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 Ophthalmology

Anatomy & development of eye

Father of modern ophthalmology

Albrect Von Graefe

①
> Ablate spheroid
→ Cornea

Orbit
Base - Quadrangular

It
Shape - Conical

Eye is a eyeball roughly spherical in shape know as ablate spheroid, cystic in

consistency kept distended by intraocular pressure inside it

IOP = normal value = 11 to 21 mm of Hg

 Superior wall ( roof )
→ Base ( quadrangular shape )

Medial
Lateral
Inferior
( floor ) Mc to get fracture known as blow out fracture

Orbit ( Pyramidal / conical )

÷ . Apex

1. Medial walls are parallel to each other

2. Lateral walls are perpendicular to each other
3. Angle between medial wall & lateral wall is 45
4. Thinnest wall is medial wall
5. Thickest wall is lateral wall
6. Mc to get fracture is inferior wall

Coats / Tunics / layers

1. Outer fibrous coat Cornea = anterior 1/6th part

: Sclera. = posterior 5/6th part
Junction is called as limbus

2. Middle / vascular Uveal tract

'
t t t
Iris Ciliary body Choroid

3. Inner / Nervous Neural function Retina

Optic nerve

Ciliary body Ciliary processes

i¥i¥÷
Choroid
Limbus

Sclera
Cornea
Retina ( 10 layers )
Lens

Vitreous cavity
Optic nerve ( 1 layer )

Ciliary zonules I
R

i.
I
Posterior chamber
Anterior chamber

S
Posterior segment
Lens

Vitreous cavity

-
 Segments

v v
Anterior Posterior

Structures anterior to lense including lense Structures posterior to lense

Aqueous humor ( water like consistency ) Vitreous humor ( gel like consistency )
Water = 99.9% Water = 80%

F Amount of vitreous fliud= 4 ml ( fixed )

Anterior chamber Posterior chamber
v
r
Depth : 2.5 mm (2-3 mm) Primary = Present in Intra uterine life mainly

}
Amount of fluid = 0.25 ml Amount of fluid = 0.06 ml Secondary After birth
Tertiary

ii
Anterior Hyaloid membrane Collagen bundles

Densely attached to
posterior part of Hyaluronic acid
capsule by
circular ligament
Lens

Known as Vitreous cavity Posterior hyloidal membrane

Weigert ligament
OR
Hyloido capsular ligament Loosely attached to retina

Posterior vitreous detachment

due to ageing

Canal of cloquet

Hyaloid artery

Hyaloid artery supplies primary vitreous in Intra uterine life

Mesodermal in origin
"

III to IV months of Intra uterine life

:
Hyaloid artery starts regressing

Primary vitreous shows regression

i
New vitreous is formed ( secondary vitreous )
. Neuroectodermal in origin
At birth whole of vitreous is secondary vitreous

Canal of cloquet - doubtful existence after birth

Sometimes = PHPV ( Persistent Hyperplastic primary Vitreous ) associated with Patau syndrome

⑦
Leucocoria

✓
a
Whitish pupillary reflex

Fibrotic band

Tertiary vitreous = ciliary zonules formed by secondary vitreous = Neuroectodermal origin

 Dimensions of eyeball

23 mm

23.5 mm

Vertical Horizontal Anterior-posterior

Smallest Largest
v
u

23 mm 23.5 mm 24 mm

Volume Weight Circumference

6.5 ml 7 gm 7.5 cm

Eye at birth

< Adult eyeball retina

Small eyeball = 16.5 mm ( 70% of adult size )

Hypermetropic at birth = +2 to +3 D
Emmetropia by age of 5 to 6 years

Reflexes

1. Fixation reflex > Critical period =2-4 months

2. Macular differentiation > 4-6 months

> Central part of retina > Cones > Colour vision

3. Stereopsis / 3D perception > Starts at = 6-8 months

> Completes at = 5-7 years

Minimum age for Nursery class = 5 years

 Embryology

Development of eye

Starts at 3rd week ( day 22 ) POG ( period of gestation ) & completing at 9-10 weeks
V

8 somites

Gene responsible is PAX 6 gene

Structures
>
Neural plate
1. Optic vesicles > Neuro ectoderm
2. Lens vesicles > Surface ectoderm PLACODE
^

3. Surrounding mesenchyme > Neural crest

4. Visceral mesoderm > Mesoderm
>
Thickening > Optic pit

Neural plate

:
Thickening (Placode ) at junction of prosencephalon & diencephalon

Small depression known as optic pit

> Optic sulcus

:
Optic sulcus

Optic vesicle > Neuroectoderm

V
Elongates & grows towards surface ectoderm
Thickening known as Lens Placode
> Optic vesicle
-
.
v
-
s
Surface ectoderm
÷ Pit
=

Optic nerve
u V
=
^
÷
Sulcus

①
=
Optic
Optic stalk Vesicle ÷ r

Lens vesicle
÷
=
I =
Neuroectoderm
÷
÷

÷
÷
"

:o÷÷÷÷÷÷
-
a

Optic Lens
÷
Optic stalk Vesicle Vesicle
÷
÷
÷
÷

>
Pigmented
=
Outer layer - v

r i
'
It forms pigmented layers of > Retina

}
-

Ciliary body Pigmented epithelium

÷
>

"
'
' '
*
* I > Iris
l .
✓
Optic cup

Neuroectoderm
×
. i T
Lens
Optic stalk Vesicle
er l
aye
r ÷ . Inner layer of retina know as neurosensory retina
.

% n
Inn T 7 Secondary vitreous
.
, .

q =
= > Ciliary zonules ( tertiary vitreous )
=
T > Smooth muscles of iris
÷
 Optic cup grows superiorly and laterally over lens vesicle

Therefore it is deficient inferio nasally know as Choroidal or embryonic fissure = obliterate at Day 33-35

Failure to fuse = Cologoma ( Absence of tissue )

Typical coloboma present inferio nasally

Neural > Surrounding mesenchyme ( NC )

tube

✓ u

Outer / fibrous Inner / vascular

V V V V
Anterior Posterior Anterior Posterior

V V V v v

Cornea Sclera Iris Ciliary body Choroid

u r

Stroma Stroma
+
Ciliary muscle

Development of eye

Ectoderm Mesoderm
v v v
Surface ectoderm Neuroectoderm 1 vitreous
v
( Neural plate ) Chorio capillaries
Lens ✓ Sclera ( only temporal part )
Epithelium of conjuctiva Non
} } Blood supply
keratinised
squamous RPE Retina
Epithelium of cornea epithelium
Neuro sensory
Epithelium of lacrimal apparatus Ligaments
Optic nerve
Lacrimal gland Epithelium of ciliary body Extra ocular muscles ( 7 pairs )
Epithelium of iris Vascular endothelium of eye and orbit
2 & 3 vitreous
Smooth muscles of iris
V

Normally muscles are developed from mesoderm

Extra ocular muscles are developed from mesoderm

Neural crest
v v

Mesenchymal Neural
V
v

Orbit > bony part Schwann cells

> connective tissue
Melanocytes
Trabecular meshwork

Stroma >Cornea
> Sclera ( all except Temporal )
> Iris
> Ciliary body
> Choroid

Ciliary muscle

Corneal endothelium
 Visual acuity

Mc used - Snellen’s chart

Normal visual acvity = 6/6

Patient stands at 6 meters

6< Patient is standing at a distance of 6 meters

>
60r

Distance from which normal can read this letter

1
Minimum visual acvity recorded by snellen’s chart
60
v

Finger counting at 1 meter

Finger counting near face

Hand movement

Perception of light

v u

Positive Negative

v r

Check projection of rays Absolutely blind

Superior

Nasal Temporal

Inferior

Arc of 1 minute

T Arc of 5 minutes MAR

f
Nodal point
'

6 meter testing distance

Each letter substends angle of 5 minutes of the arc at the respective distance

Eg : 6/60 = this will make an angle of 5 minutes at 60 meters For school children and adults
6/36 = this will make an angle of 5 minutes at 36 meters 1. Snellen’s test type
2. Landolt’s test type

What is angle substended by top most letter at 6 meters For 3-5 years
Ans : 5 minutes at 60 meters 1. Illiterate E- count
hence 5 x 10 = 50 minutes of the arc at 6 meters 2. Tumbling E- test
3. Isolated hand - figure test
4. Sheridan- Gardiner HOVT test
5. Pictorial vision test
6. Broken wheel test
7. Bork candy bead test

For 1-2 years

1. Marble game test
2. Sheridan’s ball test
3. Worth’s ivory ball test

For infants
1. Optokinetic nystagmus test
2. Preferential looking test
3. Visually evoked response
4. Catford drum test
5. Indirect assessment- Blink reflex, Menace reflex
 Lens

Avascularity Biconvex shape Crystalline nature

Lens gets nutrition from Aqueous humor Bioconvex in adults But Spherical at birth Crystallins : It contains sequestered antigens

V V v

Alpha Beta Gamma

Largest size MC = 55%

HMW ( High Molecular Weight proteins )

1 2 3 4

Water soluble Water insoluble

Increased in cataract

Structure of lens

Anterior pole ' Anterior surface ( less curved )

More radius of curvature = 10 mm

Anterio posterior thickness

3.5 - 5 mm
Equatorial diameter
9-10 mm ⇐ Equator

. Ciliary zonules
. Posterior surface ( more curved
Posterior pole
Less radius of curvature = 6 mm

Power of the eyeball Refractive index

60D
> Cortex ( surface ) > 1.39
✓

Cornea Lens
2/3rd 1/3rd
N
43-45D > Nucleus ( centre ) 1.42
15-17D y

Lens structure

1. Lens capsule : thickest basement membrane in body

l
Pre equatorial areas (4) - maximum thickness = 22-23 um

: .
Minimum thickness = posterior pole = 4 um

2. Anterior epithelium

Posterior side

÷÷÷÷÷ ÷
Single layer of cuboidal cells which
Lens cavity

Lens
becomes columnar at the equator
Vesicle

Anterior side
÷ . :
Actively dividing throughout life

Secondary lens fibers.

Cells of posterior epithelium
.

No part of epithelium after birth

Primary lens fibres
 3. No posterior epithelium

4. lense fibers > Primary > Embryonic nucleus 0 - 3 months of IUL

> Secondary > Fetal nucleus 3 months to birth

✓
> Infantile nucleus Birth to puberty
> Adult nucleus After puberty u

>

Cortex
>
>
>

Lens
v v

Nucleus Cortex
v v

Contain oldest cells Youngest cells

Metabolically inert Metabolically active

Lense
H2O
65% = water 3Na+ This causes relative dehydration
34% = proteins H2O
1% = lipids
Nucleus

Helps to maintain transparency

+
2K

Ageing
V

Decrease efficiency of Na+/ K+ATPase pump

Water will retain inside cortex

Over hydration in cortex

Denaturation of cortex proteins ( crystalline proteins )

Opacification known as cataract

Lens metabolism Factors maintaining lens transparency

V

Mainly anaerobic type 1. Avascularity

80% - O2 glycolysis 2. Crystallins

v
3. Relative dehydration in the lens ( Na+-K+pump )
v

Lactic acid Free radicle 4. MIP-26 ( Major Intrinsic Protein ) - Basic role in lens transparency
v u

Diffuse in aqueous humor Ageing

v r

Provide lens nutrition Cataract

To prevent cataract

:
Antioxidative mechanism

Consists of B Caratinoids ( precursors of Vit A )

+ Vit B, C, E
Catalase
+ 3 Enzymes > SOD ( super oxide dismutase )
Glutathione peroxidase

Transport of Vit C / ascorbate in lens

Myoinositol phosphate ( MIP )

 Cataract

MC cause of blindness - 70 in India & 50% in world

Cataract
v v

Congenital/ developmental Acquired - MC

Causes
:
Senile / Age related - MC

1. Idiopathic - about 1/3 cases Cortical - MC

2. Genetic - Autosomal dominant V

3. Known causes - 1/3rd cases Cuneiform - MC

v v

Maternal Fatal
v v v v

1. Infections : TORCH group = Toxoplasma, Other, Rubella, CMV, HSV A B C

V

Leucocoria in neonate
V V

V Anoxia/ Hypoxia Birth trauma Congenital or metabolic disorders

White
L J

Pupil Test V V v

Whitish pupillary reflex v

Eg : RDS Eg: Operative Eg: 1. Lowe’s syndrome
Serum Ab titres intervention u

With H/O fever and rashes in mother Occulo cerebro renal disease

during antenatal period 2. Galactocemia

2. Mal-nutrition > Especially Vitamins and Minerals

3. Drugs = Thalidomide & Steroids

4. Radiational exposure : X-Rays ( most cataractogenic )

Types of congenital/ developmental cataract

1. MC congenital/ developmental cataract = Blue dot / punctate

-

,
"

"
"

"
" "

J Not visually significant

I

2. MC congenital cataract which is visually significant = Zonular / Lamellar cataract

V

Etiology > Autosomal dominant

> Hypocalcemia / def of Vit D
>
Meternal Rubella especially in 7-8th week of gestation

Resemble spokes of wheel known as Riders

:
3. Total congenital cataract

Congenital Rubella syndrome TRIAD

v v v

Eye Heart Ear

v S

1. Congenital cataract L
MC : PDA Sensory neural hearing loss
(MC - Nuclear pearly ) Ventricular septal defect
2. Salt & paper retinitis Pulmonic stenosis
3. Microphthalmos ASD is not seen
 Morphological cataract

> 1.Capsular > Anterior

> Posterior

2. Subcapsular Anterior ( ASC )

"Posterior ( PSC )
>

3. Cortical > Anterior

'
>

Posterior A. Visually most handicapping type of cataract

: Peripheral ( coronary ) B. MC morphology in other acquired cataract
. .
t
4. Nuclear L 6. Polar > Anterior
> Posterior > Shows onion ring pattern
L S Associated with y Posterior lenticonus
5. Supranuclear / Lamellar PHPV
; Persistence of Hyaloid remnants

Anterior polar cataract can lead to opacification beneath it with

Hk clear area in between known as Reduplicating cataract

Acquired cataract

Senile cataract : MC
Age >60 years
Male = Female > Slightly Mc in females

Risk factors
1. Hereditary
2. UV rays : Welding areas
3. Smoking : more cyanates
4. Mal-nutrition : lower socioeconomic status
5. Dehydrational crisis : Nuclear cataract
Ageing
Dehydration
>Yellow pigment
o
Due t
>
✓

Hardening of nucleus known as nuclear sclerosis > Eg : Urochrome

Due to
✓
> Deposition of pigments in nucleus
n
Increase in Refractive index of centre of nucleus
amino acid metabolism Eg: Tryptophan
u >
n
Progressive index myopia
lens protein breakdown

:
Improvement of near vision

Can be able to read near print event without near glasses

Known as second sight

+
Diminition of vision for distant objects

v r

Day light Dim light

° '
Pupil constricted
f
%
Pupils dilated

s÷
. : s÷ .
.
:
Central opacity
Clumsy vision more in day time p
Known as day blindness
 Cortical cataract
✓ v

A. Cuneiform cataract >

MC in senile cataract B. Cupuliform cataract s MC in other acquired cataract
v
Posterior subcapsular cataract
Form periphery towards centre
^ Starting from centre of posterior
cortex towards equator

N N BB
"

Central part is affected

L
v

- Day blindness
Mostly peripheral part is involved - Early loss of vision

Night blindness

Symptoms of cataract
i

1. Earliest : Glare = Light sensitivity Intolerance to bright light

v

Not photophobia ( fear of light )

2. MC presenting feature : Frequent change of distant glasses

Increase in Refractive Index in nuclear sclerosis: Myopia

Cortical cataract : over hydration > Softening

:
Decrease in Refractive Index

Hypermetropia

Myopia -
-
Hypermetropia L

3. Uniocular polyopia
V V

One Many Not diplopia

>

Eye Images >

Cataracted eye > Due to uneven opacification

v
Feature of early cataract / Incipient cataract

4. Coloured haloes
> Rings

D/d > Cataract s Due to water droplets s Scattering of white light 7 Coloured halos
> Acute congestive glaucoma
> Acute muco purulent conjunctivitis

5. Diminition of vision or loss of vision

V
Gradual, painless, progressive
> D/d : Cataract
Primary open angle glaucoma

Grades of Nuclear sclerosis

I - Greyish
II - Light yellow
III - Amber / golden yellow
IV - Brown / Cataracta Brunescens
V - Black ( Cataracta nigra )
✓

Red ( Cataracta Rubra )

 Maturation of cortical cataract

1. Formation of vacuoles
2. Lamellar separation } Glare

3. Early or incipient cataract : uneven opacification

Uniocular polyopia
4. IMSC / Immature senile cataract
-

Partial opacification
Colour of the cataract : Greyish white
Presence of iris shadow : clear cortex present
Oblique light
:# u

Formation of iris shadow

c- → .
Shadow of iris on IMSC seen through clear cortex
- -

-sBos£

Swollen lens in IMSC

Woo

i i.
Normal outflow
.
ii Obstruction in aqueous outflow

:
Increase in intraocular pressure

Phaco morphic glaucoma

L
Lens s
Morphology

5. MSC / Mature senile cataract

V

Total opacification ( no clear cortex )

No iris shadow present

Also called ripe cataract or Stage 4 cataract
Diminition of vision
Pearly cataract ( motiya Bind )

6. Hyper mature senile cataract

Chalky white or milky white

v v

Morgagnian Sclerotic

:
Lysis of cortex proteins with intact capsule

i fi i i
-
Trabecular meshwork Passing through the capsule into aqueous humor
g
in

90% outflow
ak

:
Le

Blocking trabecular meshwork

Posterior chamber
Anterior chamber

Decrease in aqueous outflow

÷ Phaco lytic glaucoma or lens protein glaucoma

 B. Sclerotic hyper mature senile cataract

Disintegration of cortex ( fluid comes out )

Shrinkage of lens

:
Degeneration of ciliary zonules
Also we have Iridodonesis
Subluxation of lens ( partial displacement ) ✓

✓
> Also known as Phacodonesis ( trembling of lens ) v
Shivering/ trembling of iris
Anterior subluxation Posterior subluxation

v u

Displace into anti chamber Dissolve into vitreous cavity

v v

Block aqueous outflow No glaucoma

Glaucoma known as Phaco topic Glaucoma

Lens c > Position

Other acquired cataract

1. Traumatic cataract
v r

MC: blunt trauma Penetrating trauma

v u

Rosette cataract Sunflower cataract

Star shaped

2. Complicated cataract
Occurring as a complication of ocular disease
1. MC : Chronic anterior uveitis
2. High myopia
3. Retinitis pigmentosa
4. Primary and secondary glaucoma MC morphology : PSC >posterior capsular
5. Intra ocular tumors

2 important features

v
✓

Poly chromatic lusters Bread crumb appearance

V
Many L
Colour
J
Shining reflexes V

V Granular appearance
Know as Rainbow cataract

3. Metabolic cataract
A. MC : Diabetic cataract
-

v r

Pre senile : MC True metabolic ( rate but specific )

v r

Senile cataract at younger age ( 50 years ) Due to enzyme : Aldol reductase

v g
Etiology DM - glycemic and products > Sorbitol pathway
-
S Diabetic V

> Atopic dermatitis Snow flare cataract

> Myotonica dystrophica
 B. Galactocemia
Inborn error of galactose metabolism
v v

Classical galactocemia Non classical

i v

Due to deficiency of Gal-1-phosphate uridyl transferase Due to deficiency of Galactokinase

v u

Oil droplets cataract Lamellar cataract

+
Systemic features
>
Due to cerebral hypoglycaemia
V
Leucocoria with convulsions, diarrhea,
vomiting ( intolerance ), failure to thrive,
hepatospleenomegaly

C. Wilson’s disease
Inborn error of copper metabolism
Associated with hepato lenticular degeneration
Low levels of ceruloplasmin which then lead to Charcosis ( copper deposition in alloy form )
v

Sunflower cataract

MC ocular feature of Wilson’s disease : K F ring (Kayser Fleicher ring)

Deposition in descements membrane of cornea
Golden brown in colour seen through cobalt blue filter ( slit lamp)
Reversible on treatment with D- pencillamine

f
'
First occurs in superior and inferior
quadrants and later forms ring

Associated with patients having neurological involvement : 95-100 %

Also associated with hepatic involvement : 65%

Only reversible cataract : Galactocemic cataract

> Sunflower cataract is not reversible but K F ring is reversible

4. Electric cataract > Sustained electric current = Punctuate opacities in lens

5. Radiational cataract
X rays
Neutrons
UV rays
Gamma rays
IR rays > Glad Blower’s cataract
Ionising > non ionising
MRI - no radiation exposure

6. Toxic/ drug induced

Anticholinesterase, allopurinol, amiodarone > Anterior subcapsular cataract
Busulphan GTCS
n n
Topical - Glaucoma
Corticosteroids ( posterior subcapsular cataract ) Systemic - cataract

Chlorambucil, chalcosis ( copper deposition )

v

Sunflower cataract ( anterior subcapsular cataract )

Chlorpromazine (anti psychotic ) > anterior subcapsular cataract

Deposition of iron ( siderosis ), gold ( rheumatoid arthritis )
 7. Dermatogenic cataract > MC atopic dermatitis
,

Atopic cataract
or
Shield cataract

Osseous cataract
Eg: Pagget’s disease of bone

Dystrophica myotonica Also associated with 1. Pre senile cataract

;2. Frontal baldness
'

"

Christmas tree cataract s Posterior subcapsular cataract

, Polychromatic needle opacities

Treatment of cataract

Cataract extraction with PCIOL implantation

u '

Aphacia ( absence of lens ) Decreases power by 15-17 D

Hypermetropia ( power approx 40D )

Intra ocular lens = Pseudophacia

:
:
Anterior chamber Posterior chamber
ACIOL

ACIOL PCIOL

PCIOL ( ciliary sulcus )

PCIOL ( capsular bag )

Best site

Techniques of surgery

1. ICCE : Intra capsular cataract extraction

Oldest, now obsolete

.
Posterior capsule is also removed
> Ciliary zonules should be weakened
,

No PCIOL is not possible

Incision size : 10-12 mm

Only indication now a days : subluxation of lens

2. ECCE : Extra capsular cataract extraction

Posterior capsule is not removed >

y IOL : In the bag implantation

Remove anterior capsule + lens

 > Haptics

(
Dialing holes: for central fixation
> IOL dialer
<
> Optic ( lens for refraction )

Incision : 7-8 mm

> Interrupted radial sutures

3. SICS : small incision cataract surgery

:
ECCE via small incision ( 5.5-7 mm )

Manually

A corneo scleral tunnel is made

4. Phaco emulsification > Most advanced technique

>
Dissolution of lens particles in irrigating solution

45 O

Small incision : 3-3.5 mm ( by keratome or crescent knife )

>
>
Phacoemulsification

15
u
o

Side port entry : side port blade >

>
Irrigation and aspiration of cortical matter

> Titanium needle > Diameter 1 mm

or Vibrating at 40,000-60,000 per second

Phaco probe Due to piezo electric crystal in Phaco probe
v

Emmits the ultra sonic waves

Phaco machine
 Steps of surgery

1. Incisions Main

i .

Side outer

2. AC entry

3. Anterior capsulectomy > trypan blue dye is used

v u

Circular curvilinear capsulorrhexis Can opener technique

÷
Preferred

4. Side port — Irrigation

Best irrigating solution : basal salt solution with glutathione

5. Hydro dissection : separating capsule from the cortex

6. Hydro delineation : Separating Epi nucleus from endo nucleus

Required when there is high grade of nuclear sclerosis
not always required

7. Phaco emulsification

8. Irrigation and aspiration of residual cortex

9. IOL entry

10. Sutures : depends on type of surgery

2 advances in Phaco emulsification technique

1. Micro incision technique - < 2 mm

2. Phaco NIT - needle incision technique

Titanium needle = 1 mm
1 mm incision

FLACS - Awaited

Femto second laser assisted cataract surgery

Wavelength = 1053 nm
Baseless and sutureless

Cornea Sclera

it
Power of IOL Calculated by Biometer
Calculated by keratometer

:
1. SRK formula P = A - 2.5L - 0.9K Corneal curvature
Power .
.
.
:
Axial length
IOL constant
Calculated by A Scan ultrasound
Amplitude (1-D USG )

2. SRK II formula for very high axial length

 Materials of IOL

1. Normal, rigid ( 1 piece ) IOL — used for ECCE, SICS,

V

Made up of PMMA ( poly methoxy metha acrylate )

2. Foldable IOL — used for Phaco emulsification

V

Made up of acrylic, silicone

3. Rollable/ ultra thin IOL’s — made up of hydro gel

I
✓ v

Hydro phobic Hydrophilic

> Most commonly used

Complications of surgery

v ✓

Intra operative
Post operative > Early

. Late
2.
5m
m

El
5 .

J
1. Corneal injury
V

6 layers of cornea

A B C Pre D D E

Anterior epithelium Bowman’s membrane Connective tissue stroma Pre descements membrane descements membrane Endothelium

Most prone to trauma as it is always remain in state of tension

Due to trauma

:
Recoiling of descements membrane

Known as descements stripping/ descements membrane detachment

2. Injury to iris Iridodialysis D shaped pupil

÷
Iris Detachment from its root

Root of iris

y Margins of iris

±
3. PCR - Posterior capsular rupture — most severe Intra operative complication

"
1. No PCIOL

2. IOL drop of lens drop

"

First step — stop the surgery

÷
Refer to Vitreo retinal surgeon

Vitrectomy

¥i¥¥
ACIOL implantation Rupture of posterior capsule

3. Vitreous loss

In patients of
4. Expulsive choroidal haemorrhage Uncontrolled hypertension
, Heart disease
✓

Due to rupture of posterior ciliary artery , Short

> Long

2. Early post operative Complications

1. Hyphema - MC : blood in anterior chamber

2. Iris prolapse due to high Intra ocular pressure

:
Change the shape of pupil
o
Peaked pupil ⇐
'

.
hi
To reduce the complication anti glaucoma drugs are given
Eg : Acetazolamide
250mg x 2 H/S
2 tablet x morning

3. Striate keratitis
✓
7 Corneal inflammation
Deeper layers

4. Flat anterior chamber : collapse of anterior chamber due to no acquired humor

*
1. Ciliochoroidal detachment

: 2. Pupil block

JJ >
3. Wound lead

5 .
 5. Bacterial endopthalmosis : most severe complication ( overall )

Risk : 0.2- 0.5%

Maximum risk from parents own flora
Best prophylaxis - single drop of 5% Povidone Iodine

Etiology

V V

Early onset ( < 3 weeks ) Late onset ( >3 weeks )

Mc < 7 days
Especially first 48-72 hours
V

:
Staphylococcus epidermidis Proipionebacterium acenes

Previously - trimming of eyelashes

3. Late post operative complications

1. MC - PCO - posterior capsular opacification due to proliferation of LEC ( lens epithelial cells ) ( equatorial cells of anterior epithelium. )

Diminition of vision

Therefore know as after cataract or secondary cataract

v u

Sommering’s Ring cataract Elsching’s Pearl cataract

> Vacuolated cells

It is same - laser posterior capsulectomy

Opening
> Opening in posterior capsule >
my
Na: YAG > Neodymium Yettrium Aluminium Garnet lw'
1064 nm
MOA : Photo disruption

2. CME - cystoid macular edema in pseudophacia

Known as Irvine-Gass syndrome

3. Vitreous touch syndrome - bullous keratopathy is occurring due to virus loss

Occur in corneal endothelium

4. Glaucoma

5. IOL related complications

A. UGH Syndrome due to ACIOL

L V J

Uveitis Glaucoma Hyphema

7
7

B. Toxic lens syndrome : door to ethylene gas used in sterilisation of IOL

 C. Subluxation/ displacement of IOL
Superior - sun rise syndrome
Inferior - Sun set syndrome
Total - lost lens syndrome

6. Retinal detachment : specially in children due to the dense Adhesion

Aspirate lens Traction on Weigert’s ligament ' Anterior Hyaloid membrane

t¥
:
Vitreous gel

Posterior Hyaloid membrane

Retina

Renal detachment

Treatment of congenital cataract

1. Timing of surgery

÷
Unilateral dense cataract Bilateral dense cataract

Urgent surgery Early surgery within 4-6 weeks of life

Because high risk of amblyopia ( lazy eye ) Before development of fixation reflex
(2-4 months of 8-16 weeks )
Anisotropic amblyopia
Stimulus deprivation amblyopia

2. Technique of surgery

A. Lensectomy / lens aspiration/ Phaco aspiration . Risk of retinal detachment

B. Theodore better is lensectomy with anterior vitrectomy

.

Remove the vitreous Adhesion before lensectomy

3. ECCE with PCIOL ( preferably > 2 years of age )

Full development of eye: after 5-7 years

Done along with prophylactic posterior capsulotomy

Known as primary posterior capsulotomy due to high risk of PCO
4. Power of IOL
Under correction is done to negate myopic shift

Hypermetropia at birth > Emmetropic at 5-7 years

1. Under correction by 20% if age is < 2 years

2. Under correction by 10% if age is 2-8 years
3. Full correction after 8 years

Congenital anomalies

1. MC : Ectopia lentis > Abnormal position of lens

MC cause of subluxation - trauma

MC congenital anomaly associated with Ectopia lentis : A. Marfan’s syndrome (AD )

L s
Superio temporal subluxation Aortic regurgitation

B. Homocysteinuria (AR ) > Inferionasal subluxation

C. Ehler- Danlos syndrome > Subluxation + blue sclera

D. Weil- Marchesani syndrome

Micro sphero Phacia > Small spherical lens

+
Short and stout fingers
+
Short stature

2. Coloboma of lens > Absence of lens tissue

v

Usually present unilaterally and on inferior side

3. Lenticonus > Conical protrusion of lens

v v

Anterior Posterior

u v

Alpert syndrome Lowe’s syndrome

Alport syndrome: Anterior is more common than posterior

 Uveal tract
V

Middle vascular coat of eyeball

v r v

Iris Ciliary body Choroid

Most vascular part
Normal colour: Dark brown Basal lamina : known as Bruch’s membrane
Structure : collaratte pattern -
( resemble spokes of wheel appearance ) Remains in contact with outermost layer of retina (RPE )

:-.
Pars plicata

Rough anterior part

Pars plana

Smooth posterior part

Blood supply

:
Major arterial circle
:
Minor arterial circle

Present at root of iris Present at pupillary border

MC source of bleeding in
Traumatic hyphema

Venous drainage

Cortex veins
Superonasal

+
Superotemporal

Involved in malignancy
Eg: malignant melanoma of choroid

Infero nasal
X Infero temporal

Uveitis

Inflammation of uveal tract

MC etiology : allergic/ autoimmune
Not infectious

Types - Anatomical classification

V V ✓

Anterior Intermediate Posterior

:
Iris + pars plicata
:
Pars plana
:
choroid + retina

Iridocyclitis Pars planitis Chorioretinitis

Pan uveitis : while uveal tract is involved

 Anterior uveitis
Anterior uveitis Ciliary muscles spasm

i÷i
Induced myopia Blurred vision

÷÷i÷
'

Pain and redness

Clinical features : Sudden painful diminition of vision ( for cataract : gradual painless diminition of vision )
r n

t
Door to ciliary muscle spasm

Signs

1. Earliest sign : Aqueous flare/ turbidity

Due to protein deposits

eiiisiiii
÷
Aqueous cells present
I
R
I
Posterior chamber
Anterior chamber

Anterior chamber Hyphema Blood

: Hypopyon
: Pus

2. Most important sign: KP’s ( Keratic precipitate )

Inflammatory cells deposited on posterior surface of cornea in base down triangular fashion

Known as Artt’s triangle

Keratic precipitates
f v

Small pigmented Mutton fat

v u
Lymphocytes Macrophages

v v

Non granulomatous disease Granulomatous disease

Keratic precipitation : corneal opacity : Blurring of vision

3. Pupil : small constricted, fixed, can be irregular due to adhesions

If
Atropine >
Known as festooned pupil
% .

Relative deep anterior chamber

 4. Circumflex corneal congestion / deep ciliary injection

It
Not blanched by phenylephrine

± .
E
'
is
5. Iris : colour changes to muddy brown change in the normal structure

Iris nodules - Topical granulomatous uveitis

D/D
v v

Busacca nodules Koeppe nodules 1. Lisch nodules — NF-1 ( Iris hamartoma )

v
2. Iris pulse — leprosy
v

Base of the iris of the mid periphery At pupillary border 3. Brush field spots — Down’s syndrome

Rubeosis iridis — Neovascularisation over iris

Posterior synechiae > Between iris and lens

w.r.t. to iris ( g Adhesions

Types - 3
1. Segmental synechiae 2. Angular/ Ring synechiae 3. Total synechiae

v tr
u
Pupillary margin
Adhesions present in few areas
>

w Total Adhesion of iris to lens

u
✓

Ili Ili
Degeneration of ciliary epithelium
.

No/ Aqueous formation

.

v
No glaucoma

tf
L

Pupils
Posterior chamber

. Aqueous
v collection
Irregular behind the
Anterior chamber

¥ iris

Tf
Posterior chamber

Hii
-

Push the iris anteriorly

J
N
*

U
.¥
- Posterior chamber

Iris bombe formation

Posterior chamber

f)| Anterior chamber

a
Anterior chamber

. 7

uh
Posterior chamber

ed
e at
t r
Posterior chamber

un
.

ft
No glaucoma Le
"
.

V
Peripheral anterior synechiae
\ s

.my Iridiocorneal contact v

Adhesion between iris and cornea

✓
Sudden closure of angle of anterior chamber ✓

Synechial angle closure glaucoma

✓

Acute congestive glaucoma .

Known as Chronic congestive glaucoma

 6. Lens changes

Complicated cataract ( Rainbow cataract )

- Exudates
- pigments

Treatment
Ciliary spasm
V

1. Mydriatics and cycloplegics

Dilated pupil C > Paralyses ciliary muscles

MOA: 1. Relieve ciliary spasm

2. Breaks posterior synechiae
3. Prevent posterior synechiae

Treatment of choice : mydriatics and cycloplegics > steroids

2. Topical steroids
MOA : 1. Anti inflammatory
2. Anti allergic
3. Anti fibrotic

Steroids are given for short period because

Topical steroids cause glaucoma
Systemic steroids cause cataract

3. NSAID’s : to relieve pain

4. Hot fomentation > Dry heat

> Wet heat

Antibiotics are not mandatory

Complications of anterior uveitis

MC complication of air uveitis — cataract
MC complication of recurrent uveitis — glaucoma

:
Inflammatory cells in trabecular meshwork — 90% drainage

Acute inflammatory glaucoma

:
Recurrent cases

Ring synechiae

:
Acute congestive glaucoma

Chronic congestion glaucoma

Treatment — Steroids
In steps responders
 Intermediate uveitis Pars planitis

Painless condition

i÷÷¥¥
BBB , Vitritis Floaters ' Black spots

:
Blurred vision

CME ( Cystoid Macular Edema )

Diminition of vision

Signs

Snow ball opacities & snow banking

'

-
-
Settled at periphery

Di ①
Clumps of due to gravity
exudates in
vitreous cavity

D/D of snow banking

Candidiasis
Sarcoidosis
Ocular toxocariasis
Multiple sclerosis

Treatment
Treatment of choice — Steroids

Kaplan stepladder approach

Peri ocular steroids

Posterior subtenon injection

:
Systemic steroids

Immunosuppressive drugs

:
Laser PC ( Photo- Coaggulation ) or cryotherapy ( vitreous cavity )

PPV Pars plana vitrectomy

 Posterior uveitis/ Chorioretinitis

Painless condition

ei÷÷÷
÷i÷÷÷i÷÷
Choroiditis

gift No image in this area — scotoma

Retinitis

Vitritis

Optic neuritis

-
Clinical features
1. Vitritis Floaters
: Blurring of vision

2. Retinitis ( neural tissue ) Photopsia - flashes of light in front of the eye

÷ Micropsia or macropsia
Metamorphopsia - distorted images - due to macular involvement

3. Choroiditis - positive scotoma

Can be appreciated L ) Blind spot

-
Vacuum > Blind spot > Negative

Test for positive scotoma

Amsler grid test ( macular function test )

> Positive scotoma

> Fixation point

•a•

, 400 squares

5 mm x 5 mm

4. Optic neuritis

Treatment
Treatment of choice - Systemic steroids
 Acute anterior uveitis with Arthritis

1. Ankylating spondylitis HLA B27 - positive

2. Reiter’s syndrome
I

> Spine — Lower back pain

>
Triad > Urethritis
> Arthritis +- Uveitis
>
Conjunctivitis

History of > Tour

> GIT infection with Shigella

3. Psoriatic arthritis

4. Inflammatory bowel disease > Ulcerative colitis

> Crohn’s disease

5. Juvenile chronic arthritis/ juvenile rheumatic arthritis

v v

< 16 years Rheumatoid factors always negative

v v v

Pauciarticular Poly articular Still’s disease

V V V

Few or less than 5 joints More than or equal to 5 joints Systemic features
V Eg : hepatospleenomegaly
V V ANA +ve V

Type I
'
Type II ANA +ve
ANA = Anti Nuclear antibody
r u

ANA +ve ANA -ve

Sero positive Sero negative

Chronic anterior uveitis v

Acute anterior uveitis/ Iridocyclitis

Systemic diseases

1. Sarcoidosis > Granulomatous, pan uveitis

:
Most imp- Pars planitis

Snow banking

Etiology : Retinal periphlebitis

Peripheral Inflammation of veins

:
Pouring of exudates in vitreous cavity

:
Known as candle wax dropping

Pre retinal nodules

( Lander’s sign )

Gland involvement : most imp > Lacrimal gland

Mikulicz’s syndrome
> Salivary gland
 2. Behcet’s syndrome > Granulomatous pan uveitis
> HLA B5 +ve v

Most imp is non granulomatous Acute anterior uveitis

Triad : > Oral ulcers ( Aphthous ulcers ) : very painful

> Genital ulcers
> Uveitis

3. Toxoplasmosis ( TORCH ) > Granulomatous pan uveitis

#

v v

Congenital Acquired

Triad > Hydrocephalus ( convulsions ) Typical appearance in posterior uveitis

> Chorioretinitis
v

> Intra cranial calcification Head light in fog appearance

Patch of choroiditis > Vitritis

Early macular involvement : early diminition of vision

Most common cause of posterior uveitis in India

4. VKH syndrome — Vigo Koyanagi Horada

4 organs involved

V V u
v

C O N E
v V V V

Cutaneous Ocular Neurological Ear

v v Uveitis > Meningism s

Sensory neural hearing loss
Hyper pigmentation Hypo pigmentation > Neuropathies > Tinnitus

Vitiligo

5. FUS ( Fuch uveitis Syndrome ) Fuch Heterochromic Iridocyclitis

Female, unilateral
Grey, stellate ( star shaped ), KP’s
Rubiosis iridis
Patches of iris atropy
Secondary glaucoma ( inflammatory )
Complicated cataract
Posterior synechiae always absent

Treatment
Steroids

6. Posner Schlossman Syndrome Glacomatous cyclitic crisis

Males, unilateral attacks of increased Intra ocular pressure due to the trabeculitis
No congestion > Therefore eye is white
No posterior synechiae
 7. Sympthetic ophthalmitis

Bilateral granulomatous pan uveitis due to trauma ( penetrating/ perforating ) of ciliary body ( knowns as dangerous area of eye )
V

Penetrating wound : only entry wound present

Perforating wound : Entry + exit wound present

MC etiology : Allergic origin > Uncovering of the hidden antigens

:
Formation of immune complexes

Inflammation of eye

Sympathising eye
>
^

w eeks
Trauma eye 4-8
Known as
Exciting eye > Other eye

Symptoms : Earliest > Photophobia

> Transient weakening of accommodation ( ciliary muscles )

Signs : Earliest > Retro lental flare

Most imp > Dalen Fuch Nodules

Treatment
It is rare but serious
1. Meticulous repair of perforation
2. Steroids ( contraindicated in perforations) > Doc
3. Assess visual acuity in exciting eye

Hope of useful vision

v u

No Yes

v r

Enucleation Continue medical treatment

Within 2 weeks

Removal of the eyeball + part of optic nerve

Congenital anomalies

MC : Coloboma

Defect in closure of embryonic fissure

Absence of tissue

v u

Mc inferionasal quadrant Other 3 quadrants

v r

Typical Coloboma Atypical Coloboma

ST SN

8.6
IT IN
 Glaucoma

Multifactorial optic neuropathy characterised by the retinal ganglionial cell death by apoptosis

Normal IOP = 11 - 21 mm of Hg
IOP
^

At least 2 should be present to call it Glaucoma

Triad
Optic disc changes Visual field defects

If IOP, But no Optic disc changes

: : Visual field defects Ocular hypertension

>30 mm of Hg

Ocular hypertension with high risk factors > Only needs to be treated
Otherwise only screening ( follow up )

If we have optic disc changes and visual field defects with normal or low IOP > Normal/ Low tension glaucoma

Pathophysiology
^
IOP ( due to more aqueous humor )

v v

More formation Less drainage

i*i÷¥
Periphery of retina Peripheral diminition of vision

:
I
R : Night blindness
I
Posterior chamber

.
Anterior chamber

Aqueous humor S
Lens

99.9% water
RI : 1.33 Optic neuritis
pH : 7-7.5
0.01% solutes

Structures

1. Ciliary body 2. Angle of anterior chamber 3. Aqueous outflow

'
Site of production of aqueous formation

me
-

Pars plana
:
Pars plicata Diurnal variation of IOP

Ciliary processes (70-80) <

IOP morning > IOP evening
w Normal variation = 5 mm Hg
Non pigmentation epithelial cells Suspicious of glaucoma = 5-8 mm Hg
Diagnostic = > 8 mm Hg

!
-0
P Receptors c
p Blockers

Aqueous formation ( 2-3 ul/min )

✓

By. Diffusion
,

Secretion ( most imp )

i Ultra filtration
Enzyme : carbonic anhydrase to CA inhibitor
 2. Angle of anterior chamber

A. Root of iris B. Ciliary body band C. Scleral spur D. Trabecular meshwork E. Schwalbe’s line
v v

Projection Sieve like v

Prominent end of descements membrane of cornea

Angle is visualised by Gonioscope ( slit lamp )

v r

3 mirror 4 mirror ( handle )

D. Trabecular meshwork
A. Root of iris

:
E. Schwalbe’s line '

B. Ciliary body band

C. Scleral spur

Pupillary margin

If all structures are visible on gonioscopy - Open angle > Open angle glaucoma
If no structures are visible on Gonioscopy - Closed angle > Angle closure glaucoma

Shaffer’s classification ( based on gonioscopic findings )

Grades No of structures visible

IV 4 - CCB, SS, TM, SL - Open angle

III 3 - SS, TM, SL - Mild closure

II 2 - TM & SL - moderate closure

I 1 - SL only - Severe closure

0 No structures visible - Total closure

3. Aqueous outflow system

v v

Trabecular outflow system 90% Uveoscleral outflow system 10%

Starts with trabecular meshwork Ciliary body

( max resistance at just juxta canalicular meshwork ) v
u

Near schlemn’s canal Supra choroidal circulation

u Venous route
Schlemn’s canal ( oval )
Lined by endothelial cells L v s

Ciliary body Choroid Sclera

:<
Aqueous vein

Episcleral veins Inflammatory cells - inflammatory glaucoma

> Pigmented cells - pigmentory glaucoma
'
Episcleral vein
Aqueous vein TF Schlemn’s canal
Lens proteins - Phacolytic glaucoma

, Trabecular meshwork Capsule proteins - Phacotoxic glaucoma

¥*±
>

Trabecular block y r .

Glaucoma
Open angle glaucoma
 Classification of glaucoma

V
v

Congenital glaucoma Acquired glaucoma

re

v
v

Primary No known cause Secondary Cause is known

v v

Open angle Angle closure Open angle Angle closure

v v v v

POAG PACG SOAG SACG

> Most common

Congenital glaucoma

3 types
1. True congenital glaucoma : Present since birth ^
IOP
2. Infantile glaucoma : Present since Birth - 3 years of age <3 years
3. Juvenile glaucoma : Present since 3-16 years of age

:
Low scleral rigidity

Size of the eyeball

^

Buphthalmos >
Bilateral
Bull like eye/Big size eye MC in boys
> Autosomal recessive Blue baby boy
Etiology : malformation in angle of anterior chamber

v u

Concave iris insertion Flat iris insertion

Barkan’s membrane

Clinical features > Triad 7

BilateralC

L v

B P L 7

V
L S

Blepharospasm Photophobia Lacrimation

V
v v

Lid Earliest sign Most common

Non specific

2. Corneal edema due to IOP = Haziness known as Frosted Glass appearance ( earliest + specific )
^

3. Size of cornea (>13 mm ) = Diagnostic

^

Normal size at birth = 10 mm >

Spherical
Adult = 11.7 x 11 mm > Elliptical

4. Haab’s striae : Horizontal striations due to rupture of Descement membrane of cornea

5. Blue sclera : Due to stretching of eyeball
>
6. Backwards subluxation of the lens
7. Deep anterior chamber
8. Optic disc changes
9. Axial length of eyeball = patient will develop axial myopia
^

Asymmetrical

Anisometropia
: > Amblyopia Lazy eye

10. IOP ( only Mild ) ( due to increased size of eyeball )

^
 Treatment
Surgery

u v

Clear cornea Hazy cornea

v
v

TOC : Goniotomy Trabeculotomy

Opening in trabecular meshwork at opening in schlemn’s canal

If fails
v

Trabeculectomy
Fistula between anterior chamber and sub conjunctival space
Filtration surgery

Now a days combined trabeculotomy + trabeculectomy is done

Primary open angle glaucoma Chronic simple glaucoma

No known cause < > Trabecular block v

s No congestion
Gradual diminition of vision D/d : Cataract
v

Painless

Risk factors
1. Age >60 years, male = female
2. Hereditary, Genes > Optineurin Chromosome no 1
> Myocillin .

3. Diabetes, hypertension, thyrotoxicosis

4. Myopia ( deeper anterior chamber )
5. Cigarette smoking
6. Retinal vascular diseases

Etiology
1. Trabecular sclerosis = Thickening of trabecular spaces

:
Decrease in aqueous outflow

Increase in IOP

Symptoms
1. MC : frequent changes in reading glasses ( near vision changes )

IOP = ciliary muscle spasm = Defect in accommodation

^

:
Problem in near vision

Frequent change in near glasses

2. Defect in dark adaptation : because rods are affected D/d : night blindness
3. Tunnel/ Tubular vision
4. Gradual painless progressive diminition of vision

Signs
A. IOP : IOP >21 mm Hg at least two consecutive occasions 24 hours apart ( to avoid diurnal variation )
^

> Measured by tonometer

:
MC Schiotz tonometer

Indentation
Truncated cone

O
Affected by corneal rigidity

Soft cornea = false low value

: Hard/scarred/edematous = false high value
 > Foot plate
> Used when reading is less than 3
> Phunger
Extra weights > 5.5 gm
> 7.5 gm
> 10 gm
> 15 gm

Pointer > Fridienwald monogram tables

✓

Gold standard tonometer : Goldmann’s applanation tonometer >

O Flattening of cornea

Affected by corneal thickness

To measure

Pre requisite : Pachymetry

Principle : Imbert Fick law

Pressure = Force
Area
>
Fixed area tonometer
3.06 mm diameter of cornea

:
or variable force tonometer

P F
r or P = F x 10 = IOP
mm of Hg L J
In grams
Probe
Stain = Fluorocein stain

Mires >
Touching inner ends
✓ Circle of contact
J
l l
f

L
s 0.2-0.3 mm

Splitted
by 3.06 mm
biprism Diameter

Optical endpoint

Dial reading greater Dial reading less than Dial reading equals
than pressure of globe pressure of globe to pressure of globe
 B. Optic disc changes
Normal optic disc Optic nerve head
^

<

Neuro retinal rim

: Hollow area ( cup )

Normal Cup/ Disc = 0.3 to 0.4

Glaucoma = optic neuropathy = increase in size of cup

ISNT Rule
V

Thickness of neuroretinal rim I > S > N > T

:
Violated in glaucoma

Optic disc changes

1. Increase in size of cup known as cupping
2. Asymmetrical cupping : significant when difference > 0.2
3. Vertical oval cupping : due to early loss of superior and inferior fibres of neuro retinal rim
4. Splinter hemorrhages over optic disc
5. Visible pulsation of retinal arteriole over optic disc
6. Laminar dot sign seen at Lamina Cribrosa
Layer Sieve like
V

Part of sclera through which optic nerve fibres emerges out

Openings are distended and visible upto optic disc margins

V

Laminar dot sign

7. Nasal shifting of blood vessels

> This part is not visible L Double bending

l V
or
Z-bending
or
l

Appearance of being broken off at margins

,

8. Bayoneting sign
9. Total cavernous (cave like ) optic atrophy

C. Visual field defects

Extent of visual field : S-NIT > Blind spot between 10 - 20

Superior > Nasal > Inferior > Temporal > Lies in temporal visual field
50 60 70 90-100 ( i
BAB l l l >
10 20
 Temporal visual field

Physiological Blind spot

Negative

'

:
%
Optic disc
Macula
Optic nerve

Visual field charting

v v

Central visual field Peripheral visual field

v
u

0 - 30 30 - beyond
v
v
,
Campimetry Perimetry

Visual field defects

> 3. Para central scotoma - earliest significant visual field defect

/

I
>
1. Isopter contraction
Not significant

EL s
2. Sparing of blind spot

(
<

5. Arcuate /
Bjerrum’s scotoma
' s Horizontal raphae
10 20
c

6. Double arcuate scotoma

>
Sickle cell shaped
Nasal visual field Temporal visual field ✓
4. Seidel’s scotoma
7. Nasal step <
( merging of blind spot and para central scotoma )
due to uneven contraction

8. Central/ Tunnel vision <

9. Central vision also affected

10. Last to go : temporal visual field

Temporal region

:
Superior and inferior arcuate fibres

Arcuate scotomas in nasal visual field

:
Most sensitive to glaucomatous damage
Hence nasal visual field is more affected than temporal visual field

Bjerrum’s area - arcuate fibres between 10-20

Bjerrum’s scotoma
 Treatment of open angle glaucoma

A. Medical treatment
B. Laser
C. Surgery

A. Medical treatment

First line of therapy > Anti glaucoma drugs

1. B- blockers: mc used but not DOC

-

MOA : decreased aqueous formation

Types l

u
v

Non selective Selective

v
✓

Timolol - most popular Betaxolol

Contraindicated in cardiopulmonary diseases Non contraindicated in cardiopulmonary disease

:
Bronchial asthma Also improves profusion of optic disc

DOC in normal tension glaucoma

Carteolol
DOC in low tension glaucoma
Doc in hyperlipidemia

ADR
A- allergic Blepharoconjuctivitis
B- blurring of vision
C- corneal hypoesthesia - decreased sensations ( Esthesiometer )
D- dryness of eye - superficial punctuate keratitis

2. PGF2 Analogues Now DOC

MOA : increases uveoscleral outflow
Eg : Latenoprost, Bimetoprost, Travoprost

ADR
1. Hyper pigmentation > Iris > Heterochromia of iris
> Periocular skin

2. Elongation of eyelashes
3. Reactivation of H. simplex
B blockers preferred
4. Intra ocular inflammation
5. Cystoid macular edema in diabetic patients

3. AAdrenergic analogues

MOA : 1. Decreasing the aqueous formation

2. Increasing aqueous outflow

Still not DOC because of ADRs

ADR > Allergic reactions

> Tachyphylaxis ( Tolerance )
 Types

v v

Selective Non selective

-

V V V V V

Apraclonidine Brimonidine Clonidine Dipivefrine Epinephrine

Not used > Precursor of Epinephrine
v v

Trabecular outflow Uveoscleral outflow DOC in hypertension uveitis ( inflammatory glaucoma )

n n

v
v c

Before procedures that can IOP Ocular ( IOP ) ADR 1. BP

^ n n
y
t

Neuro Protection 2. Cystoid macular

But avoided in systemic hypertension edema in aphakia
v

CNS depression > Apnea

> Drowsiness
v

Hence contraindicated in infants

4. Carbonic anhydrase inhibitors

MOA : v Aqueous formation

u v

Topical Systemic

Dorzolamide Acetazolamide > Mc used

Brinzolamide Methazolamide

:
Sulpha drugs

Contraindicated in sulpha drug allergy

V

Topiramate causes angle closure glaucoma

By ciliary body effusion

Narrowing of angle of anterior chamber

5. Hyperosmotics

Emergency drugs > Mannitol > IV

> Glycerol > Oral

Contraindicated in volume overload >

CHF
> ARF
MOA : shifting fluid from vitreous to ECF

6. Rho kinase inhibitor > Nitarsudil

MOA : 1. Aqueous formation

V

2. Aqueous outflow
:
3. Episcleral venous pressure

ADR : Vertex keratopathy

 Laser trabeculoplasty

Argon/ Diode/ frequency doubled NdiYAG

> Wavelength = 1064/2 = 532 nm

:
Collagen shrinkage in trabecular meshwork

Opening of trabecular spaces

t
Aqueous outflow
^

TOC in other eye for prophylaxis

Surgery

1. Trabeculectomy : Fistula

Aqueous humor come out

> Filtration bled

:
Fibrosis

Surgery fails
V

Another surgery done - Seton surgery

Artificial glaucoma shunt devices or drainage devices keep bleb petent

Eg : Ahmed Glaucoma valve ( India ) - latex
Express mini shunt - Stainless steel

Provocative tests

Best for POAG - water drinking test

IOPbaseline 1L of water > IOPfinal

Increase in IOP > 8 mm Hg = Diagnostic

 Primary angle closure glaucoma
No known cause of sudden closure of angle of anterior chamber

Risk factors

> 50 years, females

Hereditary
Small eyeball
Small cornea
Shallow anterior chamber
Hypermetropia
Type A personality Hurry

÷ Worry
Curry

Attack due to mild dilatation of pupils Rainy season

: Emotional stress
Mydriatics/ cycloplegics
i Dark room procedures

\ # 7 c

Iridolenticular Apposition
← →
f r

Aqueous collection behind iris

÷
Iris bombe formation

±÷ is:* .

Acute congestive glaucoma

Peripheral anterior synechiae

Chronic congestive glaucoma

Stages
1. Latent stage ( hidden ) - only oculudable angle present
^

No > Optic disc changes

-

y Visual field defect

g
n
IOP Treatment of choice

Laser irodotomy
2. Intermittent stage : IOP intermittently or
^

Few seconds/ minutes/ hours Surgical P I ( Peripheral iredectomy )

Still No > Optic disc changes

> Visual field defect

3. Acute congestive glaucoma - ophthalmic emergency

Sudden painful diminition of vision
Stony hard eye due to very high IOP D/d : Acute red eye
Circum corneal congestion Present
Nausea, vomiting
Coloured Halos

Slit lamp examination : Vogt’s triad : 1. Patches of iris atrophy

2. Glaucoma flackens ( anterior subcapsular cataract )
3. Pigments on corneal epithelium

Pupil : mid dilated, vertically oval, fixed

 Treatment
1. IOP urgently : IV drugs > Acetazolamide I >
v Aqueous formation
> Mannitol II > v Vitreous volume

2. After v IOP 7 DOC = miotic- topical pilocarpine

✓

MOA : Active miosis ( acting on sphincter )

3. IV > Anti emetics

> Opioids

4. Topical drugs > Steroids ( to v Inflammation )

> Anti glaucoma drugs

5. Next day, TOC > Laser iridotomy or surgical Peripheral iredectomy

s
ail
If f
<

6. Trabeculectomy

7. TOC for prophylaxis of fellow eye - Laser iridotomy or surgical Peripheral iredectomy

4. Chronic congestive glaucoma

Peripheral anterior synechiae present

Laser iridotomy or surgical Peripheral iredectomy No use

Pilocarpine

Treatment of choice - Surgery - Trabeculectomy

5. Absolute glaucoma > Glaucomatous stage of Intra ocular tumors

Total optic atrophy

:
Painful blind eye

IOP
^

:
By destruction of ciliary epithelium

Laser photo coagulation/ Cryotherapy / Diathermy

If fails

TOC - Enucleation
-

Provocation test
Best for PACG - Prone for dark room test
IOP baseline >
Patient lies in prone position in a dark room awake for 30 minutes > Take IOP final
If increase in IOP > 8 mm Hg = Diagnostic

Fincham’s stenotic slit test To differentiate in coloured haloes between cataract and ACG

> Intact 7 Glaucoma (ACG)

Patient looks through slit >
Coloured haloes
J
Scattering > Cataract
 Secondary glaucoma
V

Cause is known

1. Lens induced : A. Phaco morphic glaucoma : due to immature senile cataract

B. Phaco lytic glaucoma : mc lens induced glaucoma

> Caused by Morgagnian stage of hyper mature senile cataract

Lysis of cortex proteins

>
Phaco anaphylactic uveitis
V

Lens has sequestred antigens

C. Phaco topic glaucoma : due to Sclerotic type of hyper mature senile cataract

D. Phaco toxic glaucoma : due to posterior capsular rupture

2. Inflammatory glaucoma : due to uveitis

or hypertension uveitis ( DOC : Dipevifrine )

MOA : 1. Acute inflammatory glaucoma - due to trabecular blockade

2. Door to ring synechiae
3. Steroids ( topical ) induced

3. Neo vascular glaucoma : due to Rubeosis iridis

Neovascularisation over iris > Zip like adhesions in the angle of anterior chamber

Etiology - mc PDR ( Proliferative diabetic retinopathy )

- CRVO ( Central retinal venous Occlusion )
>
Also known as 100 day glaucoma
- Eale’s disease
- Sickle cell retinopathy
- Intra ocular tumors

4. Pigmentory glaucoma : due to pigment deposition in trabecular meshwork

>
Open angle glaucoma
2 imp signs

v u

Krukenberg spindles Sampaolesi’s line

v v

Pigments on posterior surface of cornea Gonioscopic finding pigments on along the Schwalbe’s line

5. Steroid induced glaucoma

Main etiology : Deposition of GAG ( Glycoso amino glycan ) in trabecular meshwork
> Secondary open angle glaucoma

Steroid responders

v v
v

High Moderate Low

v v

Develop glaucoma
v
<

5% 35% 60%

6. Epidemic dropsy : Hyper secretary glaucoma ( Secretion of aqueous humor )

^

Secondary open angle glaucoma

Occur due to food poisoning
Due to Sanguinarine ( alkaloid ) present in Argemone mexicana present as adulterant in mustard oil
 7. Traumatic glaucoma
Mechanisms : 1. Uveitis
2. Hyphema - blood in anterior chamber ( mc due to major arterial circle )
3. Angle recession - tear of ciliary body face below root of iris and scleral spur

8. Ciliary block/ malignant / inverse glaucoma

Due to mis-direction of ciliary processes during Intra ocular surgery

i*÷:I÷
Accumulation of aqueous humor in vitreous cavity

No outflow channel
90% outflow
Malignant glaucoma
Lens

Vitreous cavity 1. Treatment of choice : Atropine Mydriatic is TOC

:
:
.

Breaks ciliary block Inverse glaucoma

Dilated pupil and pull ciliary body

Pull ciliary processes

Opens block

2. IV mannitol > To decrease vitreous volume

✓ IOP
3. Acetazolamide : to decrease aqueous formation

4. Vitreous aspiration by posterior sclerotomy

 Retina

Inner Most coat of eyeball

Extent : from orra serrata to optic disc margin

÷* :i÷
Origin Uneven Thinnest area of retina

Ciliary body Ciliary processes

Choroid
Limbus

Sclera

iii.
Cornea
Retina ( 10 layers )

Optic disc margin

Lens

Vitreous cavity
Optic nerve ( 1 layer )

Lamina cribrosa

Ciliary zonules

Parts of retina

i r

Central Periphery

v r

Optic disc Macula lutea

( nasal side ) ( temporal side )
Temporal visual field
v r

Optic nerve Head Yellow spot Physiological Blind spot

ii
Negative

or
Blind spot of mariotte Due to Xanthophyll & urochrome

Optic disc
Macula
Optic nerve
Macula: 5.5 mm 2 DD = 2 x 1.5 = 3 mm

Temporal Nasal

Optic disc 1.5 mm

:
Fovea centralis
1.5 mm
Blind spot on temporal side

Foveola
0.35 mm

=
Sharpest image is formed Which side of eye is this ?
Ans : If macula is present on right side then it is right eye
If macula is present in left side then it is left eye
Densely packed with cones no rods
So it is right eye
Floor Thinnest part of Retina
Fovea centralis
: Rim
: Thickest part of Retina

Overall thinnest part - Orra serrata

 Foveola - foveolar reflex ( Shinning reflex )

FAZ (Foveal avascular zone) - inside foveola centralise and outside foveola
0.4 - 0.6 mm in diameter
V

No vascular supply

Laser photo coagulation is contraindicated

Ophthalmoscopy
-

V v
v

Distant direct ophthalmoscopy Direct ophthalmoscopy Indirect ophthalmoscopy

✓
V

Done by direct ophthalmoscope Done by indirect ophthalmoscope

Used when
V

Hazy media, uveitis, cataract

Direct ophthalmoscope Indirect ophthalmoscope

Used to see central fundus Used to see periphery
Area seen : 2 DD Area seen : 8 DD
Image formed : Virtual, Erect, Magnified Image formed: Real, inverted, magnified
Magnification : 15 times Magnification : 5 times

Distant direct ophthalmoscopy : Direct ophthalmoscopy form distance

25/33/40 cm

Left eye
Nasal, Right side Temporal, Left side

> Red glow - due to chorio capillaries

>
Physiological cup

Macula
Vein <
 Blood supply

÷
Outer 4 layers + macula
:
Inner 6 layers

By choriocapillaries Central retinal artery

Layers of retina

1. RPE - Retinal Pigment Epithelium

' Melanin
.
Bruch’s membrane of choroid

Sub retinal space . Contains sub retinal fluid

2. Layers of rod and cones ( Photoreceptors ) .

First order neurons . Contains outer segment and inner segment

3. External limiting membrane Outer segment

Layer of rods and cones

:
Inner segment
4. Outer Nuclear layer - Nuclei of rod and cones
External limiting membrane
Outer Nuclear layer

:*
5. Outer plexiform layer - synaptic cleft and Rods and cones Outer plexiform layer

Synaptic cleft

6. Inner nuclear layer - Contains nuclei of bipolar cells ( II order ) > amacrine, horizontal, muller cells

7. Inner plexiform layer - Synapse between ganglionic cells ( III order ) and bipolar cells

8. Ganglion cell layer - contains dendrites of Ganglionic cells

9. Nerve fibre layer - contains axons of Ganglion cells

Continues to form optic nerve

"
In optic neuropathy - Ganglion cell death

10. Internal limiting membrane

Choroid

④
RPE
Retina Sub retinal space Neurosensory retina

:
Neurosensory retina ( 9 layers )
RPE

:
Vitreous
Transparent/ colourless
Sub retinal space
Red glow from choroid

1. The layer Most resistant to radiation : RPE > GCL

2. The layer Most sensitive to radiation : Layer of rods and cones
3. Optic nerve : NFL
4. Layer Most prone to pathology : OPL & INL
5. Macula- contains all 10 layers

Fovea Foveola centralis

u v

5 layers 6 layers

1. RPE 1. RPE
2. Layer of cones 2. Layer of cones
3. OLM ( ELM ) 3. OLM ( ELM )
4. ONL 4. ONL
5. ILM 5. OPL ( Henle’s layer )
6. ILM
 Histology of retina
> Internal

>
<
This is on internal side — Internal Nuclear layer
( 7

Dark layers are nuclear layer

c
>
> This is on external
>
side — External nuclear layer

Inner segment

outer segment
> photoreceptors

Pigmented Epithelium > External

Blood retinal barrier

v u

Outer Inner
V

By tight junction of RPE Retinal vascular endothelium

v u

Broken in > CSR ( Central serous retinopathy ) Broken in > Diabetic retinopathy
S CME ( Cystoid Macular Edema ) ) Hypertension retinopathy
 Pathologies of retina

1. Roth spots : Present in the SABE ( Sub acute bacterial endocarditis )

>
Roth spot > Multiple superficial hemorrhages

it h
W

L
>
White dot > Fibrin clot

Etiology : Retinal Hypoxia

2. Vitreous haemorrhage

>
Blood in vitreous cavity

Clinical features: Sudden painless diminition of vision > Mostly posterior segment pathology

Floaters due to climbing in vitreous gel

Absence of the fundal glow ( no red glow )

Etiology : mc cause of vitreous haemorrhage- spontaneous > trauma

mc cause of recurrent vitreous hemorrhages

v v

Young Elderly

v
V

Eale’s disease PDR ( proliferative diabetic retinopathy )

Due to hyper sensitivity reaction to TB patients

I

TOC : Steroids + ATT

3. CRAO ( Central Retinal Arteriolar Occlusion )

Ophthalmic emergency
Due to

Central Retinal artery - 4 end arteries - No collaterals

More common in males of >50 years

MC cause : Thrombosis (80%) > Embolism (20%)

Occur due to Cholesterol crystals known as

Hollen Horst plaques
Retinal hypoxia time 60-90 mins
7
MC site : Lamina cribrosa

Clinical features : Sudden painless loss of vision

RAPD present ( due to optic nerve disease ) >

Signs > Cherry red spot

> Cattle track appearance 7 Segmentation of blood column in veins

> CRAO — pale retina

U

Milky white in colour due to exudate collection in ganglionic cell layer

V

Absent in fovea centralis

>
Fovea centralis y Ganglionic cell layer absent
> Supplied by choriocapillaries
V
>
Cherry red spot : only area through which choroid continues to shine
 D/D of cherry red spot

Niemann pick disease Sand hoff disease

n
n

Cherry Trees Never Grows Tall in Sand and Mud

.

Metachromatic leucodystrophy
C V

CRAO Tay Sach disease J

V
Blunt trauma
Gangliosidosis and Gucher disease
Macular edema
( Berlin’s edema )
Pseudo cherry red spot
L

Treatment 1. Immediate lowering of Intra ocular pressure to dislodge the the thrombus

IV > Mannitol
Acetazolamide

:
Ocular massage
Paracentesis ( aspiration of anterior chamber )

2. Carbol mixture : 95% O2 + 5% CO2 = for vasodilation

To maintain respiratory drive

( if 100% O2 given : Respiratory depression )

3. IV > Steroids
> Anti coagulants > Streptokinase, urokinase, tPA
> Embolysis

4. CRVO ( Central retinal venous Occlusion )

Less severe but more common than CRAO

Types

u v

Non ischemic Ischemic

Mild changes Severe changes > Edema

> Hemorrhages
✓

Hemorrhages > Tortuosity

Edema
✓

Tortuosity Ischemia

No treatment required V

VEGF release

^
V

Neovascularisation > Newly formed vessles are fragile

✓

Neovascular glaucoma ( 100 day glaucoma )

:
It is complication of CRVO Vitreous hemorrhage

Splashed tomato appearance

<
Treatment : Laser photo-coagulation
 5. Hypertension retinopathy

1. Earliest sign : Nasal angiospasm : thinning of blood vessels in nasal quadrant

Directly proportional to severity of hypertension

2. Arteriosclerosis : increase in total peripheral resistance

^

Vicious cycle
:
Increase in diastolic B.P.

More angiospasm

Directly proportional to duration of hypertension

3. Increased vascular permeability

v
t u
Flame shaped hemorrhages

Flame shaped hemorrhages Cotton wool spots Retinal edema

v
v

Superficial hemorrhages Soft exudates

> V

Present in nerve fibre layer of retina I

Keith, Wagner, Barker — Stages of hypertension retinopathy

I — Mild angiospasm ( A:V from 2:3 to 1:3 )

II — Moderate angiospasm + Salu’s sign
III —Copper writing of f arterioles + grade II changes + Gunn sign and bonnet sign
IV — Silver wiring of arterioles + grade III changes + papilloedema ( marker of stage IV hypertension )

Spasm > Change in colour in blood vessles

Bright red

:
Dark red

Copper coloured > Grade III

No blood >
Silver wiring > Grade IV Artery vein .

£
L

Tapering/ deflection of f veins W.R.T. AV crossings Av

crossing

1. At AV crossing : Salu’s sign

2. Distal to AV crossing : Bonnet sign
3. Perpendicular to AV crossing : Gunn sign

Mc cause of diminition of vision in hypertension retinopathy — Maculopathy ( Not papilloedema )

6. Diabetic retinopathy
Risk factors : 1. IDDM ( Type I )
2. Females
3. Hypertension
4. Anemia
5. Pregnancy
 Most important factor for pathogenesis of diabetic retinopathy — Duration of Diabetes Mallitus ( >10 years )
Diabetic retinopathy is micro angiopathy
>
Small
C v i

Arterioles Capillaries Venules

Maximum ischemia

:
Maximum VEGF

Maximum neovascularisation > MC - Recurrent vitreous haemorrhage in elderly

MC cause of neovascular glaucoma

ETDRS — Early Treatment Diabetic Retinopathy Study

Stage of Diabetic Retinopathy — 4

1. NPDR ( Non Proliferative Diabetic Retinopathy ) or Background DR — Earliest stage >

> Earliest sign — Micro aneurysms > Pin point hemorrhages

V
Due to loss of pericytes from the capillary walls
> Present in Inner Nuclear layer of retina
Deep hemorrhages — called as Dot- blot hemorrhages
L s

Hard exudates are present in Outer Plexiform Layer

> Lipids and lipoprotein deposits
Micro aneurysms
-
• y

b t Circinate retinopathy
v -

OO
OO
AV shunt
a

IRMA : Intra Retinal Micro Vascular Abnormality >

Eg : venous changes >

Bleeding
>
Loops
Eg : AV shunts ( Arterio- Venous shunts )
Retinal edema

Severity of NPDR : 4-2-1 Rule

Criteria > 1. All 4 quadrants have micro aneurysms

> 2. Venous changes in at least 2 quadrants
> 3. IRMA ( AV shunts ) in at least 1 quadrant

If any 1 criteria present : Severe NPDR

If any 2 criteria present : very severe NPDR

Neovascularisation Micro aneurysms

2. PDR ( Proliferative Diabetic Retinopathy ) — Always occurs after NODR

Neovascularisation ( Hallmark )
/ ° '

NVE
.

NVD ①
-0
u
v

Elsewhere Disc
.

. .

Along major blood vessles Optic Disc

.
 3. Diabetic Maculopathy — Macular involvement

CSME - Clinically Significant Macular Edema

1. At macula > Edema

> Exudates

or, 2. Within 500um from centre of macula

with 3. Increased retinal thickening atleast 1 DD ( due to edema )

Maculopathy can occur after > NPDR

> PDR

4. Advanced Diabetic Eye Disease — Complications

Neovascular glaucoma (NVG), Tractional Retinal Detachment (TRD),

Screening of Diabetic Retinopathy

IDDM/ Type I NIDDM / Type II

u v

Start within 5 years of diagnosis Immediately/ ASAP

> Early onset so duration is less Adult onset so duration is less c

Follow up

NPDR — Mild : Yearly

Moderate : 6 monthly
Severely : 3 monthly

PDR — 2 monthly

Diminition of vision in Diabetic Retinopathy

v v

Sudden Gradual > Cataract

> Tractional Retinal Detachment (TRD)
v u

NPDR PDR > Diabetic retinopathy

v v

MCC : Maculopathy MCC: Recurrent vitreous haemorrhage

Most important test to see changes in Diabetic Retinopathy

t
Breakdown of Inner Blood Renal Barrier

Fluorescein Angiography

Fluorescein dye is injected in Anti cubital vein

 Treatment of Diabetic Retinopathy

1. Control of Blood Sugar because chances of Diabetic Retinopathy are due to glycemic end products
2. PRP ( Pan Retinal Photo coagulation ) — Laser
Whole Retina : 2000-3000 Laser spots
Each laser spot : 500 um foot 0.1 second
Distance between 2 spots : 500 um
Started from periphery to centre leaving macular area (FAZ = Foveal Avascular Zone)

> Blind spot

Total area = Ring scotoma

Diminition of vision in Diabetic Retinopathy is irreversible

PRP is done to prevent complications

3. Maculopathy Focal laser Photo coagulation ( lesser energy )

: or
Intra vitreal Injection of Triamcinolone (Steroid)

4. Intra Vitreal Injection of anti VEGF agents Severe / very severe NPDR

÷
PDR
Ranibizumab or Lucentis
Bevacizumab or avastin
Pegaptamib or macugen

5. PPV : Pars Plana Vitrectomy — Aspiration of fibro vascular tissue from vitreous cavity through Pars Plana to prevent TRD

7. ROP ( Retinopathy of Prematurity )

<28 weeks - Period of gestation

<1.7 kg - Birth weight

Exposed to high [O2]

Prone to obliteration because of immature retinal vasculature

t
Due to release of VEGF

Intense fibrovascular proliferation especially behind the lens

Hence called Retrolental fibroplasia

Leucocoria d/d
-
1.PHPV
Leucocoria '
2. Congenital cataract
3. Retinoblastoma

Stages of ROP - 5
TRD
1. Dermarcation of line : Between the vascular and avascular retina
2. Ridge : permanent line
3. Ridge with fibro vascular proliferation
4. Subtotal RD ( TRD )
5. Total RD
 Zones and Extent -

v v

3 Clock hours

Zone I : Concentric circle centered on optic nerve

Radius = 2 x distance from nerve to fovea
= 2 x 2 DD = 6 mm

Zone II : concentric annular area from outer border of zone I

l
2DD
l
to the Orra serrata nasally and just beyond equator temporally

Zone III : Temporal crescent from outer border of zone II to temporal orra serrata

ROP — Plus Disease

TAVE n n
Tortuous arteries
Engorged veins

Treatment of ROP

t
Threshold Disease

5 contiguous areas or 8 non contiguous areas in stage 3 + Zone I/II with plus Disease

Pre threshold Disease

1. Zone I + any stage + plus disease

2. Zone I + stage 3
3. Zone II + plus disease + stage 2

Treatment : Photo coagulation upto the orra serrata ( to burn fibro vascular proliferation )

Screening

v
V

<28 weeks >28 weeks

V
u v

Examined within 2 weeks <1.7 kg >1.7 kg

u v

Examined within 3 weeks Examined Within 4 weeks

2-4 weeks from birth/ 32-36 weeks from periods of gestation

8. Retinitis pigmentosa

MC hereditary pigmentory dystrophy of Retina affecting Photo receptors ( rods >> cones )
V

Involve RPE Degenerative

:
More common in males
Bilateral
Symmetrical

Inheritance : MC - sporadic (35%) > familial

Most common
AR>AD>XR
Best prognosis C 7 Worst prognosis

Symptoms : 1. Rods >Cones -

Earliest sign > Night blindness
2. Delay in dark adaptation 7

3. Tunnel vision or Tubular vision

Signs : Triad
1. Pale yellow wavy optic disc
>
2. Pigmentory spicules
3. Attenuation of retinal arterioles
>

> Ring scotoma

Tests : EOG ( Electroculography ) & ERG ( Electroretinography )

EOG done in sitting position and ERG done in supine position
v v

Eye Retina

"

Resting potential between cornea ( + ve charged ) and macula ( - ve charged )

Resting potential
+ —

> Light adapted state ,

Spikes Maximum spike

X 100 = Arden’s Ratio
>
Dark adapted state Minimum spike
y

Normal : >185 %
Borderline : 180-150%
Sub normal : < 150
Flat : <125
ERG ( Electroretinography )
V

Change in the potential induced by flash of light

3 waves > a - negative wave

> b
Positive wave
> c

a - from Rods and cones ( I order neurons ) Rods are affected > a wave affected

b - From muller cells s to

II o
rder
g oe
tial
ot e n
- shows activity of bipolar cells ( II order neurons ) <

Affe
c te d
p

c - RPE activity (pigmentory dystrophy) - abnormal Wave

Hence all waves are affected

Therefore best test for retinitis pigmentosa = ERG
 Systemic associations of Retinitis pigmentosa

>

Acanthocytes /
spurr cells

Ocular associations of Retinitis Pigmentosa

POAG
Myopia
Keratoconus
VKC
CME
 9. CSR ( Central Serous Retinopathy )
V V

Macula SRF Collection

Spontaneous detachment of neurosensory retina from RPE in macular area = collection of SRF

Foveal depression

l I
Neurosensory retina
i
-

CSR Sub Retinal space

RPE

More common in males

20-50 years
Type A personality Hurry

÷ Worry
Curry
Stress, Smoking, Steroids

Clinical features : Sudden painless diminition of vision (6/9 to 6/24)

Metamorphopsia ( Distorted images ) Metamorphopsia ( Distorted images )

Acquired hypermetropia '

Correctable with plus lenses
Du e
to
'
'
Decrease in effective axial length

Tests : 1. Slit lamp Bio-microscopy or Direct ophthalmoscopy

> Better
v

< Circular ring sign

Normal
2. OCT (Optical coherence tomography) >

Neurons sensory retina Foveal depression

"

>
a OCT findings in CSR patient

^ SRF

RPE

3. Confirm by FFA ( Fundus Fluoroscein Angiography )

=
Mushroom pattern/ Ink Blot pattern/
Umbrella pattern/ Enlarging dot sign
Smoke stack pattern
>

<

Treatment : Just wait and watch for spontaneous resolution ( usually self limiting : 4-12 weeks )
10. CME ( Cystoid macular edema )

Cyst like spaces in macula due to collection of fluid in outer flexiform ( Henle’s layer ) and INL

Etiology : Mc inflammation after cataract surgery known s as Irvine-Gass syndrome

Retinitis pigmentosa
Posterior uveitis
Niacin toxicity
Prostaglandin analogues
Diabetic Retinopathy
Epinephrine (CME in aphakia )
CRVO /BRVO

Clinical features : Sudden painless diminition of vision

Metamorphopsia

Tests : 1. Slit lamp Bio-microscopy or Direct ophthalmoscopy > Honey comb appearance

2. OCT (Optical coherence tomography)

3. FFA : confirmation : Flower petal appearance

Due to radial/ petalloid arrangement of the fibres in the Henle’s layer

Treatment: Steroids + Causative treatment

 11. ARMD (Age Related Macular Degeneration)
>60 years
Males = Females
Bilateral
Symmetrical

MC cause of irreversible diminition of vision in developed countries

ARMD

v
u

Dry/ Geographic (90%) Wet (10%)

t
-

Main lesson : Drusens Choroidal neovascularisation After thickening of Bruch’s membrane

v v

Extra cellular eosinophilic deposition between the Bruch’s membrane and RPE Dysfunctional Bruch’s membrane
+
Atrophic areas in retina
+
Irregular pigmentation RPE
Choroid

Mild or no diminition of vision ✓

Treatment: No treatment
Multivitamins + anti oxidants -
RPE PED
Choroid

:
Pigment epithelial detachment

CNVM
Drusens ( Choroidal Neovascular Membrane )

Clinical feature : Severe diminition of vision

Treatment
-

v v

Extra Foveal area Foveal / sub Foveal area

u r

Laser photo coagulation 1. TOC : Anti VEGF agents

2. Previously TOC : PDT ( Photo Dynamic Therapy )

Using a light activated compound

Known as Verteporfin

Followed by Diode laser

3. Transpapillary thermotherapy

RPE

PED

Choroid
 12. Angiod Steaks

Pigmented Steaks due to changes in elastic fibres of Bruch’s membrane of choroid

Etiology : P - pseudoxanthoma Elasticum - MC

E - Ehler Danlos Syndrome
P - Paget’s disease
S - sickle cell Retinopathy
I - Idiopathic

13. Salt and Pepper Retinopathy

Yellow and black flecks in retina

Congenital Rubella
Congenital Syphillis
Fungus flavimaculatus
Atypical Retinitis Pigmentosa
Phenothiazine toxicity ( Thioridazine )
Cerebro Maculo facial Degeneration

14. Photo Retinitis

Retinopathy by light >
IR > Emitted by Sun during solar eclipse known as Solar/ Eclipse Retinopathy
-

>
UV
> Visible blue

"
Causing foveolar defect

RPE defect surrounded by mottled pigment

Rarely cause FTMH ( Full Thickness Macular Hole )

Latent period : 4-6 hours

Fundus is normal

15. Macular dystrophy

MC - Stargardt’s disease ( Fundus flavimaculatus )

Autosomal recessive
Diffuse deposition of lipofuschin ( Golden brown pigment ) in RPE of macula — Beaten bronze appearance
V

FFA - fluoroscein dye — Auto fluorescence

Lipofuschin covers fluorescence

< Silent choroid or Dark choroid

EOG > Subnormal / Normal C ERG

Age : young
Best Vitelliform macular dystrophy/ Best disease
2nd mc macular dystrophy
Autosomal dominant
Mutation of Bestrophin gene >

Localised deposition of lipofuschin in RPE of macula — Egg yolk appearance

Age : Children and young

Best test for Best disease : EOG

Abnormal EOG with relatively Normal ERG
v u

EOG : measures resting potential ERG : a wave : Rods and cones : Normal
Macular dystrophy : affects -ve charge of macula b wave : Bipolar cells : Normal
Hence abnormal EOG is obtained c wave : RPE : Abnormal
Only decreased c wave

Bull’s eye Maculopathy / Annular Benign Concentric Macular Dystrophy

Patients present with Fundus and FFA findings

Patients taking 500 mg/ day Hydroxychloroqine

Chloroquine derivatives
- Drugs used in treatment of malaria, rheumatological and dermatological disorders
- Toxicity : CQ - 3 mg/ kg/ day, HCQ - 6.5 mg/ kg/ day for 5 years
Cumulative dose: > 460 g for CQ and > 1000 g for HCQ
- MOA : Drug + Melanie in RPE > prolonged effect
- The primary damage is to the Photo receptors and as the ONL degenerates, there is secondary disruption of the RPE

Screening of Chloroquine toxicity

- Aim - Early detection and minimisation of toxicity
- Baseline examination within 6 months of prescription
- Routine ocular follies up every 6-12 months
- Amsler grid once a week
- If abnormality suspected: Automated VF, SD-OCT and mfERG

Rule of 5 ( screening purposes ) > Visual acuity and Fundus examination

>
Fields ( perimetry ) : central/ paracentral
> Multifocal ERG : potential
> Spectral OCT : layers of Retina seen
> Auto fluorescence : lesions

Risk factors : Rule of 5

1. Daily dose : > 3 g/kg/day for CQ and >6.5 g/kg/day for HCQ

2. Cumulative dose : > 460 g for CQ and >1000 g for HCQ

3. Liver/ Renal disease

4. Duration : > 5 years

5. Also using Tamoxifen

 Retinal detachment

Misnomer : It is actually separation of RPE from neurosensory retina

Retinal Detachment

V v
v

Rhegmatogenous (MC) Exudative Tractional

"
RRD ERD TRD
Retinal hole : most imp risk factor
Due to pushing of retina towards vitreous cavity Occurs due to pulling of retina towards vitreous cavity
MC Shape — Horse shoe shaped by collection of exudates/ fluids / tumor cells due to dense fibro vascular tissue in vitreous cavity
: Site — Superotemporal quadrant
-

Old vitreous hemorrhages

:i
Other risk factors
Smooth convex RD
Males, old age, trauma, High myopia, Etiology : PDR - mc
lattice Degeneration, pseudophakia Sclera Eale’s disease
Choroid
Aphakia RPE Trauma
Neurosensory retina
Sickle cell Retinopathy
Clinical features
Sudden painless diminition of vision Sudden painless diminition of vision Only RD which causes Gradual painless DOV
Photopsia + floaters : Unique to RRD No photopsia or floaters
B scan USG
- v

Flashes of light Dark spots

Curtain like effect Greyish reflex present

TRD
Shifting fluid levels - Pathognomic
Ophthalmoscopy : Greyish reflex Movement Concave / tent shaped

N : Red reflex

Sheffer’s or Tobacco dusting sign : pigment

Dispersal in anterior vitreous Change in the levels of the fluid due to
movement of patients due to gravity Treatment :
Lincoff rule : to locate retinal hole 1. Laser photo coagulation
On Indirect Ophthalmoscopy Etiology : Renal hypertension
u

In 99.9% cases Eclampsic Retinopathy to stop vitreous hemorrhages

( Gestational HTN + proteinuria + seizures )

Hole is 1-2 clock hours on most Coat’s disease 2. PPV : pars plana vitrectomy
( idiopathic vascular telengiectasia )
convex side of RD
12 1 -
11
VKH syndrome Vitreous aspiration of fibro vascular tissue
Intra ocular tumors :
1. Retinoblastoma 3. RD surgery
2. Malignant melanoma of choroid
Test : RAPD present in large RD
Indirect ophthalmoscopy Treatment of ERD : Causative treatment
Confirm : B scan USG
Coat’s disease

!
Brightness/ 2D USG

Unilateral, idiopathic vascular telengiectasia

Total funnel Shepard RD
more common in boys, <10 years

TRD : B scan
-

Posterior vitreous detachment

Vascular malformation
Confuse with: CD /PVD / RR ✓

Choroid detachment v

Inflammation
Combine A and B scan

:
High spike
rn
ea
RD Exudates
Co '

' Sclera

i Complicated cataract
Inflammatory glaucoma
Leucocoria
ERD
M spike : CD
No spike : PVD
Treatment
1. Sealing of retinal hole by lesser Photo coagulation
2. Scleral buckling/ encirclage operation '
Most imp step

Silicon patch Convex

Encircling sclera

e Fix the retina

ERD : B scan
Suturing

3. Internal temponade:

>
Reverse hypopyon
Silicon oil
or
Heavy gases : SF6 gas

:
Remove within 3 months
because of ADR
Eg: Oil granuloma ^

Inverse hypopyon
4. Drainage of SRF especially in long standing cases

<

Horse shoe shaped

Funnel shaped Optic nerve shadow

B scan
 Tumors of eye

✓ v

Primary Secondary ( metastasis )- mc

v u

Intra orbital Intra ocular

V V V V

Adult Children Adult Children

V V
✓ V

Cavernous hemangioma Rhabdomyosarcoma Malignant melanoma of choroid Retinoblastoma

Benign Malignant

Malignant: NHL Benign : dermis cyst

NON HODGKINS LYMPHOMA

Retinoblastoma

Arises from blast cells of Retina

Gene mutation 13q14
Knudson’s 2 hit hypothesis
MC age of diagnosis : <3 years ( 1.5 years )

Types

v u

Sporadic (90%) Familial (10%)

>Unilateral > Mostly : Bilateral

v u

Somatic Germ line

Non hereditary Hereditary
(2/3) (1/3)
Unilateral Bilateral

Total no of bilateral cases : 25-40%

MC tumor associated with Retinoblastoma : Pinealoblastoma

MC secondary tumor ( patient is disease free ) : Osteosarcoma

>
Unilateral
Retinoblastoma > Bilateral
> Trilateral = Bilateral Retinoblastoma + Pinealoblastoma

Microscopy > Mc : Flexner–Wintersteiner rosettes

Homer wright rosettes >

Pseudorosettes
Fleurettes

4 stages
1. Quiescent/ Asymptomatic : Signs >> symptoms
Earliest sign : Leucocoria ( 1st MC ) >

2nd MC : Squint ( convergent )

Nystagmus, poor vision, ERD

1.5 year baby with leucocoria

1st d/d should be Retinoblastoma

2. Glaucomatous ( 3rd MC sign )
Buphthalmos ( IOP )
^

3. Local spread - MC Optic nerve

4. Distant metastasis > Direct route

> Lymphatic
> Blood route ( most severe )

Liver
> Most common cause of death

Tests : B - scan
CT - scan - calcification, not preferred in children
MRI - better to see calcification
>
It will also show optic nerve involvement

Plasma LDH levels : Not diagnostic, only prognostic value

Treatment :1. Unilateral, <10 mm — tumor destruction by laser photo coagulation or cryotherapy
2. Unilateral, >10 mm — TOC : Enucleation
3. Bilateral, metastasis present : TOC — chemo

:
VEC regimen

Vincristine, Etoposide, Carboplatin + life long surveillance

Rb can mimic inflammatory condition Pseudo uveitis or Masquerade syndrome

 Neuro-Ophthalmology

Visual perception > 4 senses

1. Light sense
2. Colour sense
3. Contrast sense
4. Form sense

Visual sensation
How a visual impulse is transmitted ?

Optic nerve Through visual pathway

Cornea Aqueous humor Lens
> > Visual cortex
Vitreous humor Retina

Rods and cones ( photoreceptors )

Periphery Centre First order neurons
: : 6.5 million
120 million

II Order neurons ( Bipolar cells )

!
III Order neurons ( Ganglionic cells )
(Axons of Ganglionic cells lies in NFL and continues to form the Optic nerve)
III Order neuron

IV Order neurons ( Lateral geniculate body )

Visual pathway

Retina
Form temporal retina From nasal retina
-

Optic nerve
na
e ti
Te

lr
m

sa
po

Na
ra

:
lr

Temporal fibres Nasal fibres

et
in
a

Ipsilateral Cross over

.

Optic nerve
Lateral chaisma Optic chaisma

Ipsilateral > Optic tract C Contralateral

:
Lateral geniculate body

Optic radiations
Sensory fibres passing through 2 lobes

v
v

Parietal lobe Temporal lobe

Superior fibres Inferior fibres

Visual cortex
> Occipital cortex C

Brodman area 17,18,19

 Optic nerve

• Continuation of NEL of Retina

• Each optic nerve contains 1.2 million axons
• Total length : 47-50 mm

4 parts

1. Intra ocular 2. Intra orbital 3. Intra canalicular 4. Intra cranial

v v v v

Optic disc/ Myelinated Optic canal In brain

Optic nerve Head Extra ocular part ( other content : Ophthalmic artery ) Above cavernous sinus
1 mm 30 mm 6-9 mm 10 mm
Shortest part Longest part
Non myelinated

Superior Rectus & Medial Rectus

Adherent to pial sheath near optic foramen

Optic Tract

I
• Each Optic tract contains temporal fibres of same side & Nasal fibres of opposite side

Lateral geniculate body

6 layers

Layers 1,4,6 : Receives input from contralateral Hemiretina

Layers 2,3,5 : Receive input from Ipsilateral Hemiretina
 Pathways

i i
Magnocelluar Parvocelluar

Large size cells Small size cells

Layers : 1,2 Layers : 3–6

movement Colour
Depth Texture
flickering Shape
Fine details

Visual cortex

Blood supply : PCA ( Posterior cerebral artery )

Tip of the visual cortex : PCA + Middle cerebral artery

v u

Macula Double blood supply

T N N T

i
Right eye Left eye
Na
na

sal
e ti

ret
lr

Te a
sa

in
i

mp et
na
Na

o ral lr
ra
re t in po
m
a Te

*
1. Optic nerve

2. Optic chaisma

3. Bilateral lateral chaisma 3.

4. Optic tract

5. L G B L G B

④k
6. Optic radiation

7. Visual cortex
 Visual pathway defects ( Right side )

1. Optic Nerve
T N N T
Eg : Trauma, Tumor, Optic neuritis, CRAO

Total blindness on side of lesion with normal vision on other side

2. Optic chaisma > Nasal fibres from both sides

Right eye Left eye

Bilateral hemianopia T N N T
^ 7 h
7

Right side Left side Right side Left side

Heteronymous
Different L j
Sides

Eg : Craniopharyngioma Pituitary adenoma

t
V
V

(Towards crown) (Towards pedal)

.

Superior nasal fibres are affected Inferior nasal fibres are affected

v u

Inferior visual field effects Superior visual field is affected

Inferior heteronymous quadrantanopia Superior heteronymous quadrantanopia

3. Bilateral lateral chaisma

Eg : Hydrocephalus Right eye Left eye

✓
T N N T
Bilateral temporal fibres 7 r 7 r

Right side Left side Right side Left side

Heteronymous
V

Binasal hemianopia

4. Optic tract

Right optic tract

u
r

Temporal fibres of Right side Nasal fibres of left side Right eye Left eye

v v
T N N T
Nasal visual field of Right side Temporal visual field of Left side > r y
r

Right side Left side Right side Left side

v

Contralateral Homonymous hemianopia Homonymous

V

MC visual pathway defect

Optic tract lesion = incongruous type

Different in extent and severity in 2 eyes

 5. Lateral geniculate body
Supplied by anterior choroidal artery
.

Contralateral homonymous hemianopia

: Supplied by lateral choroidal artery

Lesion of anterior choroidal artery

Key hole/ tongue shaped defect

6. Optic radiations Contralateral homonymous hemianopia

:
Parietal lobe

Superior fibres
t
Temporal lobe

Inferior fibres

Inferior homonymous quadrantanopia Superior homonymous quadrantanopia

or or
Pie in floor Pie in sky

7. Visual cortex > Contralateral homonymous hemianopia

Congruous type

P H
Lesion of Posterior cerebral artery

Macular sparing
Due to double blood supply

Traquiare’s junctional scotoma

Junction of Optic nerve and optic chaisma

( Proximal lesion )

Anterior knee of Von Willebrand

# NR
t Inferionasal fibres loop around the optic nerve before decussating in the optic chaisma
TR
N
TR

R
Su

Left optic nerve Temporal

pe
ro

: Nasal
na
sa
lf
ib
re
s

T
-

Total blindness in left side

Infe
ro
nasa
l fi
bres

Right eye : inferionasal fibres are affected

Superio quadrantanopia
 Optic neuritis < 70%
n

Etiology : 1. MC Demyelinating disorders, eg : Multiple Sclerosis

2. Inflammation : Posterior uveitis
3. Hereditary : Leber hereditary optic neuropathy (LHON)
4. Idiopathic
5. Toxic optic neuropathy : Methyl alcohol, Ethyl alcohol, Chloroquine, Ethambutol, Digoxin, Amiodarone, tobacco
6. Ischemic diseases: Anterior Ischemic Optic neuropathy ( AION )

Types -3

i
- v

1. Papillitis 2. Neuro-retinitis 3. Retro Bulbar Neuropathy

Optic nerve Head • Least common type • Most common type

.

• Not found in multiple sclerosis • Most symptomatic

Only optic disc involved • Involves : Optic disc + macula • Found in Extraocular part
• Present in viral infections • Adults

Clinical features
Symptoms : 1. Mostly unilateral
2. Sudden diminition of vision ( Profound/ complete )
3. Mostly painful ( Deep retro-orbital pain )
4. Pain increases on ocular movements

Medial Rectus
Superior Rectus

:O
-

Superior Rectus and medial Rectus are adherent to pial sheath

Optic nerve
Lateral Rectus
.

Inferior Rectus

5. Defect in colour vision : Red-Green ( Blue-Yellow in macular lesions )

6. Defect in depth perception : Pulfrich phenomenon

7. Uthoff symptoms

"

Aggravation of symptoms Heat ¥

; Exertion
.

Optic disc edema Macular Star formation/

Normal Puckering

Signs : 1. Earliest : RAPD

2. Tenderness at the insertion of Superior Rectus and Medial Rectus
3. Central or centrocaecal scotoma

✓
Visual field charting
Involves blind spot
.

Best test
4. Optic disc edema ( much less than papilloedema )
5. Fundus

i. Papillitis ii. Neuro retinitis iii. Retro bulbar neuritis

+
-

Hyperaemic disc

Blurred margins
i
Optic disc edema + macular exudates

Macular Star formation/ Puckering

t
Behind eyeball

Fundus normal
 Treatment : Steroids

IV : Methyl prednisolone x 3 days

Oral : Methyl prednisolone x 11 days

Taper in next 3 days

Toxic Optic neuritis

Painless
Bilateral contraction of visual field
Gradual progressive diminition of vision

Treatment : IM Vit B12 > 1000 units weekly x 10 weeks

3 5
Leber hereditary optic neuropathy (LHON) M P

Clinical features : unilateral to bilateral vision loss

LHON usually presents as painless, subacute, central visual loss in one eye. Weeks

• Mitochondrial inheritance
to months later, the second eye becomes involved, with a median delay of 6–8 week

Diagnosis : Hyperemic optic disc with telangiectasia

• Optic disc hyperemia
• Peripapillary telangiectatic blood vessels

• Maternally transmitted
• Vascular tortuosity
• Swelling of the retinal nerve fiber layer (RNFL) around the optic disc without corresponding leakage on fluorescein
angiography (sometimes termed “pseudoedema”)
Differential diagnosis:
• Demyelinating optic neuritis

• MC manifested in Males
• Neuromyelitis optica spectrum disease
• Toxic optic neuropathy
• Compressive optic neuropathy

• Painless
• Primary optic atrophy
• Pupillary reactions normal
• Pseudopapillitis present
• Peripapillary telangiectatic microangiopathy

Anterior Ischemic Optic neuropathy ( AION ) 7 Altitudinal hemianopia

V
Due to Occlusion of short posterior ciliary artery

v v

Arteritic 5% Non arteritic 95%

Classic symptoms:
Patients may state that their headache has been
occurring for a duration of 2 to 3 months and

( Giant cell Arteritis ) >

worsens with exposure to cold and at night when
the pressure of the pillow causes pain to the artery
( DM, HTN )

Pale optic disc Hyperaemic optic disc

t
Transient ischemic attacks

Transient obscuration of vision ( ocular ischemic syndrome )

.

Superior altitudinal hemianopia

• Scalp tenderness
• Jaw claudication ( Ischemia of masseter muscle )

First investigation : ESR ( very high )

I

ESR ≥ 50 mm/h

Investigation of choice : Carotid Doppler USG

Treatment : High dose of steroids

Inferior is more common than superior

Papilloedema
> Optic disc/ Optic nerve Head

• Passive optic disc edema due to ICP

• Always bilateral

ICP

Axostasis

Stasis in flow of plasma

Stasis in optic nerve Head

v
u

Mechanical Vascular

1. Extra cellular edema 1. Hyperaemic optic disc

2. Earliest - Nasal blurring of disc margins 2. Venous engorgement/ congestion
3. Obliteration of cup 3. Retinal hypoxia/ NFL infarcts
4. Elevation of optic nerve Head
v

5. Retinal / choroidal folds known as Paton’s lines Cotton wool spots D/D
4. Splinter hemorrhages
5. Macular star formation

>
Clinical features : 1. ICP : Throbbing headache, Projectile vomiting, Amauror’s fugax
^

2. Normal colour vision & depth perception

3. Uthoff’s symptoms : absent
4. Optic disc edema : 7-8 times than optic neuritis

:
5. Enlargement of Optic nerve Head

6. Enlargement of blind spot

Grading of papilloedema
 Grade 1. C shaped halo
Grade 2. Circumferential halo
Grade 3. Loss of major blood vessles as it leaves optic disc
Grade 4. Loss of major blood vessel at least 1 on optic disc
Grade 5. Loss of all blood vessles

Treatment : Only of cause

Optic atrophy

Primary Secondary Tertiary

Without previously optic disc edema With previously optic disc edema Consecutive to retinal disease

Etiology : Brain lesions Etiology : Optic nerve lesions Etiology : Retinal disease

Chalky white in colour Dirty white in colour Pale yellow waxy

Eg : LHON Eg : Papillitis Eg : CRAO

Trauma AION CRVO
Tumor Papilloedema Retinitis pigmentosa
Toxic Optic neuropathy

Pupillary Reflexes

u
v

Light reflex Accommodation

-

Pathway of accommodation reflex is same as light reflex

v u

Direct light reflex Indirect/ consensual light reflex Except LGB instead of Pre tectal nucleus

v r

Same eye constricting Other eye constricting

Light

t.tt
Sphincter pupillae
n
Sphincter pupillae
n
v

Retina
Ciliary ganglion Ciliary ganglion
Optic nerve
III Nerve III Nerve
Optic tract
EWN
n
EWN
n

Forms the basis of indirect light reflex

Pre tectal nucleus
V

( Anterior to LGB )
-
 Abnormal pupillary reflexes

1. Argyll Robertson pupil ( ARP )

Accommodation reflex present
i

Lesion of bilateral pre tectal nucleus

Light reflex absent on both sides

Accommodation reflex present on both sides

V
Light near dissociation

Eg : Neuro-syphillis

Isocoria present
> Same size of pupil on both sides

2. Adie tonic pupil

Non reactive to > Light reflex

> Accommodation reflex

Unilateral lesion of ciliary ganglion

Affected side Normal side

DLR : absent DLR : Present
ILR : absent ILR : Present
AR : Slow/ absent AR : Present

v u

No reflex All reflexes Present

v u

Pupil dilated Pupil constricted

Anisocoria Present

Denervation hypersensitivity Present

Therefore Adie’s Tonic Pupil constricts even with 0.1% pilocarpine

Right eye Left eye

3. RAPD ( Relative Afferent Pupillary Defect )
> Optic nerve

Also known as Marcus Gunn pupil

Earliest manifestation of Optic nerve disease
V

Optic nerve defect

Eg : Optic neuritis, CRAO, Ischemic Large Retinal detachment, CRVO

Tested by Swinging flash light test

*÷ DLR : Present
.

ILR : Present

ILR : absent
¥÷ DLR : absent
.

Paradoxical dilatation of pupil

RAPD present in left eye

 4. Hutchinson pupil : due to ICP
^

Temporary constriction of pupil due to meningeal irritation of III Nerve followed by permanent dilation due to III Nerve palsy

5. Wernicke’s reaction :

Lesions of Optic tract

# NR
t Both DLR and ILR are absent of the light shown to

TR
N
TR

R
Temporal half of affected side and nasal half of opposite side
While both are present vice versa

)
"

Right temporal Left nasal

> a

DLR : absent DLR : Present

ILR : absent ILR : Present

6. Horner’s syndrome

'
Oculo sympthetic palsy
Upper lid

:O
Ptosis

Inverse ptosis
: Lower lid
:
Muller’s muscle

Inferior tarsus muscle

.

Sympthetic supply

>
Narrowing of palpebral aperture >
Palsy of dilator pupillae : Miosis

Apparent enophthalmos/
Pseudo enophthalmos
+
Loss of ciliospinal reflex

Diagnosis : 1% aprachlonidine / 4% cocaine test

No dilatation in normal pupil Dilatation in Horner’s syndrome

7
v u

No dilatation in Horner’s syndrome Dilatation in normal eye

Horner’s syndrome

"

1% amphetamine test

.
/
Dilatation : Present

Pre Ganglionic
,
Dilatation : Absent

Post Ganglionic
 Anisocoria : Difference in pupil size > 0.4 mm

Normal eye Horner’s syndrome

÷
Anisocoria increases in dark

In dark condition,
Normal pupil dilate, Horner’s syndrome not dilated due palsy of dilator pupillae

Colour vision

Trichromatic — 3 primary colours

Red Green Blue

Given by Young Helm Hottz

Test for colourblindness : 1. MC : Ishihara colour plates ( Screening )

>
38 colour plates

2. Lantern test
3. Holgren’s test
4. Most sensitive : Farnsworth Munsell 100 hue test
>
85 caps

5. Nagel’s anomaloscope
6. Hardy Rand Rittler test

Colour blindness

XLR , M>F
-

v
v

Partial/ Anomaly Total/ Anopia

Red Protanomaly Protanopia

Green Deuteranomaly Deuteranopia

> MC

Blue Tritanomaly Tritanopia

Drugs
✓

1. Digoxin : Xanthopsia ( Yellow vision )

2. Ethambutol : Red-Green blindness
3. Chloroquine : Red-Green defect ( not blindness )
4. Sildenafil : Transient Blue Green anomaly
 Congenital anomalies of Optic disc

1. Coloboma Absence of the tissue 2. Drusens

i
Inferior crescent
Drusens

3. Hypoplasia of Optic disc

Small sized optic disc surrounded by yellowish or pigmented ring

4. Mediated optic nerve fibres

Normal myelination starts from brain — upto Lamina cribrosa

Sometimes, it reaches Optic disc
Enlargement of blind spot

5. Morning glory Syndrome

• Displastic condition
• Absence of Lamina cribrosa
• Scleral defect
• Large cup surrounded by neuroglial tissue
 Squint

Anatomy of extra ocular muscles

7 pairs = LPS + 4 Rectus muscle + 2 Oblique

j
Levator palpebral superioris

Elevation of upper lid

Rectus : SR, IR, MR, LR

Oblique : SO, IO

Angle between visual axis and orbital axis = 23

c
.5
22
=
/2
45

Nerve supply : ALL3 SO4 LR6

All extra ocular muscles are supplied by III Nerve
Except SO : IV & LR: VI

Elevation
>
Straight

Intorsion

Addiction
Abduction

Extortion

Depression
 Rectus Oblique

Straight EOM Titled EOM

Same direction Opposite direction

Eg : SR : elevation Eg : SO : depression
IR : depression IO : elevation

Primary action Elevation Primary action Intorsion

: Depression : Extortion

Inserted straight into sclera Inserted in a tilted manner

anterior to equator posterior to equator
-

Anterior pole

Lateral Rectus Medial Rectus

Equator

Inserted at 0
Hence no secondary and tertiary actions

Rectus EOM are inserted 23 Lateral to visual axis

°

23
Boffo ,

Hence Rectus muscles do maximum elevation and depression

23
@f°
in abducted eye

Oblique EOM are inserted 51 medial to visual axis

Hence oblique muscles do maximum elevation and depression

in adducted eye
 Sin n
Radd n

Superiors are intorters Rectii > Adductors > Superior Rectus

Hence SR and SO : intorters > Inferior Rectus
Tertiary action
Inferiors are extorters Obliques > Abductors > Superior oblique
Hence IR and IO : Extortion > Inferior oblique

Actions of EOM’s

EOM Action Primary Secondary Tertiary

SR Elevation Intorsion Adduction

:
IR Depression Extortion Adduction
Maximum in abducted eye

MR Adduction

LR Abduction

SO Intorsion Depression Abduction

IO Extortion Elevation Abduction

Maximum in adducted eye

Longest EOM : Superior oblique ( Cheating muscle )

Shortest EOM : Inferior oblique

Origin of Rectus muscles

Medial Rectus
Superior Rectus
Annulus of zinn <
✓

Optic nerve
-
Lateral Rectus

Inferior Rectus

Rectus origin : From common tendinous ring known as Annulus of zinn at the apex of orbit
Rectus insertion : Rectus muscles are inserted straight into sclera at fixed distance from limbus

M I L S
Medial Rectus Inferior rectus Lateral rectus Superior rectus

( in mm ) 5.5 6.5 6.9 7.7

Closest to limbus
 Origin of oblique muscles

Superior oblique
V

1. Body of sphenoid
2. Tendinous attachment with SR Passing through a fibrocartilagenous pulley known as trochlea

Insertion : Supero- lateral part of sclera behind equator

Inferior oblique
V

Floor of the orbit ( not from Annulus of Zinn )

Insertion : Infero lateral part of sclera behind equator

Ocular movements

V
V

Uniocular/ Ductions Binocular

v v u
v v

Horizontal axis Vertical axis Antero-posterior axis Conjugate/ version Disconjugate/ vergences

< > v v
^
Same direction Opposite direction
✓ v

v Eg : Right : Dextroversion
u
v

Left : Levoversion Convergence Divergence

Elevation Adduction Intorsion Up : Supraversion
& & & Down : Infraversion
> c c >
Depression Abduction Extortion Right + Up : Dextroelevation
Right + Down : Dextrodepression
Left + Up : Levoelevation
Left + Down : Levodepression

Positions of Gaze 9

V v
V

Primary Secondary Tertiary

f
u
v

One Four Four

Dextroelevation 7
Levoelevation

×
n r
v
Straight up

Straight ahead

<
Straight right Straight left
>
Straight down

L J
Dextrodepression Levodepression

/
 Cardinal positions

:
In which all EOM can be tasted
1. Dextroversion 2. Levoversion 3. Four tertiary positions

Groups of EOMs

1. Synergist : 2 EOM having same action in 1 eye

Eg : SR and IO wrt elevation

2. Antagonist : 2 EOM having opposite action in 1 eye

Eg : SR and IR of 1 eye

3. Yolk muscles : pair of EOM one from each eye which contracts simultaneously during conjugate movements
Eg : Dextro version RLR and LMR

Levoversion LLR and RMR

Dextroelevation
Abducted Adducted

RSR LIO

Dextrodepression C C
RIR LSO

u u
Levoelevation
Adducted Abducted

RIO LSR

Levodepression O O
RSO LIR

Dextroelevation Levoelevation

\
7
RSR LSR
LIO ✓ VV
Flip the EOM
RIO c

Dextroversion Levoversion

%
RLR LLR
LMR RMR

L J
Dextrodepression Levodepression
RIR LIR
LSO RSO

4. Contralateral antagonist : Pair of EOMs, one from each eye which contracts simultaneously during disconjugate movement

v v

Convergence Divergence
Medial Rectus of both sides Lateral Rectus from both sides
 Laws of inervation

1. Herring’s law : Equal and simultaneous energy flows to a pair of yolk muscles

Dextroversion > RLR, LMR

2. Sherrington’s law of reciprocal inervation : Increased flow of energy to contracting muscle is accompanied by decrease in flow to relaxing muscles

Dextroversion : RLR and LMR ( Energy )

:
LLR and RMR ( Energy )

Binocular single vision

3 grades

1. Simultaneous perception of 2 images ( even dissimilar )

2. Fusion of 2 similar images
3. Stereopsis

Flowers
Tail

÷
Two dissimilar but
incomplete images
fuse to form complete
image

Normal retinal correspondence

Point to point correspondence

Fovea Fovea

Seen simultaneously

to
Fusion

Single image

Abnormal retinal correspondence In squint

Fovea

Fovea

"
Correspond to extra Foveal point

Crude form of binocular single vision

 >
Binocular single vision

Test of suppression/ sensory anomalies

1. Worth 4 dot test - least physiological test

Normal — 4 lights without squint

ARC — 4 lights with squint
Right eye suppression — 3 Green
Left eye suppression — 2 Red
Diplopia — 5 lights ( 3 Green + 2 Red )
Alternating suppression — 3 Green/ 2 Red alternatively

2. Bagolini striated glasses test — most physiological

Right eye Left eye

135 45

Without squint — Normal

With squint — ARC

Right eye suppression

l Normal cross without squint : NRC

l Normal cross with squint : ARC

L R

Diplopia

Right eye suppression

Left eye suppression

X Central suppression
 Squint Strabismus

Misalignment of 2 visual axis

Perfect state of alignment of 2 eyes known as Orthophoria

Types
A. Apparent/ pseudo squint
B. Latent squint
C. Manifest squint

A. Apparent/ pseudo squint

V
V

Pseudo convergent ( ESO ) Pseudo divergent ( EXO )

> c c >

Causes :
Telecanthus : Increase in inter canthal 1. Increase in Inter canthal distance
distance with normal inter pupillary distance with increase in inter pupillary
distance
Epicanthus : Vertical semilunar fold of skin 2. Wide inter pupillary distance
over medial canthus

>
60 mm

> 30 mm

V
In telecanthus = 45 mm

B. Latent squint

Squint is kept hidden by fusional reserve of EOM’s known as Phorias

V V V V

Eso phoria Exo phoria Cyclo phoria Hyper phoria

V V u V

Convergent Divergent Rotatory Upward

Patient will manifest squint due to fatigue of EOM

Eg : excessive near work, dim light, etc

Tests by breaking fusion

1. Cover-uncover test
No simultaneous perception

Eso
V

Exo
t
No fusion

Squint manifest
Recovery movement Recovery movement
L s

Use : Presence and type of squint

v v

Outwards Inwards

No movement : No squint
 2. Maddox rod test

Consists of cylinders parallel to each other

Maddox rod converts point source of light into a red line perpendicular to its axis

What patient will see

1
-

Vertical squint
.

= Horizontal squint

Always kept parallel to plane of squint

:
Dissimilar images

No fusion
-

v
v

Orthophoria Diplopia
Simultaneous perception present
✓

I > Latent squint

Evaluation of latent squint

1. Visual acuity and refraction under full cycloplegia > Most imp step

2.
 3. Prism bar cover uncover test Cover eye ( squint ) with prisms of increasing power ( apex towards deviation )
and perform cover uncover test until there is no recovery movement

4. Maddox rod test Dissimilar images

Fusion broken

5. Maddox wing test

o w
arr
hite
lw
ica
Measures phorias for near ( 33 cm )
t
Ver

Right eye arrow

l red
iz onta
Hor

Horizontal
L
Vertical >

( white ) ( red )

Treatment of latent squint

C →
O P >
S

1. C : Correction of Refractive error

2. O : Orthoptic exercises to improve fusional reserve
3. P : Prisms ( In glass ) > Synaptophore
4. Surgery > After 4-5 years of age

v
u

Recession Resection

Weaken EOM
t
Loosening of EOM

v
n
t
Shortening the EOM

Strength

Eg : Divergent squint

v v

Overaction of Lateral Rectus Under action of Medial Rectus

u v

Sx : Reccesion Sx : Resection
 C. Manifest squint

u v

Comitant/ non paralytic Incomitant/ paralytic

Amount of squint remains sane in all positions of gaze Amount of squint is not same, maximum when patient tries to look in direction of EOM

No limitation of ocular movements Ocular motility restricted

No palsy Present Palsy Present

Primary deviation = Secondary deviation Secondary deviation >> Primary deviation

Comitant/ non paralytic

Etiology : 1. Refractive Errors >

Amblyopia ( lazy eye )
2. Anisometropia

Gross difference in Refractive power of 2 eyes

3. Using wrong specs for long time

4. Dense > Corneal opacities

> Cataract
> Macular lesions

Comitant/ non paralytic

v u

Esotropia ( convergent ) Exotropia ( divergent )

v u

Accommodative Non accommodative

Associated with accommodation reflex Not associated with accommodation reflex

1. Congenital — Present since birth

u v

Refractive Non refractive 2. Primary — 2-5 years

3. Secondary — Adults ( eg : Cataract )
High hypermetropia High AC
A Ratio 4. Consecutive — Over correction of divergent squint

AC : Accommodative convergence
A : Accommodation

Treatment of comitant squint

C # O1 O2 S P >
Oclude normal eye
1. C : Correction of refractive error
V

2. O1 : Occlusion therapy ( Amblyopia ) >

Most imp To stimulate squint eye
3. O2 : Orthoptic exercises

:
4. S: Surgery Rule of Occlusion
5. P : Prisms for remaining corrections
x : 1 ( 1 day normal eye is kept open )
No of days of Occlusion = Age in years

Eg : at 1 year = ratio is 1:1 at 2 years = ratio is 2:1

l

at 5 years = ratio is 5:1

Amblyopia becomes refractory after 5-6 years

 Evaluation of comitant squint

1. Visual acuity and refraction under dilatation ( Fundus ) > Most imp step

2. Hirschberg corneal reflex test

① No squint
>

15 Squint ( pupillary border )

; 45 Squint ( Limbus )
>
30 Squint

3. Krimsky test

4. Synaptophore

5. Meddox wring test > Measures squint for near ( 33 cm )

6. Direct cover test

7. PBCT >
Prism + direct cover test till no recovery movement

Strength of prism where movement becomes nil = amount of squint

 Incomitant squint

3 types : 1. Paralytic
2. Restrictive
3. A-V pattern

Paralytic squint

Palsy Present ' EOM

. Nerve . III
IV
iVII

O O Normal eyes

I. L

2 visual axes are perfectly aligned with each other

t
Simultaneous perception of images

Fusion

Steropsis

Binocular single vision

Eg : LR palsy ( VI nerve ) LR : abduction

O O . Abduction deficit

No alignment of visual axes

t
No simultaneous perception

No fusion

1 Diplopia . Most imp symptom of the paralytic squint

off
'

Crossed Uncrossed

Divergent squint Convergent squint

¥
Temporal retina Nasal retina Nasal retina Temporal retina

Temporal retina Nasal retina Nasal retina Temporal retina

Right eye Left eye

Exo
Eso

Temporal field
Nasal visual field Image of RE
.

Image of Left eye on left side

Right side of left eye
 2 Compensatory head tilt

"
In the direction of action of the paralysed EOM

t
Same side

Lateral Rectus palsy

t
Opposite side

Superior oblique palsy

Intorsion
:Depression in adduction

3. Diplopia : Confusion, vertigo

4. Visual acuity : Normal
5. No amblyopia
6. Limitation of ocular movement
7. Ocular deviation

O O
:
Normal eye

Deviation of normal eye under cover

t
Squint eye

Primary deviation . Hirschberg corneal reflex test

O O No squint
>

>RMR , LLR
-
:

Occluder 15 Squint
: 45 Squint
✓
Only fixating eye

:t
Uses paralysed extra ocular muscle

According to Herring’s law

Equal and simultaneous energy to yolk muscles

i
Equal energy in LLR ( palsy ) and RMR ( normal )

Right eye will deviate more

Hence secondary deviation is more than primary deviation

Treatment : 1. Treat the cause DM, HTN

: Surgery/ aneurysm/intraocular Tumor/ Space occupying lesion
2. Systemic steroids for any non specific inflammation
3. Vitamin B complex : acts as a neurotonic
4. Surgery if required

Isolated nerve palsies

v V
v

III IV VI y Most common

µ
> Etiology: mc : ICP^
> False localising sign
Lateral Rectus Cavernous sinus thrombosis
Orbital apex syndrome
Convergent squint / Esotrophia Caratico cavernous fistula

Uncrossed diplopia

Due to VI nerve palsy : Diplopia in lateral gaze

 IV nerve palsy
V

Superior oblique paralysis

V

Intorsion >
Normal functions
Depression Maximum in adducted eye
>

Abduction
>
Hypertropia
u

Peculiar features of IV nerve

v
• Thinnest nerve
• Longest Intracranial course
• Only nerve to emerge from dorsal aspect of brain stem
• Only nerve to have crossed inervation

III Nerve palsy > Most important

Supplies all EOM except SO4 and LR6

Only actions left

v r

Superior oblique Lateral Rectus

v v

Intorsion Abduction
Depression
Abduction -Maximally spared

Eye is down and out

LPS palsy : ptosis
Pupil is dilated ( Pupillary reflexes — Efferent nerve : III Nerve )

Pupillary sparing III Nerve palsy

.
>
Constrictor fibres > Not affected in DM, HTN

III Nerve

§
Surgical causes : compression of constrictor fibres

Pupil is involved
 Restrictive squint

Limitation of movement due to fibrosis

1. Duane’s Restrictive squint / Duane’s Retraction syndrome

Fibrosis of medial Rectus or lateral Rectus or both

On attempting adduction > Narrowing of palpebral aperture

> Enophthalmos

On attempting abduction > Widening of the palpebral aperture

> Proptosis

2. Brown’s Superior Oblique Syndrome : Fibrosis of superior oblique

Inability of inferior oblique to contract

Limitation of elevation in adduction

3. Strabismus fixus : fibrosis of medial Rectus of both eyes

A & V pattern squint

Increase in amount of squint by 10 & 15 respectively in Upgaze and downgaze

> c Esotropia c r s Exotropia

A pattern V pattern

< > Exotropia c or Esotropia

Maddox rod test

Temporal visual field

Right eye Nasal visual field
^
Left eye ^

I
#

Esotropia Exotropia

>
Uncrossed diplopia S
Crossed diplopia

Nasal visual field

✓ v v

Temporal visual field L

Same side

Dot reflex on right side of red line Dot reflex is on left side of red line
Left Right
 Forced duction test

To differentiate between paralysed and the restrictive squint

Local anaesthesia is used

Forceps : limbal area

I
Patient looks in direction of action of paralysed muscle

' Passively move the eyeball in direction of action of paralysed EOM

ti
If restriction Present Restriction absent

No movement Movement present

Forced duction test positive Forced duction test negative

Restrictive squint Paralytic squint

Titmus fly test

> Right side

Left side < r

Crude stereopsis
✓
Fine stereopsis
 Best test

Frisby test

Lang test
TNO test
 Park’s 3 step test

Eg : Right hypertropia which increases in Right gaze and right head tilt

Relative right hypermetropia

Right eye hypertropia or Left eye hypotropia Step 1

:I
Right eye depressor palsy

Right inferior Rectus

t
Left eye elevator palsy

Left superior Rectus

Right Superior oblique Left inferior oblique

Increase in Right gaze Step 2

( Right eye C Left eye

v v

Abduction Adduction

✓
V
V L

Rectus will cause maximum Oblique will cause maximum

elevation and depression elevation and depression

v r
RIR LIO

Increase in Right Head tilt

v v
Step 3
L L
j j

Right eye Left eye

f
Intorsion Extortion
:

f
Superior muscle Inferior muscle

:
RIR LIO .

Left hypotropia

Relative right hypermetropia

Eg : 2. Left hypertropia increase in left gaze and left head tilt

Step 1 : Left hypertropia or Right hypotropia

I
Left eye depressor palsy

LIR
.
t
Elevator palsy in Right eye

RSR
LSO RIO

Step 2 : increase in left gaze Step 3 : increase in left head tilt

j
L

j
J
L L
'

Right eye > Left eye > Right eye Left eye

v v

Adduction Abduction Extortion Intorsion

v v V ✓

Oblique muscles Rectus muscles Inferior Superior

V v
v v

RIO LIR RIO LIR

 Optics and refraction

Light : Visible portion of electromagnetic spectrum

400-700 nm

VIBGYOR
Lowest wavelength < > Highest wavelength

Power of the eye : + 60D

v r

Cornea Lens
43-45 D 13-17 D

Refractive Index : Cornea : 1.376

Lens > Cortex/ surface= 1.39

> Nucleus/ cortex = 1.42

Aqueous humor = Vitreous humor = 1.33

Refractive surfaces of eye : 4 1 2 3 4

1 2
Anterior and posterior surface of cornea
Aqueous humor Vitreous humor
3 4
Anterior and posterior surface of lens

Most imp refractive surface : Anterior surface of cornea

Max difference in Refractive Index at anterior surface of cornea

Purkinje image based test

No of images formed = No of refectory surfaces

Normal eye = 4 images

Aphakia = 2 images
Pseudophakia = 4 images
Cataract
>

IMSC 4 images
>

>

Mature 3 images
>

Out of 4 images, first three are visual and erect

While 4th is real and inverted

Hirschberg corneal reflex test : Used first Purkinje image

 Emmetropia

Normal state of refraction

>
Parallel rays of light coming from infinity

>
focused at retina with accommodation at rest
>

Ametropia / Refractive errors

✓

Abnormal refraction
MC cause of low vision/ ocular morbidity

✓ v

Myopia Hypermetropia
J
j
Short sightedness Far sightedness
> >

> >

> >

DOV for distant objects DOV for near objects

Etiology : 1. Increase in Axial length : Most imp Etiology : 1. Decrease in axial length

Increase in axial length by 1 mm will produce 3D myopia Decrease in axial length by 1 mm will produce 3D of hypermetropia
Ratio = 1:3 Ratio = 1:3

Eg : Buphthalmos Eg : Congenital Rubella syndrome

v v

Axial myopia Micro ophthalmos

2. Curvature of refractive surfaces > Cornea 2. Curvature of refractive surfaces > Cornea
> Lens > Lens

v
u

If Increase in curvature : Myopia If decrease in curvature : Hypermetropia

Ratio = 1:6 Ratio = 1:6
Increase by 1 mm : 6D of myopia Decrease by 1 mm : 6D of hypermetropia

Eg : Keratoconus Eg : Cornea plana

3. Refractive index 3. Refractive index

v v

Increase in RI will cause Myopia Decrease in RI will cause Hypermetropia

Eg : Nuclear sclerosis Eg : Cortical cataract

t
t
-

Increase in RI Over hydration

Progressive index Myopia Decrease in RI

Index hypermetropia

4. Posterior displacement of lens 4. Anterior displacement of lens

 Signs : 1. Large eyeball Signs : 1. Small eyeball
2. Large cornea 2. Small cornea
3. Deep anterior chamber ( POAG ) 3. Shadow anterior chamber ( PACG )
4. Large and pale optic disc 4. Small and shiny optic disc/ Silk shot appearance/ pseudopapillitis

Treatment : Simple Myopia Treatment : Simple Hypermetropia

i : Concave/ diverging/ minus lens i '

Convex/ converging/ plus lens

v v
Minification of image r
Magnification of images

Refractive surgery Refractive surgery

v v

Age : 21 years Age : 21 years

Minimum corneal thickness : 450 um Minimum corneal thickness : 450 um
Stable refraction for at least 1 year Stable refraction for at least 1 year

MC : LASIK Hypermetropia

v v
T
Lifting a flap with hinge : 180 um Latent/ hidden Manifest
Minimum thickness of stromal bed : 250 um
Laser applied on stromal bed
v
=
MC laser used : Eximer laser Kept hidden by inherent tone of Facultative Absolute
ciliary muscles approximately 1D
MOA : Photoablation
v v

For Myopia : flattening of Central cornea Compensated by patient’s Remaining hypermetropia

own accommodative efforts

Myopia : Diverging lens

Total hypertropia = Latent + Facultative + Absolute

i
Trouble in near vision

:
:
Especially small printed stuff Remove ciliary tone Remove accommodation

Preferable to under correct Myopia Cycloplegics Mydriatics

Dilates pupil
High myopia / Degenerative/ Pathological
For hypermetropia : refraction under cycloplegics and Mydriatics
v

Due to over stretching of eyeball outside normal biological variation

u

t
Give full treatment
Degenerative changes in eyeball

>6 D of myopia, progressive

Posterior staphyloma
✓
1. Sclera : Posterior ectasia of eyeball
Crescentic degradation
Known as Posterior staphyloma -

Staphylos = bunch of grapes

Cresentric edge here

Lacquer cracks

2. Choroid

v u

Hemorrhages Breaks in Bruch’s membrane

v v

Foster Fuch spots Lacquer cracks >

 3. Retina : Peripheral retinal degeneration (Lattice)

Night blindness
V

Retinal hole

Rhegmatic Retinal Detachment

4. Vitreous Degeneration - floaters known as Muscae volitantes

5. Lens : Nuclear cataract

Complicated cataract
Pigmentory glaucoma

6. Fundus
Tigroid Fundus

Peri papillary degeneration

>
- -
-
-

tame
.
,
'
I

: i s

Vessles HERE . e
'
'

Optic disc

t
. -

' Myopic / temporal crescent

Tessellated or Tigroid Fundus >

Visible choriocapillaries due to atrophy of RPE

Treatment of high myopia

TOC : Contact lenses

Because of anisometropia ' Anisokonia

n n
v

Difference in image size between 2 eyes

v

Difference Refractive error between 2 eyes g

For specs 1D anisometropia leads to 2% Anisokonia

:
Dissimilar images

No fusion

v
v

5% of anisokonia : best tolerated Diplopia

2.5D of anisometropia : Best tolerated

Types of contact lenses

Hard Rigid/ semisoft Soft

O2 permeability Little / no Average Maximum

Refractive quality Best Average Good

Material PMMA PMMA + Silicon HEMA

TOC : Rigid/ semi soft

MC infection in contact lens users is pseudomonas

 Aphakia

• Absence of lens from pupillary plane

• MC etiology : Cataract surgery

• Optics : 1. Jet black pupil

2. Limbal scar
3. Deepening of anterior chamber
4. Loss of accommodation
5. Power of eye decreases : Highly hypertrophic

TOC : PCIOL : Posterior Chamber Intra Ocular Lens

Specs usually 10 D convex lens

1. 1D = 2% images magnification
10D = 20% images magnification : Not tolerable

High plus
>
2. Spherical or chromatic aberration High minus

3. Pin cushion distortion

4. Jack in the box phenomenon/ Roving Ring scotoma >

5. Cosmesis

Astigmatism
v

Cylindrical error >

Different refractive power in at least 2 principle meridians

Spherical errors >

Myopia Power is same in all meridians
> Hypermetropia

>

Etiology : Uneven Refractive surface >

Cornea MC
> Lens
> Retina
V

Known as Toric surface

Strum’s conoid

The rays are not coming to a point focus rather forms focal lines

Distance between 2 foci known as focal interval of Sturm.

FV
FH
 -

Types
r
v

Regular Irregular

v u

2 meridians ( M1 & M2 ) are perpendicular to each other 2 meridians ( M1 & M2 ) are perpendicular to each other

Eg. Keratoconus

Types of regular astigmatism

1. With the rule :

M1 Vertical

"
Vertical > Horizontal

M2 Horizontal

Eg : Pterygium

2. Against the rule :

M1 Vertical
Vertical < Horizontal

M2 Horizontal

3. Oblique astigmatism
M1 '
M2

t M1 and M2 are perpendicular but not horizontal and vertical

-2 +4
In terms is power
Myopia > emmetropia > hypermetropia
ATR ATR
✓

More the myopia more is the power

Lesser the hypermetropia more is the power -5 0

Power of cylinder acts as perpendicular axis

Classification of astigmatism
-

Simple Compound Mixed

-
One meridians is emmetropic Both meridians have different power with same signs One meridians myopic and other is hypermetropic
-
Other is myopic or hypermetropic

v v V

Simple myopic astigmatism Both myopic Both hypermetropic

Simple hypermetropic astigmatism c

v
> s >

> > > > >

<

M2 M1 M1 M2 M1 M2 M1
>
M1 M2
> 7
M2 > >

> > > > >

> > 7

Simple myopic astigmatism Simple hypermetropic astigmatism Compound myopic astigmatism Compound hypermetropic astigmatism

O +2 -3 +2 +2

-2 O -2 +4 -4
 Strum’s conoid

A. Vertical : Converging ( hypermetropia )

Horizontal : Converging ( hypermetropia )
Vertical > Horizontal
Compound astigmatism with the rule

B. Vertical : Emmetropic
Horizontal : Converging
Simple hypermetropic astigmatism

C,D,E. Vertical : Diverging ( Myopia )

Horizontal : Converging ( Hypermetropia )
Mixed astigmatism > Least symptoms due to circle of diffusion

F. Vertical : Diverging ( Myopic )

Horizontal : Emmetropic
Simple myopic astigmatism

G. Vertical : Diverging
Horizontal : Diverging
Compound hypermetropic astigmatism

Type of astigmatism from power given

1. -2DC and -3DC at 180

I

-2 -3
L

-5
Power of cylinder acts at perpendicular plane
Compound myopic astigmatism with the rule
>
-2 -2

2. -2DS and -1 DC at 90

-2 -2

Compound myopic astigmatism against the rule

-2 -1 -3
 3. -2DS and +2DC at 90

-2 -2

Simple myopic astigmatism with the rule

-2 +2 0

4. +3 DC at 180

+3

Simple hypermetropic astigmatism against the rule

0

How to prescribe spectacles

Refractive error = Retinoscopy - Distance factor - Tonus allowance of mydriatics and cycloplegics

Distance factor = 1
Distance ( in meters )

Tonus allowance of mydriatics and cycloplegics A C H

V V V

Atropine Cyclopentolate Homatropine

+3

With Retinoscopy at 1 meter, Atropine

+5

+3 -1 -1 +1

+5 -1 -1 +3

Take one meridians as spherical

Hence Other will be cylinder

+1DS and +2DC at 90

+3DS and -2DC at 180

Retinoscopy
u
v

Dry Wet

v v

Without mydriatics and cycloplegics Refraction under dilatation with mydriatics and cycloplegics
Refraction undilated

1. Atropine : 1% eye ointment : used in infants : Strongest and longest acting mydriatic
Onset : 3 days only at night
DOA : 2-3 weeks

2. Cyclopentolate

3. Hometropine
 4. Adults : mc : Tropicamide : Shortest acting

DOA : 4-6 hours 30-40 mins

5. Phenylephrine same onset and DOA as Tropicamide

• Only mydriatic no cycloplegic effect
• Preferred in old patients
• Contraindicated in systemic Hypertension due to vasoconstriction

Interpretation of Retinoscopy

1. Neural/ no movement : Myopia = 1D

2. With movement = Myopia < 1D or Emmetropia

3. Against movement = myopia > 1D

Refinement of refraction
v v

Spherical Cylindrical

v v

Duochrome test Jackson cross test >

V Astigmatic fan test

>
More clearer
v

Myopia or over correction of hypermetropia

- by Edward Jackson
>
More clearer - Combination of sphere and cylinder
Hypermetropia over Correction of myopia
V

- Power of sphere = half the power of cylinder with opposite sign

If equal = Emmetropic Eg : -0.5DS and +1DC

+0.5DS and -1DC

-0.5 -0.5

-0.5 + 1 +0.5

<
2 cylinders of equal power in 2 meridians with opposite signs

:
First check axis then power

Technique known as flip cross technique

If one line looks more clearer : astigmatism present

Pin hole test 1. If visual acuity improves : Refractive error Present

2. No improvement : Organic pathology

V

3. In visual acuity worsens : macular pathology

 Accommodation
V

Power to see near objects clearly

Note Diverging rays from near object

During accommodation

Contraction of ciliary muscles

:
Loosening/ relaxation of ciliary zonules

Change in ROC of lens

10 mm >
6 mm
While posterior ROC remains same (6mm)

V
Increase lens thickness

:
Accommodate

Amplitude of accommodation (A) = P - R

P = Power of eye in full accommodating eye

R = Power of the eye at rest

A=P-R

1 1
A=
Near point ( meter ) Far point ( meter )
> Usually at infinity 7 1 =0
as

:
In this case

1
A=
Near point ( meter )

Spasm of accommodation : Involuntary, excessive, sustained accommodation

:
More convergence

Pseudo myopia

Etiology : 1. Uncorrected hypermetropia in children

2. Mitotics

Treatment : Cycloplegics

Insufficiency of accommodation
Due to ageing > Lens
> Ciliary muscle

Specially after 40 years of age known as presbyopia ( Not a Refractive error )

Treatment : A. Standard correction according to Age
40-45 years = + 1D
45-50 years = +1.5 to +2D • Increase by 0.5 upto 1D
51-55 years = +2.5 to +3D • Never should be over corrected
56-60 years = +3.5 to 4D
B. Near addition over distance correction
Bifocals
x
Distance

-
Near -

Distinctive line
> 7 Seam
Should always pass through pupillary plane

Trifocals '

E I
Distance
Intermediate
Near

Multifocals : No distinctive line

Orbit

• Pyramidal in shape
• Apex lies posterior and base lies anteriorly
• Quadrangular base
• Volume : 30 cc
• Orbit lies between anterior cranial fossa and maxillary sinuses

Supra orbital foramen ( junction of lateral 2/3 rd and medial 1/3rd )

Supra orbital nerve and artery ( not vein )

Floor of the orbit >

Blow out fracture

Optic canal : Formed by greater and lesser wing of sphenoid

Supra orbital fissure : Formed between greater and lesser wing of sphenoid
 O
Orbit

Pyramidal/ conical shaped

Apex posteriorly, base anteriorly
Volume : 30cc > Quadrangular

Thinnest wall : medial wall

Thickest wall : lateral wall
Medial walls : parallel to each other
Lateral walls : perpendicular to each other
Floor : mc Blow out fracture

Apex
v u
Optic canal Superior orbital fissure

v v

Formed by greater and lesser wing of sphenoid Lies between greater and lesser wing of sphenoid

v u

Ophthalmic nerve Annulus of zinn divides it into

Ophthalmic artery

u
v
v

Superior Middle Inferior

v v v

Superior orbital vein Nasociliary Inferior ophthalmic vein

+ Abducent
L : Lacrimal Occulomotor > Upper division
F : Frontal > Lower division
T : Trochlear

Orbit lies between anterior cranial fossa and maxillary sinuses

Contents : Eyeball
EOM’s
Optic nerve
Blood vessles
Fat
Lacrimal gland
Lacrimal sac

Volume : 30 ml
 Proptosis

Anterior displacement of eyeball beyond the lateral orbital margin

>21 mm or difference of >2 mm between 2 eyes

Term Exophthalmos : Reserved for thyroid eye disease

Proptosis

Unilateral or bilateral
Axial or non axial
Acute : Hemorrhages, emphysema
Intermittent : orbital varix
Pulsatile : Caratico cavernous fistula ( CCF )
Increase in bending or moving forward or valsalva = varix

MC cause in children

u
r

Unilateral Bilateral

Orbital cellulitis

Inflammation posterior to orbital septum

t
Metastasis

AML ( Chloroma )
&
Etiology : Staph Neuroblastoma
Strepto > Pyogenes
> Hemolyticus
Mc : secondary to ethmoidal sinusitis

Chandler’s classification

Proptosis in Adults

MC cause unilateral, bilateral, Male, Female : TDE ( Thyroid Eye Disease )

90% : Hyperthyroidism
6% : Ethyroidism
4% : Hypothyroidism

Risk factors : Women

Middle age
Smoking

Pathology : Orbital fibroblasts

i t
Myofibroblast Lipofibroblast

Fibrosis in EOM GAG accumulation in orbital cavity

✓ V

Restrictive squint Edema

+ +
Motility defects Proptosis

Forced duction test positive

 EOM
Whole belly is affects sparing origin and insertion ( tensions are not affected )

Thyroid eye disease

Order of EOM
Tendons are not affected

I S LucknOw Whole belly affected c

M
S

v v
u v v

IR > MR #
SR LR Obliques >

>

S First affected : Restriction of elevation

MC sign : UL retraction > proptosis

Due to over action of Muller’s muscle

Due to sympthetic stimulation

v
 No wrinkles
on forehead

Proptosis
v u

Nafzigger’s view Worm’s views

v u

Head end Foot end

Instrument

Exophthalmometer
-

v u

Hertel’s Exophthalmometer Luede’s Exophthalmometer

Cavernous sinus thrombosis

Centre
t
v

Internal carotid artery

Lateral wall
t
v

III Nerve
Abducent nerve IV Nerve
V1,2

MC etiology : 1. Infections over dangerous areas of face

2. Ethmoidal sinusitis
3. Orbital cellulitis

Clinical features : Unilateral ( proptosis ) > 50% bilateral

High grade fever with chills and Rigors
Optic disc congestion
Conjunctival congestion
Ophthalmoplegia > first diplopia in lateral gaze > Due to VI nerve involvement
Pathognomic sign : Mastoiditis

Increase pressure in mastoid emissary vein

Ophthalmic emergency

No vision loss due to no optic nerve involvement

Treatment : 4 hourly monitoring

Admission to hospital
Antibiotics
Analgesics
Anticoagulants

CCF - Caratico cavernous fistula

Fistula between internal carotid artery or its branches and cavernous sinus
i.e. high pressure area to low pressure area

Clinical features : similar to cavernous sinus thrombosis

H/O : Trauma

Bandy’s triad

PCB
Pulsatile proptosis Chemosis Bruit ( noise in Head )

Conjunctival edema

SOFS - Superior Orbital Fissure Syndrome

Ty
Compression Superior orbital vein Nasociliary Inferior ophthalmic vein
Abducent
L : Lacrimal Occulomotor Upper division
F : Frontal Lower division
T : Trochlear

No involvement of Optic nerve

OAS - Orbital Apex Syndrome / Jacob syndrome

Ty
Involvement 1. Optic canal
2. Superior orbital fissure

Clinical features : Superior orbital fissure syndrome + Optic nerve involvement

Orbital pseudotumors/ Idiopathic orbital inflammatory disease

o • Space occupying lesions in the orbit

• Non infective, Non malignant
• 40-60 years of age
 Tolorosa hunt syndrome

- • Chronic granulomatous inflammation of orbital apex, SOF or cavernous sinus

Blow out fracture

MC cause : blunt trauma

MC site : Inferior wall/ floor

Clinical features : 1. Periorbital edema & sub conjunctival ecchymosis

2. Emphysema in eye lids
3. Anaesthesia or paresthesia in areas supplied by inferior orbital nerve
4. Acute inflammation and edema Proptosis
5. Lately Enophthalmos

Due to — fibrosis Pulls eye inwards

— Decrease in volume of orbital contents

6. Entrapment of EOM in long fragments

Motility defects

Restrictive squint Forced duction test positive

7. Double diplopia Upgaze Tear drop sign

Downgaze

Diagnosis : X Ray orbit Water’s view

Hanging drop / Tear drop sign

Treatment : wait for surgery for 10-14 days for edema to resolve

Management : 1. Cold compresses

2. Avoid nose blowing
3. Antibiotics : to prevent secondary infection ( maxillary sinus )
4. NSAIDs
5. Surgery : After 10-14 days
 To conjoin

Translucent membrane joining eyelids to sclera

Eyelids

OSclera

Parts : 1. Palpebral Below eye lids

> Orbital
>
Orbital
Tarsal plate >
Tarsal
> Tarsal
> Marginal >
Marginal

2. Bulbar Over eyeball

3. Fornix Conjunctival pouch

Structure : 1. Epithelium : Non keratinised stratified squamous epithelium contains goblet cells — Mucin secretion

Maximum in nasal bulbar conjunctiva

: Minimum in upper temporal fornix

2. Adenoids 3. Fibrous

v
u
Follicles Together known as Substantia propria

v v

Aggregations of lymphocytes Degeneration

v
v

Infectious : mc Non infections

t
Bacterial ( mc )

Staph aureus ( mc )
. Yellowish discharge

Types of Bacterial Conjunctivitis -

>
Based on type of discharge

1. MC : Active mucopurulent conjunctivitis ( Sticky + pus )

• by Staph aureus >
Matted eyelids
• matted or sticking eyelids
• coloured Halos present >
Yellowish sticky discharge

2. Acute purulent ( only pus )

• by Gonococcus
• more virulent
• other systemic features : urethritis and arthritis
• Cornea may be involved
• systemic antibiotics also indicated
 3. Acute membranous conjunctivitis : membrane is formed

A. True membranous conjunctivitis

Corynebacterium diphtheriae Streptococcus hemolyticus

MC in non immunised children MC in adults

True membrane in palpebral conjunctiva

t
Bleeds on peeling off

Raw area : Symblepharon

B. Pseudo membranous conjunctivitis

• Staph, Streptococcus, N. gonorrhea

• No bleeding on peeling off

4. Angular conjunctivitis

• caused by Morxella axenfeld — Proteolytic enzyme

Excoriation of skin

• TOC : Zinc : helps in epithelial healing

Types of Viral Conjunctivitis ' MC by adenovirus

1. Acute follicular conjunctivitis

t
Epidemic Kerato conjunctivitis

Adenovirus : 8, 19, 37
t
Pharyngo conjunctival fever

Adenovirus : 3, 4, 7

2. Acute hemorrhagic conjunctivitis/ Apollo conjunctivitis

• Picorna virus family especially

• Enterovirus Type 70 , Adenovirus, Coxsachie A24
• Only bacteria : Pneumococcus

3. Herpes simplex conjunctivitis

• Unilateral
• Serious discharge
• <5 years of age
 Chlamydia trachomatis > Obligate intracellular

v r

A, B, Ba, C D to K

t
. v

Blinding Trachoma Inclusion Conjunctivitis . Spread : Veneral spread : Genitals to eye

✓
Non veneral spread : from eye to eye Autoinoculation
v u

Adults Children Right eye is mc involved

v u
Swimming pool Conjunctivitis Ophthalmia neonatorum

Trachoma : It is Chronic kerato Conjunctivitis

v v

Cornea Conjunctiva

Signs : A. Conjunctiva > Mc : upper tarsal involved

Sagograin follicles
1. Mixed response >
Follicles
> Papillary hyperplasia

2. Gross examination : Sagograin follicles >

3. Microscopic examination : Leber cells ( Large multinucleated cells ) with signs of necrosis

4. Arlt’s line : Scaring in sulcus subtarsalis Arlt’s triangle : seen in anterior uveitis

5. Concretions : Dead epithelial cells + debris

t
.

Epithelial abrasions

Corneal ulcer

Concretions Arlt’s line

✓

B. Cornea

Herbert pits : Depression seen after cicatrisation

Herbert follicles of limbal follicles

OO r

o Same as conjunctival follicles

Darker
Below the limbus Darker > While Horner-Tranta spots are lighter and above the limbus
Below the limbus
 Pannus
Vascularisation
+ > Lead to corneal ulcer

Infiltration

Pannus : Lymphoid infiltration with vascularisation of superior cornea

FISTO Classification

F Sagograin follicles

I Papillary Hyperplasia

S Arlt’s line

Trachiasis

T :
Rubbing of eyelashes over Cornea

Corneal ulcer

Trachoma : Complications : only corneal ulcer

 Trachoma : mc infection causing blindness in India

Treatment : SAFE strategy

S : Surgery for lid deformities especially trichiasis

A : Antibiotics
F : Facial cleanliness
E : Environmental hygiene
V

Tetracycline 1% eye ointment or

Single drug regimen — 1 gm Azithromycin orally once stat

WHO blanket therapy — Maintenance treatment

V
I
1% Tetracycline eye ointment B.D. X 5 days per month > For 6-12 months

Ophthalmia neonatorum

Conjunctivitis in newborn ( <28 days )

Diagnosed by any discharge even watering ( because tear formation : 4-6 weeks )

Etiology : Transfer from mother to child

D/D

v u

<48 hours of birth >48 hours of birth

v
u v
> Chemical Gonococcal 1. Other bacteria

:1
2. Herpes simplex
• Mild • Most severe 3. C. Trachomatis D to K
Leads to

• Watery
• No congestion Blindness
• No chemosis
• Severe congestion
Cred’s method • Chemosis Edema in conjunctiva

1% AgNO3
V

Treatment
V

Use is now obsolete

v

BAC therapy

V V V

Bacitracin eye ointment Atropine eye ointment IM Ceftrixone Injection

For corneal ointment

Allergic conjunctivitis

MC non infective conjunctivitis

MC allergic conjunctivitis in VKC ( Vernal kerato conjunctivitis )

VKC / Spring Cataract

• M>F
• Age : 4-20 years
• Bilateral
• Intestinal
• Recurrent
• Type I and Type II hypersensitivity
• IgE to exogenous allergens
• Hot and humid climate

Clinical features : Intense itching with ropy discharge

1
Pseudo membrane formation
:
Maxwell Lyon sign

Signs : 1. Cobblestone papillae ( Polygonal raised areas in palpebral conjunctiva )

Cobblestone papillae

2. Horner- Tranta spots

Horner- Tranta spots

Greyish white spots
Eosinophil accumulation

000.00000
Above the limbus

Greyish white spots

3. Gelatinous thinking of limbus

4. Pseudo gerontoxon / Cupid’s bow

• Seen in Recurrent cases

• Paralimbal band of lipid deposition resembling arcus senilis

Keratopathy Shield ulcer

:1
SPK ( Superficial Punctate Keratitis )

Shield ulcer

Treatment : DOC : Olopatadine

Topical steroids may be added in acute exacerbations then taper Antibiotics and steroids for shield ulcer
 VKC

Olopatadine : DOC

t
Acute + Chronic

( Anti histaminic + Mast cell stabiliser )

Fails

!
Topical steroids > Start with low potency s
Fluro metholone
Fails

Systemic steroids
+
N- acetyl cysteine ( mucolytics )

Phlyctenular kerato conjunctivitis

• Unilateral
• Nodular
• F> M
• Type IV hypersensitivity reaction to endogenous allergens ( Staph proteins > TB proteins )

Clinical features : Pinkish nodules near limbus

÷
Can spread from limbus to centre

Ulcers : 1. Sacrofulous ulcer

2. Fascicular ulcer
3. Military ulcer

TOC : Topical steroids

Topical antibiotics and atropine in case of corneal involvement

Degenerations

Pinguecula
Pterygium

Astigmatism : WTR
Pterygos

Head

Wing shaped growth Body

Tail Nasal side

Obstruction of visual axis

Stocker’s line

Bitot’s sopt
Seen in Vit A deficiency not in Pterygium

Fe deposition
Temporal side
 Pinguecula
• Bilateral, yellowish, triangular with apex Always away from cornea
• due to Elastotic Degeneration of substantia propria
• Stationary, nasal side earlier
• No active intervention required

Pterygium
• Wing shaped fold of conjunctiva over cornea
• Nasal side involved earlier than temporal
• Earliest visual loss occurs due to Astigmatism ( WTR ) then due to encroachment of visual axis ( >4 mm )
• Stocker’s line : Iron deposition anterior to advancing Head of Pterygium
TOC : Surgical excision

t
30-80% recurrence

Reduced recurrence by

L v s

Mitomycin-C Thiotepa Radiation

Conjunctival autografting from superior limbal area

Gold standard is amniotic membrane grafting

 Cornea
• Anterior 1/6th of eyeball
• Transparent, Avascular
• 2 surfaces > Anterior — +48D
>

Net power = + 43D

> Posterior — -5D
7

• Refractive Index = 1.376

• Size = 11.7 x 11 mm

-
Micro cornea

• Congenital Rubella Syndrome

Megalocornea

• Marfan’s syndrome
t
v

• Ehler-Danlos syndrome
• Alport syndrome
• Down’s syndrome

> Acellular, avascular

> Opacity

>90% thickness

: >
Thickness : 16 um
Toughest layer

+ +
> Na-K pump most vital layer

Specular Microscopy
Pre requisite for corneal transplantation
2000-3000 : Normal Endothelial count
<500 cells : Decompensation
Hexagonal cells

Specular Microscopy
Pachy meter
To measure thickness of cornea
 Kerato meter

For corneal curvature

Bio meter

Power of IOL

Keratitis

A. Bacterial corneal ulcers

• MC > World — Staph aureus

> India — Streptococcus pneumonae
• Some bacteria can penetrate intact cornea
C. diphtheriae
N. meningitidis
N. gonorrhoea
Hemophillus
Listeria
Shigella
But not pseudomonas

• Otherwise bacterial ulcer always starts with Epithelial Erosion

•Stages : 1. Polymorphonuclear infiltration

2. Active ulceration
3. Impending perforation
4. Perforation

• Clinical features : Photophobia

Sudden painful loss of vision
Acute red eye D/D : ACG and Acute anterior uveitis
Vascularisation

:
Descements membrane Iridocyclitis Anterior uveitis

iii.÷
Epithelium

:
Hypopyon . Purulent uveitis
( Pus in anterior chamber )

Descematocele Impending perforation

 Signs : Hypopyon
• Always sterile and mobile
• Most dangerous hypopyon

r
u

Pneumococcus Pseudomonas

:l
Ulcus Serpens

Characteristic Hypopyon corneal ulcer

Other bacteria causes corneal ulcer with hypopyon

Complications of perforation

:
:-.
Small Large Anterior capsular cataract

Adherent leucoma Iris prolapse Anterior staphyloma

:÷
Fibrosis '
Pseudo cornea

.
-

White opacity
False cornea

Adherent leucoma Anterior staphyloma

Grape like appearance

Treatment : 1. Fortified topical antibiotics

÷
Gentamicin 15 mg% Cephazolin 50 mg%

or Recently, 5% Cefazoline + 5% Vancomycin / Tobramycin

2. Topical mydriatics and cycloplegics for associated uveitis

3. Doxycycline in case of impending perforation

4. Don’t Topical steroids

Padding and bandaging
Frequent irritation of conjunctiva
B. Fungal ulcers

I
.

Filamentous

Aspergillus fusarium
-

Yeast like

• Candida
Fungal ulcer

• Cryptococcus

MC risk factor : Trauma due to vegetative matter

Signs >>> Symptoms Feathery margins

Mostly Asymptomatic

Signs : Dry looking, greyish white, elevated margins

Immune ring of Wesseley
Finger like extensions
Multiple satellites like lesions
Immune ring of Wesseley >

Big hypopyon
Perforation is rare
Vascularisation is away absent

TOC

Filamentous

Natamycin
f
Yeast like

Amphotericin B + Nystatin

C. Viral corneal ulcer

• Decreased corneal sensation

• Keratic precipitates ( most commonly seen in anterior uveitis )

A. Herpes simplex
#

v
v

Primary lesions Recurrent lesions

V
V

Blepharitis
Dendritic pattern
Follicular conjunctivitis
Superficial punctuate keratitis
> Multiple dot like lesions in epithelium
Steroids are contraindicated

V Amoebic ulcer/ Geographical ulcer

•
& Knobs are present
B •

Fluoroscein stain L

Rose Bengal stain

<

Seen through
Cobalt blue filter
 I. Epithelial : Dendritic ulcer

I:c: Floor — Fluoroscein stain

: Knob — Rose Bengal stain

Treatment : 3% Acyclovir
Topical steroids are contraindicated as they can hasten formation of Geographical ulcer

II. Stromal
Treatment : Both 3% Acyclovir + Topical steroids

III. Meta herpatic

Healing defect due to paralysis of V nerve
Treatment : Neither Acyclovir nor Topical steroids

B. Herpes zoster ophthalmicus

✓
v

Primary lesion Gasserian Recurrent Ganglion lesions

F
Frontal Lacrimal Nasociliary

÷
L
Strict distribution on one side of forehead

Hutchinson’s rule : Tip of nose lesions shows more chances of ocular involvement
NC

Clinical features : intense Trigeminal fever + Neuralgia

Skin eruptions

Ocular features

Nummular keratitis
Nummular keratitis Characteristic
Granular deposits surrounded by stromal haziness

Stromal interstitial and disciform keratitis

Sclerokeratitis : least common
Motor cranial nerve palsy - 3 ( mc ), 4, 6

Keratitis

t
f
Neurotrophic Neuroparacytic

V palsy Facial palsy

Orbicularis oculi

Exposure keratitis

Treatment of HZO : 1. Tab. Acyclovir 800mg

2. 3% Acyclovir
3. Topical antibiotic - Steroids ointment
4. Systemic steroids — Post herpatic neuralgia
5. Amitryptilline — Depession
6. Antihistaminics
 D. Acanthamoeba

• Free living Amoeba present in soil

• Infection is mc in contact lens users, trauma with vegetative matter, swimming pool, immunocompramised
Ring abscess

* . Radial kerato neuritis

Out of proportion pain

• Typical reticular pattern
• History of contact lens
• Pseudo dendrites ( confused with H. simplex )
• Trophozoites ( Mistaken with macrophages )

Non infective keratitis

Band shaped keratopathy

• Degenerative disease occurring due to Calcium deposition in Bowman’s membrane

Etiology : Hypercalcemia, chronic uveitis, JRA, Sarcoidosis, still’s disease
Chronic glaucoma, vitamin D toxicity, ocular trauma, phthisis bulbi
Chronic keratitis, hyperparathyroidism

Treatment : EDTA ( Chelating agent )

Keratoconus

Non inflammatory, bilateral conical ectasia of cornea associated with progressive

Myopia and irregular astigmatism
Oil droplets reflex

Signs : 1. Oil drop reflex on direct ophthalmoscope

2. Fleischer’s ring at the base of cone due to iron deposition
3. Munson’s sign : Localised bulging of lower eyelids when patient
looks in downward gaze

Complications : Acute hydrops due to rupture of descements membrane

Munson’s sign
Treatment : 1. Rigid contact lenses
2. Penetrating keratoplasty
3. Collagen cross lining by Riboflavin and UVA to arrest progression

Vortex keratopathy
Vertex keratopathy
Drugs causing : PICA
Phenothiazine Indomethacin Chloroquine Amiodarone
 Photo ophthalmia / snow blindness

• Epithelial keratitis caused by UV rays (290-311 nm) ; Latent period : 4-5 hours
• Crook’s glasses : for prophylaxis

Treatment : Cold compresses and padding and bandaging with antibiotic eye ointment

Mooren’s ulcer/ Chronic serpenginous ulcer

• Idiopathic/ degenerative/ autoimmune

• Superficial peripheral ulcer with
a. Undermined epithelium
b. Advancing borders
c. Overhanging margins
d. Very Painful ( due to early vascularisation )

Corneal transplantation

V
v
Partial Total

u
v

Anterior Posterior

v u

DSAEL DMEK

Descement stripping stromal automated endothelial keratoplasty

V
Descement’s membrane endothelial keratoplasty

Contraindications of keratoplasty

1. Infections - HIV, Hepatitis B, C

2. Intraocular tumors
3. Death due to unknown causes
4. Septicaemia
5. Rabies

Corneal preservation

1. Short term ( 1-2 days ) : +4 C : Sterile moist chamber

2. Intermediate ( upto 14 days ) : Mc Corey Kaufman medium
3. Long term ( 30 days to 1 year ) : By organ culture medium and Cryopreservation
 Eyelids

Infections

Style/ External hordeolum

-
Internal hordeolum Chalazion

V
v
Acute suppurative Chronic Lipogranulomatous

v
v

Gland of Zeis or Moll Meibomian gland Meibomian gland

s
v v

Sebaceous gland
u
Sebaceous gland Sweat gland Sebaceous gland

Treatment : Antibiotics Systemic Treatment : Incision and drainage

" Topical

Tf
NSAIDs
Hot fomention Horizontal Vertical
Stye
u v

Skin side Conjunctival side

>Pus point towards lid margin
' '
' -
I e
\ -

\ -

l l l l l l l

Instruments :
Chalazion clamp
Chalazion scoop
Internal hordeolum
Recurrent chalazion : Risk of sebaceous cell carcinoma
Chalazion
V

TOC : Intra lesional Triamcinolone

Nodules, no pus, No signs of inflammation Multiple chalazion of upper eyelid

Ptosis

Recurrent lid infections

t
Child

v
Refractive errors
t
Elderly

DM

Ptosis

Drooping of upper eye lid

Normally upper eyelid covers 2 mm of cornea
Elevators of eyelid I LPS III Nerve
#
Accessory muscle Muller’s muscle Sympthetic inervation

Etiology :

v v

Congenital Acquired

Due to defective development of LPS

v u v

Mild : 2 mm Moderate: 3 mm Severe : 4 mm

LPS resection accordingly

 Severe congenital ptosis ( Pupil is covered )

Stimulus deprivation amblyopia

Acquired congenital ptosis

Etiology : 1. Neurogenic > III Nerve palsy

Horner’s syndrome

2. Myogenic Myasthenia gravis

> Myotonia dystrophica

3. Aponeurotic — Senile

4. Mechanical — Trauma, lid edema, multiple chalazion

Treatment of ptosis

v
v v

Mild Moderate Severe

f
u

Fasanella servat operation

:
Levator resection Levator function

Resection is conjunctiva, tarsal plate, muller muscle

v u
Good Poor

Lid tumors
MC malignant Tumor - Basal cell carcinoma

MC in lower lid
Followed by medial canthus a - Upper lid Lateral canthus
 Trauma

v v

Blunt Penetrating

Clinical features : 1. Lid edema

2. Peri orbital ecchymosis
3. Sub conjunctival hemorrhages
4. Corneal - edema, abrasions, blood staining, opacity
5. Anterior chamber — Hyphema ( Blood in AC )

MC source : Major arterial circle

— Aqueous cells. ( inflammatory cells ) > Inflammatory glaucoma

6. Iris : Iridocyclitis ( Detachment of iris from its root )

"

Leading to D shaped pupil

7. Ciliary Body : Shutdown ( detachment )

:i
No aqueous formation

Hypotony

8. Pupil : Constriction for short period due to irritation of ciliary nerves

followed by permanent dilatation of pupil

9. Lens : Subluxation
Rosatte cataract
Pigment dispersal
Vossious ring

µ Pigment deposition of miotic pupil on anterior capsule of lens

:
jy
10. Vitreous hemorrhages and avulsion of vitreous base : 4mm band of vitreous at orra serrata
11. Retinal detachment
12. Choroidal detachment
13. Optic neuropathy
14. Macular edema : known as Berlin’s edema or commotio retinae

Cherry red spot

15. Macular hole

16. Blow out fracture
 Penetrating trauma

IOFB ( Intra Ocular Foreign Body )

Risk of endophthalmitis
Cataract : Sunflower cataract
MC IOFB : Chisel and Hammer ( chips of iron )

Magnetic

MRI is contraindicated

IOC for localization of foreign body : CT Scan

IOC for visual acuity : ERG

Dont’s in IOFB
V
1. Don’t touch foreign body
2. Don’t rub foreign body
3. Don’t remove foreign body
4. Don’t wash the eye
5. Don’t cover

Do’s in IOFB

1. Measure visual acuity as accurately as possible : ERG

2. Antibiotics
3. Cover with moist cotton or loose bandage ( if required only )
4. Wash : warm water or Saline

Lacrimal apparatus

ma
l Upper punctuate
cri
La land
g
V: vertical canaliculi : 2 mm

f
H
V Total = 1 cm
H : horizontal canaliculi : 8 mm

¥÷÷:
UP

LP
Lacrimal sac

Lower punctuate

Valves : To maintain unidirectional flow of tears

D Naso lacrimal duct : 15-18 mm
NL
Direction : DOB ( Downward, Outward, Backward )

Inferior meatus of nose Valve of Hesner

i
Membranous Occlusion of NLD

Backflow of tears in lacrimal sac

:
v

Epiphora/ Watering Secondary bacterial infection

Sticky discharge

Congenital dacryocystitis
 Treatment : 1. 0-1 years : Lacrimal sac massage ( Criggler’s massage )
80% cases: spontaneous resolution
+ Topical antibiotics

2. 1-2 years : Syringing with normal saline

3. 2-3 years : Probing by Boman’s lacrimal probe

4. 3-4 years : Alternate syringing and probing

5. > 4 years : DCR ( Dacryo Cysto Rhinostomy )

Opening between lacrimal sac and meddle meatus

Contraindications of DCR

1. < 6 years of age and >60 years

2. Syphillis, TB of lacrimal sac
3. Tumors of lacrimal sac >
DCT is indicated
4. Atrophic rhinitis
V

5. Surgeon is unskilled Dacryocystectomy

Evaluation of Epiphora

Syringing

Patent Obstruction

u r

1. Hyper secretion Probing by Bowman’s lacrimal probe

2. Pump failure l
3. Partial obstruction
v
l v
l
Hard stop Soft stop

u v

Jones dye test I /II NLD block Canalicular block

t t
V
I : 2% Fluoroscein dye in conjunctival sac and cotton tipped bud in nasal cavity
If 5-8 mm from punctum If >8 mm from punctum
V
Look for staining
v
u

Upper/ lower canaliculi Common canaliculi

v u

No ( — ve ) Yes ( + ve )

v u

Jones dye test II Hypersecretion

v
Syringing and see staining

u
v
Yes No

u
v

Partial obstruction Pump failure

 Community Ophthalmology

Blindness

1. WHO definition : Visual acuity less than 3/60 ( Snellen’s chart ) of its equivalent

2. NPCB definition : a. Inability of a person to count fingers from a distance of 6 meters or 20 feet
b. Vision 6/60 or less with the best possible spectacle Correction
c. Diminition of field vision to 20 degrees or less in better eyes

Types of blindness
1. Economic blindness
2. Social blindness
3. Manifest blindness
4. Absolute blindness
5. Curable blindness
6. Preventable blindness
7. Avoidable blindness

Comparison of WHO and NPCB definitions

WHO-ICD Visual acuity NPCB

Low vision

Category 1 < 6/18 - 6/60 Low vision

Category 2 < 6/60 - 3/60 Economic blindness

Blindness

Category 3 < 3/60 - 1/60 Social blindness

Category 4 < 1/60 - perception of light Manifest blindness

Category 5 No perception of light Absolute blindness

Blindness : Causes
MC cause of blindness — Senile cataract

India : 70%
: World : 50%

In children : MC cause is Vit A deficiency

MC cause of low vision : Ocular morbidity

Uncorrected refractive errors

MC cause of infection causing blindness — Trachoma

 Vision 2020

Right to sight

Visual acuity of 20/20 by year 2020

Cataract
Vit A deficiency
Refractive errors
Trachoma
Onchocerciasis ( not found in India )
For India

v u

Diabetic Retinopathy ROP

v v

In adults In children

Vitamin A deficiency

Earliest symptom : Decreased sensitivity to green light followed by night blindness

Signs : Conjunctival xerosis

Ii
Bitot’s spots

Corneal xerosis :
White foamy spots : more comply on temporal side

Hyperkeratosis of epithelium

:
Keratomalacia

Xerophthalmia

Dose of Vit A

<1 year : 1 lac IU

>1 year : 2 lac IU Prophylaxis

6 months : 50,000 IU

Vitamin A deficiency : 3 doses

V
0, 1, 14 days
 Chemical injuries
• It leads to limbal injury — Loss of stem cells
• Alkali injuries are more severe than acid injuries
• Acids - cause protein precipitation : No risk of perforation
• Alkali - MOA : 1. Intra ocular inflammation
2. Necrosis > Epithelium
> Stroma 7 Perforation

• Alkali injury is an Ophthalmic emergency

• Treatment : 1. Intensive irrigation of conjunctival sac with Normal saline / RL/ BSS (best ) x 15-20 min to pH becomes normal
Don’t use a hand spray of water as it can change burned area

2. Once pH has been neutralised, through sweep of fornices with upper lid eversion to detect and remove deeply embedded particles

3. Debrigment - Removal of dead and necrotic tissue

4. Topical steroids for inflammation

5. Vitamin C as a topical drop also added with steroids to prevent corneoscleral metting

6. Topical antibiotic ointment to provide lubrication and prevent superinfection

7. Cycloplegics for comfort

8. Doxycycline reduces effects of MMP’s which can degrade Type I collagen

9. Citrates : > Anti collagenolytic

> Anti proteolytic
> Anti neutrophillic