3 layers: host

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OPHTHALMOLOGY
 LK
 More successful because
endothelium is host’s own

Q:
Maximum Rejections against: Endothelium

Indications of PK:
1. Pseudophakic Bullous Keratopathy – Vesicles/ Blisters of corneal
edema –due to corneal endothelium trauma sustained during cataract
surgery
2. Non- healing Ulcer
3. Corneal scar
4. Corneal dystrophy
5. Keratoconus
6. Chemical Injuries
7. Fuchs’ endothelial dystrophy

Therapeutic Keratoplasty:
 To eliminate infect or repair a structure defect
 Not done for visual rehabilitation

Corneal Donation:
 HLA matching is not required
 Within 6 hours of death
 Preserved in MK media( McCarey Kaufmann) media – 96 hours life
 Optisol GS - 14 days
 Cornisol -14 days

Contraindications
 HIV
 Hepatitis -B
 Septicemia
 Rabies
 Bacterial/ Fungal keratitis
 Herpes simplex vires
 Creutzfeldt Jacob disease
 Retinoblastoma
 Metastatic Brain Tumor
 Leukemias
 Lymphoma

 Age is not C/I, best corneas before 75 years of age

 Children can only donate to children
 Tamil Nadu > Gujarat: Highest donor states in India.

Corneal Ulcer:
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OPHTHALMOLOGY
Break in epithelium with underlying necrosis of cells

Hypopyon

Ant. Uveitis Ulcer

Symptoms:
1. Photophobia (earliest)
2. Pain: Cornea has highest density of nerve endings.
3. Redness
4. Loss of vision
5. Watering

4 Ulcer – Bacterial
Viral
Fungal
Acanthamoeba

Acanthamoeba Keratitis:
 Contact lens wearers
 M/c organism to attack contact lens
wearers-Pseudomonas
 Acanthamoeba Keratitis: 2nd mc
 Also bathing in pools, hot tubs, swimming
in contaminated water
Ring shape ulcer
Most painful of all the conditions in the eye.
Pain out of proportion
Radial keratoneuritis

Bacterial Keratitis:
Risk factor: Corneal trauma
CL tear
Post refractive surgery
Mc: Staph aureus (world)
Mc: Streptococcus Pneumoniae/ pneumococcus. (India)
Ulcus serpens

Bacteria Penetrating intact corneal epithelium:

1. Corynebacterium diphtheriae
2. Neisseria gonorrhea
3. Listeria monocytogenes
4. Hemophilus aegypticus

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OPHTHALMOLOGY

Fungal Keratitis:
Mc : Fusarium/ Aspergillus
Quiet ulcers, slow growing, asymptomatic
Signs > symptoms

Predisposing factors:
1. Prolonged topical steroids
2. Organic/ vegetable matter injury
Finger like projections
Feathery margins
Satellite lesions

HSV keratitis:
Dendritic

like branches of a tree

 Dendritic epithelial ulcer

 Geographic ( enlarged) Ulcer
 It cause loss of corneal sensation
Herpes Zoster Ophthalmic/Shingles :
 Cause : Varicella -Zoster  Chickenpox
 Old people > 60 , immunocompromised - DM,
Steroid therapy
Anti-cancer drugs
Radiation
 Young Patient (< 45)  sign of HIV
 Hutchinson ‘s sign-tip of nose affected , eye will be affected
 Treatment to start in 72hrs  Acyclovir 800mg × 5 times a day for 7-
10days.
 If not- PHN
(Post Herpetic Neuralgia)

Management of corneal Ulcers:

Topical drugs only
 DOC Bacteria ulcers : 4th generation fluoroquinolones
Moxifloxacin / Gatifloxacin
 DOC for fungal ulcers : Natamicin
 DOC for viral ulcers : Acyclovir/ Famcyclovir
 DOC Acanthamoeba: PHMB/Propamidine/ Chlorhexidine
Cycloplegics for pain: Atropine /Homatropine.

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OPHTHALMOLOGY

Nonhealing ulcer:
1. Uncontrolled Diabetes (most imp)
2. Wrong diagnosis
3. Dacryocystitis
Treatment: Keratoplasty for impending perforation/ perforated ulcer.

Keratoconus :
 Progressive thinning of Central
cornea  Cone shaped bulging of Cornea.
 Risk factor: Rubbing of Eye
 Blurred vision: frequent change of glasses
 Diplopia
 High myopic astigmatism
Important signs
1. Munson ‘s Sign –indentation of lower lid

2. Fleischer’s ring Kayser Fleischer’s ring: Wilson ‘s disease

Fleischer’s ring : Keratoconus

3.Vogt’s Striae- Verical folds in corneal stroma

Hydrops: progressive thinning

ruptures Descemet’s membrane causing corneal edema

Advanced keratoconus

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OPHTHALMOLOGY
Treatment:
1. Glasses
2. RGP lens (Rigid Gas Permeable) contact lens
3. Keratoplasty
4. C3 R : Corneal Collagen Crosslinking with Riboflavin - induces collagen
bonds , stiffens cornea , no further thinning

REFRACTIVE SURGERY:
Principle – change corneal curvature
Myopia – flatten cornea
Hypermetropia – Steepen cornea
Astigmatism - does both

LASIK: Laser assisted in situ Keratomileusis

 Excimer laser
 Corneal flap with microkeratome  reshaping cornea with
excimer from underlying stromal bed  replacing the flap.
 Myopia  -10.0 D
 Hypermetropia : + 4.0D
 Astigmatism : + /-4.0 D
Absolute C/I -Keratoconus

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OPHTHALMOLOGY

ARISE MEDICAL ACADEMY 94