2014’s
2014’

MataPedia
M t P di

TM

for Ophthalmologist
(Slides Compilation)
Gede Pardianto
Sumatera Eye Center
Medan Indonesia
M d -I d
i
The information provided within this book is for educational and
scientific purposes only and it should not be construed as
commercial advice.
Author thanks all of our teachers, fellow ophthalmologists,
publishers, sponsors, and all manufacturers for their works those
all being cited in this handout book.

FREE COPY
NOT FOR SALE
2
• Being an ophthalmologist doesn’t mean you can
be the rich person or you can do everything. As
a little light, the sincerity you can perform in your
meaningful life is giving a humble tribute to
humanity by serving the people against
blindness.

Gede Pardianto
May 20, 2008
3
Gede Pardianto
•

Graduate from
–
–
–

•

Office
–
–
–

•

Doctor of Medicine  Airlangga University
Ophthalmologist  Airlangga University
Doctor of Philosophy  Sumatera Utara University
p y
y
Dr. Komang Makes Hospital
Sumatera Eye Center
Sumatera Utara University, Medical School
y

Member of
–
–
–
–
–
–
–
–

IOA
InaSCRS
APACRS
ESCRS
ASCRS
EuCornea
AAO
ICO
4
Here are awarded to the souls
of the valiant who gave their
lives in the service of their
country and who sleep in
unknown graves…

All Indonesian heroes…
Some there be which have no
sepulchre.

Airlangga University - Medical School 1913

But their name liveth for
evermore.

Dedicated to 100 Years of the Spirit of Nationality 1908 – 2008
y
y
and 1 Century of Medical Education in Surabaya 1913 – 2013
5
Basic and Latest
Spirit of Bali
Only one on earth
Visual functions including :
•
•
•
•
•
•

Visual acuity
Visual fi ld
Vi
l field
Color vision
Dark adaptation
Contrast sensitivity
Binocular single vision
7
Examination

Which one goes wrong ?
8
Examination : Finger
•
•
•
•

Finger counting
Confrontation t t
C f t ti test
Digital tonometry
Open the eye lid

9
Confrontation Visual Field testing
• Technique
– Examiner sated about 1 meter opposite patient
– Patient directed to cover one eye and fixate on
y
examiner’s opposite or nose
– Patient asked whether examiner’s entire face is
visible or specific portions are missing
– Patient asked to identify a target of 1,2 or 5 presented
at the midpoint of each of four q
p
quadrants in a p
plane
halfway between the patient and examiner

American Academy of Ophthalmology

10
Confrontation Visual Field testing
– Patient is asked to add total number of fingers
g
presented in opposing quadrants (double
simultaneous stimulation)
– A h i uncooperative, sedated i t b t d or very
Aphasic,
ti
d t d intubated
young patient can use finger mimicry, pointing, visual
tracking or reflex blink to respond and allow gross
appraisal of VF integrity. If a patient saccades to a
visual stimulus in a given quadrant, the visual field
area can be considered to be relatively intact
– Check patient’s ability to distinguish color of red
object when looking directly at it
American Academy of Ophthalmology

11
Examination : At least
•
•
•
•
•
•
•
•
•
•
•
•
•
•

Optotypes charts
Phoropter and/or Trial lens and frame
Torch
Slit lamp
Jaegger’s reading chart
Lensometer
L
t
Color test  Ischihara’s pseudoisochromatic plates
Tonometer
Fluorescein for Defect and Siedel’s test
Siedel s
Ophthalmoscope
Amsler grid and Red dots
Ruler
Placido disc keratoscope
Whatman No. 41 paper by 5x30mm for Schirmer test

12
Examination : Phoropter
• A device containing different lenses used
for refraction of the eye during sight testing
• The instrument used to measure refractive
status of the eyes.
• It contains many lenses which are then
changed in front of the eyes while the
p
patient is looking at an eye chart.
g
y
• This is when the doctor usually asks,
"Which is better, one or two?"
13
Examination : Optotypes
• High contrast visual acuity
– Snellen chart
– Bailey Lovie chart
Bailey-Lovie

• Low contrast visual acuity
– Reagan chart

14
Examination : Torch
• Light perception
• Projection of Illumination / Light projection
• Macula Photostress Recovery Test
–
–
–
–
–

Measure visual acuity first
Place torch 2 cm from eye
10 seconds illumination
Measure visual acuity again
Record th ti
R
d the time needed f recovery b k t previous visual
d d for
back to
i
i
l
acuity
– 55 seconds  normal
– Larger (90 180)  macular dysfunction
(90-180)

• Pupil examination
• Crude anatomical screening
Deborah Pavan-Langston

15
Examination : Slit lamp
• How to adjust
– Up and down
– Horizontal move
– Pupil distance
– Light
– Angle
– Slit maneuver and rotation
d t ti
– Color option
16
Slitlamp examination
anterior
cornea
p
posterior
cornea

anterior
lens

limbus

anterior
iris
17
Examination : Ophthalmoscope
• How to use :
– Power switch
– Size of illumination
– Diopter
– Color  Red free
– Placido disc  Crude

18
Dilating drops
• Mydriatic
– Phenylephrine 2.5%, 10%  20 min  3 hours

• Cycloplegics
–
–
–
–
–

Tropicamide 0.5%, 1%  20-30 min  3-6 hours
Cyclopentolate 0.5%, 1%, 2%  20-45 min  24 hours
Homatropine 2%, 5%  20-90 min  2-3 days
Scopolamine 0.25%  20-45 min  4-7 days
Atropine 0.5%, 1%, 2%  30-40 min  1-2 week(s)
Will’s Eye Manual, 2004

19
Examination : Amsler grid
• Boldly cross-hatched paper
• Will b mandatory i :
be
d t
in
– Metamorphopsia
– Central scotoma
– Discomfort “perfect” vision
– Color vision disturbance

20
Amsler grid

21
To use the grid
g
• Sit in an area with good lighting, and hold the chart at
eye level and at a comfortable distance
• You may find it convenient to attach the grid to a wall at
eye level and stand 12 inches to 14 inches away
(comfortable reading distance)
• If you wear glasses, keep them on. If you wear bifocals,
use the bottom or reading portion of the lens
• Cover one eye completely
• Stare with your other eye at the central dot on the grid.
While doing this, observe the pattern of vertical and
horizontal lines
• Repeat the test with the other eye
22
Schirmer test I
•
•
•
•
•
•
•
•

Whatman No. 41 paper
p p
Filter strip 5x30mm, folded 5mm
Dimly light room
Place l
Pl
lower palpebral conjunctiva at it l t l 1/3
l b l
j
ti
t its lateral
Eye kept open and look upward
Blinking is permissible
Remove after 5 minutes
10-30 mm wet  normal or basal secretion may be low
but compensated for by reflect secretion
• Less than 5 mm wet  repeated  hyposecretion of
basic tearing
Deborah Pavan-Langston, 2008

23
Examination : Add 1
•
•
•
•
•
•
•
•
•
•
•

76 or 90 D lens
Goldmann’s 3 mirrors lens
Hruby lens
Indirect hth l
I di t ophthalomoscopy
Manual or automatic keratometry
Standard A-Scan biometry
A Scan
Retinometer
WFDT
Prisms
Streak retinoscopy
Hertel s
Hertel’s exophthalmometer
24
Examination : Goldmann s 3 Mirrors
Goldmann’s
•
•
•
•

Central
Oval
O l
Trapezium
Square

: Posterior pole
:G i
Gonioscopy
: Equator
: Periphery

25
Examination : Add 2
• Visual field test 
–
–
–
–

Bjerrum’s tangent screen
Goldmann’s perimetry
SAP, SWAP, FDT, HPRP
For AMD  Preferential Hyperacuity Perimeter (PHP) 
Foresee PHP (Notal Vision)
– For Retina  Micro Perimeter MP-1 (Nidek)

• Advanced biometry
– Partial Co e e ce Laser Interferometer
a t a Coherence ase te e o ete
– Non-contact Optical Coherence Biometry
– Laser Interferometry Technique

• Advanced High Definition AB-Scan USG
g
– Aviso (Quantel Medical)
– VuMax II (Sonomed)

• Standard digital fundus camera with FFA
g
– VisuCam (Carl Zeiss Meditec AG), AFC-330 (NIDEK)
26
Visual Field Analyzers

FDT Perimetry
Octopus 101
Perimetry

Goldmann
Perimetry

Humphrey
Perimetry

27
Examination : Add 2
• Advanced anterior examination
– Pachy-Autorefrakto-Keratometer
• PARK 1 (OCULUS Optikgeräte GmbH)
• Galilei G4 (Ziemer)  Placido and Dual Scheimpflug

– Anterior Optical Coherence Tomography
• Visante OCT (Carl Zeiss Meditec AG)
• SL OCT (Heidelberg Engineering)
• TOMEY SS-1000 (TOMEY GmbH)

– Scheimpflug Camera Pentacam  Keratometry Corneal
Keratometry,
topography, Pachimetry, Corneal wavefront, AC and angle
analyzer, Lens analyzer, Phakic IOL and Post refractive surgery
biometry
y
• Pentacam HR (OCULUS Optikgeräte GmbH)
28
Examination : Add 2
• Advanced anterior examination
– Keratograph  Oculus Keratograph (OCULUS
Optikgeräte GmbH)
– E d th li
Endothelium S
Specular Mi
l Microscope
– Advanced High Definition Ultrasound Biomicroscopy
(
(UBM)
)
• P60 UltrasoudBioMicroscope (Paradigm)
• Aviso (Quantel Medical)
• VuMax (Sonomed)

– Very high frequency (VHF) ultrasound eye scanner 
Artemis (ArcScan, Inc)
– HRT3 with Cornea Module (Heidelberg Engineering)

29
Advanced anterior examination

Artemis (ArcScan, Inc)

P60 UltrasoudBioMicroscope
(Paradigm)

Visante OCT (Carl Zeiss Meditec AG)

Pentacam HR
(OCULUS
Optikgeräte GmbH)

30
Examination : Add 2
• Advanced posterior examination
– Posterior Optical Coherence Tomography
• St t OCT (C l Z i M dit AG)
Stratus
(Carl Zeiss Meditec
• 3D OCT 2000 FA Plus Swept-Source SS OCT and
DRI (TopCon)
( p
)
• 3D OCT-1 Maestro OCT (TopCon)
• RS3000 Advance (Nidek)
• RTV FD OCT (O t
RTVue
(Optovue)
)
• High Definition Cirrus + SmartCube HD OCT (Carl
)
Zeiss Meditec AG)
• SOCT Copernicus (Reichert)
• HRA OCT Spectralis (Heidelberg Engineering)
• E i P di t i SDOCT (bi ti
Envisu Pediatric
(bioptigen)
)
31
Examination : Add 2
• Advanced posterior examination
– Scanning Laser Ophthalmoscopy
• OCT-SLO (Opko Instrumentation)
• O t Ultra Widefield I
Optos Ult Wid fi ld Imaging S t
i System (O t )
(Optos)
– Scanning Laser Polarimetry
• GDxVVC  Glaucoma Diagnosis - Variable
g
Corneal Compensation (Carl Zeiss Meditec AG)
– Confocal Scanning Laser Tomography
3
e de be g et a o og ap y
• HRT3  Heidelberg Retinal Tomography
(Heidelberg Engineering)

32
Stratus OCT (Carl Zeiss Meditec AG)
RTVue FD OCT (Optovue)

HRA-OCT Spectralis
(Heidelberg Engineering)
HRT3 (Heidelberg Engineering)

GDxVCC (Carl Zeiss Meditec AG)

Cirrus HD OCT
(Carl Zeiss Meditec AG)

33
Examination : Add 2
• Pediatric visual examination
– Pictures cards  Allen card
– Letter  HOTV
– Matching games  Lea symbols

• Binocular vision test
– Titmus, TNO, Lang, Madox’s Rod,
– Bargolini striated test
– Hering-Bielschowsky afterimage test

• Al f t t
Also for teatment 
t
– Synophtophore
– Holme’s stereoscope

• H
Hess S
Screen
• ERG and EOG
• Visual Evoked Potential (VEP)
34
Contrast sensitivity tester
• Aberrometry
• Glare
– Letter  Pelli-Robson Chart
Pelli Robson
– Grating 
•
•
•
•
•

Functional Acuity Contrast Test (FACT) Chart
Contrast Sensitivity Tester 1800
Landolt-C based Miller Nadler Glare Tester
Frankfurt-Freiburg Contrast and Acuity Test System (FF-CATS)
Grating-based Charts CSV-1000 (Vector Vision)

– Scotopic testing  lower than 0.032 cd/m
0 032 cd/m²
• Rodenstock Nytometer (Rodenstock)
• Mesoptometer (Oculus Optikgeräte GmbH)

• Scatter
– Van den Berg Stray Lightmeter

• Haloes
– Tomey G a e a d Halo So t a e ( o ey)
o ey Glare and a o Software (Tomey)
Kohnen T, Koch DD, 2005

35
Examination equipment
•
•
•
•
•
•
•
•

Well accepted
pp
Well approved
Well proven
Easy to learn its manual
Easy to use
Easy and comfortable for patient
Easy to make accurate and reliable interpretation
Reproducible
36
EMBRIOLOGY

The Marshall
dr. Norman Tagor Lubis, Sp.M

37
American Academy of Ophthalmology

Neuroectoderm
-Neuresonsory retina
-Retinal p g e t ep t e u
et a pigment epithelium
-Pigmented ciliary epithelium
-Nonpidmented ciliary epithelium
-Pigmented iris epithelium
-Sphincter and dilator muscles of iris
-Optic nerve, axons, and glia
-Vitreous

DERIVATIVES
OF
EMBRYONIC
TISSUES :
ECTODERM

Cranial Neural Crest cells
-Corneal stroma and endothelium
-Trabecular meshwork
-Sheaths and tendons of extraocular muscles
Sheaths
-Connective tissues of iris
-Ciliary muscles
-Choroidal stroma
-Melanocytes (uveal and ephitelial)
g
p
-Meningeal sheaths of the optic nerve
-Schwann cells of ciliary nervers
-Ciliary ganglion
-All midline and enferior orbital bones, as well as part of orbital roof and lateral rim
-Cartilage
-Connective tissues of orbit
-Muscular l
M
l layer and connective ti
d
ti tissues sheaths of all ocular and orbital vessels
h th f ll
l
d bit l
l
Surface Ectoderm
-Ephitelium, glands, cilia of skin of eyelids and caruncle
-Conjuntivital ephiyelium
-Lens
-Lacrimal glan
-Lacrimal drainage system
-Vitreous

38
DERIVATIVES
OF
EMBRYONIC
TISSUES :
MESODERM

• Fibers of extra ocular
muscles
• Endothelial lining of all
orbital and ocular blood
vessels
l
• Temporal portion of sclera
• Vitreous

American Academy of Ophthalmology

39
American Academy of Ophthalmology
22 days Optic primordium appears in neural folds (1 5-3 0 mm)
(1.5-3.0 mm).
25 days Optic vesicle evaginates. Neural crest cells migrate to surround vesicle
28 days Vesicle induces lens placode.
Second Invagination of optic and lens vesicles.
month Hyaloid artery fills embryonic fissure.
Closure of embryonic fissure begins.
Pigment granules appear in retinal pigment epithelium
epithelium.
Primordial of lateral rectus and superior oblique muscles grow anteriorly
Eyelid folds appear.
Retinal differentiation begins with nuclear and marginal zones.
Migration f ti l ll begins.
Mi ti of retinal cells b i
Neural crest of corneal endothelium migrate centrally.
Corneal stroma follows.
y
Cavity of lens vesicle is obliterated.
Secondary vitreous surrounds hyaloid system.
Choroidal vasculature develops.
Axons from ganglion cells migrate to optic nerve.
Glial lamina cribrosa forms
forms.
Bruch’s membrane appears.
40
.
Third
Precursors of rods and cones differentiate.
month Anterior rim of optic vesicle grows forward
Ciliary body starts to develop.
Sclera condenses.
Vortex veins pierce sclera.
Eyelid folds meet and fuse.
Fourth Retinal vessels grow into nerve fiber layer near optic disc.
month Choroidal vessels form layers.
Iris t
I i stroma is vascularized.
i
l i d
Eyelids begin to separate.
Sixth
Ganglion cells thicken in macula.
g
month recurrent arterial branches join the choroidal vessels.
Dilator muscle of iris forms.
Seventh Outer segments of photoreceptors differentiate
differentiate.
month Central fovea starts to thin.
Fibrous lamina cribrosa forms.
Chorodial melanocytes produce pigment.
Circular muscle forms in ciliary body
American Academy of Ophthalmology

41
Oculoplastic

43
Eye lid layer
y
y
• Anterior lamellar
– Skin and subcutaneus tissue
– Muscles of protraction  Ocular orbicular muscle

• Medial lamellar
– O bit l septum
Orbital
t
– Orbital fat
– Muscles of retraction
• Palpebral levator muscle
• Muller’s muscle

• Posterior lamellar
– Tarsus
– Conjunctiva
American Academy of Ophthalmology

44
OP : Ptosis
1. PSEUDOPTOSIS
2. CONGENITAL
3. ACUIRED
–

MYOGENIC
•
BLEPHAROPHIMOSIS SYNDROME
•
MYASTHENIA GRAVIS
•
PROGRESSIVE EXTERNAL
•
OPHTHALMOPLEGIA

–

NEUROGENIC PTOSIS
•
HORNER’S SYNDROME
•
MARCUS GUNN JAW WINKING
•
THIRD NERVE PALSY
•
BOTULISM
•
CEREBRAL PTOSIS

–

APONEUROTIC PTOSIS
•
INVOLUTIONAL PTOSIS
•
POST CATARACT SURGERY
•
POST EYELID TRAUMA
•
POST EYELID OEDEMA
•
POST CONTACT LENS WEAR

–

MECHANICAL PTOSIS
•
EYELID TUMOURS
•
ORBITAL LESIONS
•
CICATRIZING CONJUNCTIVAL DISORDERS
•
ANOPHTHALMOS

45
Diagnostic keys
g
y
•
•
•
•
•
•

Levator Function
Margin reflex distance (MRD)
Margin limbal distance (
g
(MLD)
)
Inter palpebral fissure
Lid lag
Bell’s phenomenon  Eye lid closing
failure without moving eye ball upward or
outward at the SAME time
• Ocular motility
46
Levator function

• The most practical measure of the strength of the
levator muscle
• Excursion of the upper lid from extreme down-gaze
to extreme up-gaze
• Normally 15 mm

47
MRD
• A simple way to measure
the height of the upper lid.
• N
Normally 4 5 mm
ll 4-5
• MRD 1 = distance of the
upper lid f
from th corneal
the
l
light
• MRD 2 = distance of the
lower eye lid from the
corneal light reflex
48
Skin
Ski crease height and strength
h i ht d t
th
• The distance from the lid margin to crease
– Men  6-8 mm, Asia  5-6 mm
– Women  8-10 mm, Asia  7-8 mm

• A weak levator muscle  creates less pull
on the skin the crease is weak
• MLD  Normal 9-10 mm
49
System for Ptosis surgery
Levator function

> 10 mm

< 10 mm

Degree of ptosis

Levator function

< 2 mm

> 2 mm

> 2 mm

< 4 mm

Fasanella
servat

Aponeurosis
surgery

Levator
resection

Brow
suspension

Collin JRO, 1989

50
System for myogenic ptosis

Collin JRO, 1989

51
Collin JRO, 1989

52
Collin JRO, 1989

53
Collin JRO, 1989

54
Fascia lata : How to get
•
•
•
•
•
•

Mark outside of thigh 1/3 distally
Skin incision 4-5
Ski i i i 4 5 mm  d ll undermine
dull d
i
Find the white fascia
Take 3 X 1.5 cm of fascia
Suture the edge of fascia
Suture sub cutan and skin
55
OP : Entropion
CLASSIFICATION :

–C
Congenital
it l
• Entropion
• Epiblepharon

– Acquired :
• Involutional
• Spastic
y
• Cycatrical
56
Entropion : Involutional
• Overriding of lower lid protractor muscle
• Horizontal eye lid laxity  lateral and
medial canthus ligament
• Disinsertion or weakness of lower lid
retractor muscle
t t
l
• Fat atrophy enophthalmos
• Anteriorly prolapse of orbital fat
57
Involutional Entropion : Examination
• Horizontal laxity
– Pi h / Distraction t t
Pinch Di t ti test
– Snap back test

• Medial canthal laxity
• Lateral canthal laxity
y
• Vertical laxity  Retractor dehisence
58
Pinch / Distraction test
• Distant between globe and lower lid
g
pull
margin after full lower lid p out
• None  5 mm
• Mild  5 7 mm
5-7
• Moderate  10-12 mm
• Severe  more than 12 mm
59
Snap back test
• Dynamic test  Pull downward lower lid
margin then rapidly released
• Normal  Lid margin back on its position
spontaneous without blinking
t
ith t bli ki
• Laxity  Not spontaneous back on
position
60
Medial canthal laxity
• Lateral distraction test  Position shift of
inferior lacrimal punctum
• Normal  The punctum must be stable on
semilunar plica while pulled to lateral
– 1 2 mm shift i youth
1-2
hift in
th
– 3-4 mm shift in elderly

• If any greater position shift  Laxity
61
Medial canthal laxity

0

1

2

3

4

5

6

Grade of Lancrimal punctum position shift

62
Cycatrical Entropion
Pathophysiology
p y
gy
• Cycatric at posterior lamellar  Posterior
lamellar shortening  lid margin inversion
to the globe  Entropion  Trichiasis

63
System for upper lid entropion
Lid closure possible?
Yes

No

Keratinisation of marginal
tarso-conjunctiva?

Corneal graft considered?
Yes

Lashes abrading
cornea?

Rotation of
terminal
tarsus

No

Posterior
lamellar
graft

Yes

No

Tarsal
excision

No
Yes
Anterior lamellar
reposition

Tarsus thickened?

Yes

No

Tarsal wedge resection

Lamellar division +/- MM graft

Collin JRO, 1989

64
Collin JRO, 1989

65
Congenital Entropion : Surgery
• Congenital epiblepharon
– Could be disappear by age
– If there any punctate keratopathy Tarsal
fixation

66
Involutional Entropion : Surgery
• Without lid laxity
– Everting suture
g
– Wies procedures

• With lid laxity
– Wies procedures with tarsal strip

67
Cycatrical Entropion : Surgery
• Mild to Moderate
– Anterior lamellar reposition (ALR)
– Tarsotomy

• S
Severe
– Posterior lamellar graft
– Terminal tarsus rotation

68
OP : Ectropion
CLASSIFICATION :

– Congenital
– Acquired :
• Involutional
• Paralytic
• Mechanical
• Cycatrical

69
Ectropion : Principal surgery
• Laxity
– Tarsal strip
– Pentagonal excision  Medial Canthal
Medial, Canthal,
Lateral
– Medial canthus ligament shortening

• Cycatrix
– Ski graft
Skin
ft

70
System of acquired
ectropion
p

Shortage of skin?
No

Yes

Normal eyelid closure?

Cicatricial ectropion

Yes

Localized defect?

No
Paralytic t i
P l ti ectropion

Yes

No

Z - plasty

Skin
replacement

Medial canthal tendom laxity?
Yes
Y

No
N
Lump in lid

Medial ectropion only?

Yes

No

Involutional
ectropion

Mechanical
ectropion
t i

Medical canthal
resection
No

Yes

Medical canthoplasty
+ lat canth. sling
lat. canth

Medical
canthoplasty

Ectropion mainly medial?

Collin JRO, 1989

Yes
No

Horizontal lid laxity?

Exess skin?
No
Horizontal lid
shortening
h t i

Yes
Horiz .lid short. +
blepharoplasty
bl h
l t

No

Yes

Excision of
diamond of
tarso-conjunctiva
t
j
ti

Med.canth. tendom lax?

No
Lazy - T

Yes
Med.canth. tendom
placation or resection

71
Collin JRO, 1989

72
OP : Trichiasis
• Cilia emerge from their normal anterior
lamellar location
• Associated with cicatrizing processes of
the conjunctiva

73
OP : Blepharospasme
• Eye lid squeezing disorders
• L
Long standing  association with :
t di
i ti
ith
– Eye lid and brow ptosis
– Dermatochalasis
– Entropion
– Canthal tendon abnormalities

74
OP : Blepharophimosis
- G
Generalized narrowing of the palpebral
li d
i
f th
l b l
fissure
- A CONGENITAL ANOMALY
- EPICANTHUS INVERSUS
- MICROBLEPHARIA PTOSIS AND
- VERTICAL STRETCHING OF THE BONY ORBIT

75
COLOBOMA PALPEBRA or
BLEPHAROSCHIZIS
• FULL THICKNESS DEFECTS OF THE EYELIDS
• RARE. UNILATERAL OR BILATERAL
• THE CONFIGURATION  TRIANGULAR OR
QUADRILATERAL
• THE CORNEA EXPOSE  CORNEAL OPACITY
• THE RISKS ARE GREAT INVOLVES THE CENTER
OF THE LID

76
OP : Blepharochalasis
p
• Thin and wrinkled eyelid skin
• Familial variant of angioneurotic edema
• Idiopathic episodes of inflammatory edema of
the eyelid
• Most frequently in young females
• Younger patient than dermatochalasis
• Different with Dermatochalasis 
• Redundancy of eyelid skin
• Often associated with orbital fat protrusion or prolapse
• Upper eye lid  indistinct or lower than normal eyelid crease
American Academy of Ophthalmology

77
Contracted sockets
• Causes of
– Radiation
– Extrusion of an enucleation implant
– Severe initial injury
– Poor surgical technique
– Multiple socket operations
–P l
Prolonged periods of conformer or prothesis
d
i d f
f
th i
removal
American Academy of Ophthalmology

78
Collin JRO, 1989

79
Collin JRO, 1989

80
Prof. dr. Mardiono Marsetio, Sp.M(K)
and
Prof. dr. Wisnujono Soewono, Sp.M(K)

Ocular surface
85
Tear film : Functions
• Maintains optical clear for cornea
• Moistening, lubricating and protecting
surface of conjunctiva and cornea
• Inhibits microorganism growth by
mechanism processes and anti-microbial
h i
d ti i bi l
actions
• Feeding the cornea
Vaughn GD, 2000

86
Tear film : Layers
y
•

Monomolecular lipid layer
–
–
–
–

•

Superficial
Origin from Meibomian glands
Inhibits evaporation
Closed palpebra  Water-tight barrier

Aqueous layer
– Origin from major and minor lacrimal glands
– Water soluble salts and proteins

•

Mucin layer
– Secreted principally by conjunctival goblet cells
– Glycoprotein  coating conjunctiva and cornea
– Absorbed by hydrophobic corneal epthelial cells membrane  on
microvilio
– Normally on 15-45 seconds of Break-up time test
– Abnormally on less than 10 seconds of Break-up time test

Vaughn GD, 2000

87
Tear film : Formations
•
•
•
•
•
•

Thickness  7-10 µm
7 10
Volume  7 + 2 µL each eye
pH  7 35  vary from 5 20 8 35
7.35
5.20-8.35
Isotonic  295-309 m osmol/L
Albumin
Alb i  60% t t l protein
total
t i
Defence mechanism by  Lisozym, Ig A,
Ig
I G and Ig E
dI

Vaughn GD, 2000

88
Tear dynamics
• Tear volume is 10 µ L or less
• The maximum volume of fluid that can be contained in
the “cul-de sac” without overflow is 30 µL.
• Th eye d
The
drop volume i approximately 40 µL
l
is
i
l
L
• The excess fluid instilled is rapidly removed by spillage
j
from the conjunctiva sac  until the tear fluid returns to
its original volume
• The reflex tearing after the instillation of an irritating drug
may produce up to 400 µL excess tears
tears.
• Dilution of 5–50 fold usually occurs in the first 2 minutes,
depending on the irritating power of the substance
Cornea, 2002

89
Ocular surface : Hyperemia
• Conjunctival
j

• Corneal
• Scleral

90
Ocular surface : Red eye
•
•
•
•

Conjunctivitis
Uveitis
Keratitis
K titi
Glaucoma

91
Acute
Conjunctivitis

Acute Iritis

Acute
Glaucoma

Acute
Keratitis

Incidence

++

+

+/-

+

Secret

++

-

-

+

VA

-

+/-

++

+

Pain

-

+

++

+/++

Injection

Diffuse, to
fornices

Circum cornea

Circum cornea

Circum cornea

Cornea
C

Clear
Cl

Usually clear
U
ll l

Cloudy
Cl d

Clearance
Cl
change

Pupil

Normal

Small

Oval dilated

Normal or Small

Light response

Normal

Decrease

None

Normal

IOP

Normal

Normal

Increase

Normal

Organism +

No organism

No organism

Only in ulcers

Swap

92
Sign
Injection
Hemorrhage
Chemosis
Secret
Pseudo
membrane

Bacterial

Viral

Allergic

Toxic

Trachoma

Marked

Moderate

Mild/ Moderate

Mild/ Moderate

Moderate

+

+

-

-

-

++

+/-

++

+/-

+/-

Purulent

Scant/
Watery

String/ White

-

Scant

+/-

+/-

-

-

-

Streptococcus/
Corynebacterium

Papillae

+/-

-

+

-

-

Follicles

-

+

-

+

+

(Medication)
Peri auricular
node

+

++

-

-

+/-

Pannus

-

-

-

-

+

(Except
Vernal)

93
Staining : Gram
g
• Older technique
–
–
–
–
–

3 seconds of Carbol Gentian Violet on fixated object glass
¾ seconds Lugol solution
1 second 90% Alcohol
Wash by water
y
3 seconds Watery Fuhcin

• New technique
q
–
–
–
–
–
–
–

½ - 1 second(s) Ammonium oxalate crystal violet
Wash by water
1-2 seconds Lugol solution
Wash by water
1 second Acetate alcohol
Wash by water
1 second S ff
d Sofframin
i
94
Staining : Giemsa and KOH
• Giemsa
– Giemsa solution : Aquadest  1 : 10
– 2 seconds Methanol on Fixated object glass
– Waste and add 10-15 seconds Giemsa stain
– Wash by water and make it dry
y
y

• KOH
– 1-2 drops 10% KOH on object g
p
%
j
glass
– Place specimens on object glass
– Covered with coverglass
g
95
Ocular surface : Conjunctiva
j
• Follicle
– Focal lymphoid nodule
y p
– With accessory vascularization

• Papilla
– Dilated, talengiectatic conjunctival blood vessels
,
g
j
– Anchoring septa
– Dot like changes to enlarged tufts, surrounded by edema and
inflammatory cells

• G
Granuloma
l
– Nodule of chronic inflammatory cells
– With fibrovascular proliferation

• Phl t
Phlyctenule
l
– Nodule of chronic inflammatory cells
– Often at or near the limbus
American Academy of Ophthalmology

96
Follicle and Papilla
p
Area to be examined

Follicles

Papillae
97
Follicle and Papilla
p
Papilla

Follicle

American Academy of Ophthalmology

98
Phlycten and Phlyctenule
y
y
Phlycten

Phlyctenule

Staphylococcus

Delayed hypersesitivity

Good

Poor

+

-

Limbus
Without progression

Limbus
To central

All ages
g

Children

Cycatrix

-

+

Recurrence

-

+

Triangular
Base at limbus

Triangular
Apex at limbus

Topical antibiotic

Steroid based on
Underlying disease

Etiology
General condition
Conjunctivitis
Location
Age

Shape
Therapy
py

99
Ocular surface: Cornea
• Epithelium
– 5-6 layer structure
– 50 100 µm thickness
50-100
– Great sensitivity
– Composed
• Basal cells layer
• Wing cells layer
• Surface cells layer
Deborah Pavan-Langston, 2008

100
Ocular surface : Cornea
• Bowman’s layer
Bowman s
– Homogenous condensation of anterior
stromal lamellae

• Stroma
– 90% of corneal thickness
– Bundles of collagen fibrils of uniform
thickness enmeshed in mucopolysaccharide
subtance
bt
– Maintain corneal clarity
Deborah Pavan-Langston, 2008

101
Ocular surface : Cornea
• Dua’s Layer
Dua s
– Discovered by examining the separation that
often occurs along the last row of keratocytes
during the big bubble (BB) technique
– Attached to the deep stroma
– is not "residual stroma."
– Distinct layer that is 10 15 ± 3 6 microns thick
10.15 3.6
between stroma and descemet membrane
EuroTimes, 2013

102
Ocular surface : Cornea
• Descemet membrane
– Basement membrane of the endothelial cells
– Can be easily stripped
– Homogenous glasslike structure
– Anterior  Composed of stratified layers of
very finecollagenousfilaments
– Posterior  Amorphous layers that increases
with age
Deborah Pavan-Langston, 2008

103
Ocular surface : Cornea
• Endothelium
– Single layer
– 5 18 µm size of approximately 500 000
5-18
500,000
polygonal cells
– Maintain corneal deturgescence
– Contributes the formation of Descemet
membrane

Deborah Pavan-Langston, 2008

104
Ocular surface : Cornea
• Blood supply
– Predominantly from
• Conjunctival vessel
• Episcleral vessel
• Scleral vessel

– Arborize about the corneoscleral limbus

• Innervation
– Sensory  mostly  ophthalmic division of the
trigeminal nerve
g
– Is via long ciliary nerves that branch in the outer
choroid near ora serrata region
Deborah Pavan-Langston, 2008

105
Ocular surface : Keratititis
Location

Marginal
keratitis
k titi
Peripheral

Bacterial
keratitis
k titi
Central

Size

< 1 mm

> 1 mm

Epithelial defect Small or absent Present
Uveitis

Absent

Present
Kanski JJ, 2007

106
Chemical trauma : Hudge Grade
I

II

III

IV

Good

Good

Intermediate

Poor

Epithelial

Epithelial

Epithelial loss

Hazy

Iris/Pupil
detail

Visible

Visible

Blurred

Very blurred

Ischemia

None

<1/3 limbus

1/3 -1/2
limbus

> 1/2 limbus

Prognosis
Broken
cornea

107
Corneal endothelial layer

• Normal  2 000 – 3 000 cells / mm²
2,000 3,000
mm
• Stressed  800 -1,500 cells / mm²
• D
Decompensate  < 500 cells / mm²
t
ll
²

108
Keratoplasty
• Penetrating Keratoplasty (PK)
• Barron’s Keratoplasty
• Sterile Cornea Allograft  VisionGraft
(TBI/Tissue Bank International)
• Deep Anterior Lamellar Keratoplasty (DALK)
• Femtosecond laser-assisted Anterior Lamellar
Keratoplasty (FALK)
• Femtosecond laser-assisted Descemet Stripping
Endothelial Keratoplasty (
dot e a e atop asty (F-DSEK)
S )
109
Keratoprostheses: Boston K Pro

EuroTimes 2006

110
Keratoprostheses: AlphaCor

EuroTimes 2006

111
Keratoprostheses: Pintucci

IJO 2011

112
113
114
Refraction

Prof. Dr. dr. Admadi Soeroso, Sp.M, MARS
115
Visual acuity
• Vi
Visual threshold
l th h ld
– Light discrimination
•
•
•
•

Brightness sensitivity (minimum visible)
Brightness di i i ti ( i i
B i ht
discrimination (minimum perceptible)
tibl )
Brightness contrast
Color discrimination

– Spatial discrimination
• Minimum separable
• Vernier acuity (hyperacuity) 
– Separated by little as 3 5 seco ds o a c
Sepa a ed
e
3-5 seconds of arc
– Considerable less than the diameter of single foveal cone
– The basis of Amsler’s grid

• Minimum legible acuities
• Di t
Distance di i i ti
discrimination
• Movement discrimination

– Temporal discrimination
• Flickering light
American Academy of Ophthalmology

116
Some basic acuity
Type

Description

Point acuity ( arc minute)
y (1
)

The ability to resolve two distinct point targets.
y
p
g

Grating acuity (1-2 arc minutes)

The ability to distinguish a pattern of bright and dark
bars from a uniform grey patch.

Letter acuity (5 arc minutes)

The ability to resolve a letter. The Snellen eye chart
is a standard way of measuring this ability. 20/20
vision means that a 5-minute letter target can be
seen 90% of the time

Stereo acuity (10 arc seconds)

The ability to resolve objects in depth. The acuity is
measured as the difference between two angles
for a just-detectable depth difference.
just detectable

Vernier acuity (10 arc seconds).

The ability to see if two line segments are collinear

Healey CG, 2005

117
Visual acuity in different notation
FEET

METERS

MINIMUM ANGLE OF
RESOLUTION

LOGMAR

DECIMAL
NOTATION

20/10

6/3

0.50

-0.3

2.0

20/15

6/4.5
6/4 5

0.75
0 75

-0 1
0.1

1.5
15

20/20

6/6

1.00

0.0

1.0

20/25

6/7.5

1.25

0.1

0.8

20/30

6/9

1.50
1 50

0.2
02

0.7
07

20/40

6/12

2.00

0.3

0.5

20/50

6/15

2.50

0.4

0.4

20/60

6/18

3.00
3 00

0.5
05

0.3
03

20/80

6/24

4.00

0.6

20/100

6/30

5.00

0.7

20/120

6/36

6.00
6 00

0.8
08

20/150

6/45

8.00

0.9

20/200

6/60

10.00

1.0

0.1

20/400

6/120

20.00
20 00

1.3
13

0.005
0 005

American Academy of Ophthalmology

0.2

118
Visual acuity : Development
y
p
Age

Visual acuity

2 months

20/400 (6/120)

6 months

20/200 (6/60)

1 year

20/100 (6/30)

2 years

20/60 (6/18)

3 years

20/30 (6/9)

y
4-5 years

20/20 (6/6)
( )
Duke Elder

119
Visual acuity : Various test in children
AGE (Years)
0-2
0-2
0-2
02
2-5
2-5
25
2-5
5+
5

VISION TEST
VEP
Preferential looking
Fixation behavior
Allen pictures
HOTV
E-Game
Snellen h t
S ll chart

NORMAL
20/30
20/30
CSM
CSM*
20/40-20/20
20/40-20/20
20/40 20/20
20/40-20/20
20/30-20/20
20/30 20/20

* CSM Method : Refers to Corneal light reflex, Steadiness of fixation and
Maintain alignment
American Academy of Ophthalmology

120
Light : Basic
• Wavelength of visible light  380-760nm
380 760nm
• Velocity of light waves 
– 300 000 k /
300.000 km/second or
d
– 86.000 mils /second

• Character of light
– Hue
– Saturation
– Brightness or Luminance
121
Illumination
• Radiometry
– Measures term of power
– Irradiance = watts per square meter, lamberts
• Sunny day = 10,000 – 30,000 foot lamberts

• Photometry
–
–
–
–
–

Measures units based on the response of the eye
1 candela = 12.6 lumens
Illuminance = lumens per square meter
Luminance of surface is amount of light that reflected or emmited
Apostlib  surface perfectly emitting or reflecting 1 lumen per
square meter
– Ideally 100 watt lamp bulb provides about minimum
• 600 foot candles 3 feet away
• 150 foot candles 6 feet away

American Academy of Ophthalmology

122
Photobiology
gy
• Scotopic vision is the monochromatic vision of the eye
in low light. Since cone cells are nonfunctional in low
light, scotopic vision is produced exclusively through rod
cells so therefore there is no color perception. Scotopic
vision occurs at luminance levels of 10-2 to 10-6 cd/m².
cd/m .
• Mesopic vision occurs in intermediate lighting
conditions (luminance level 10-2 to 1 cd/m²) and is
effectively a combination of scotopic and photopic vision
vision.
This however gives inaccurate visual acuity and color
discrimination.
• Ph t i vision  I normal light (l i
Photopic i i
In
l li ht (luminance l
level 1 t
l to
106 cd/m²), the vision of cone cells dominates  good
visual acuity (VA) and color discrimination
Lars Olof Björn, 2002

123
The cone cells
• Sharp photoreceptor
• A human eye can see wavelengths in the range of 380 to
760nm. This range is called the visible region
y
yp
,
• Trichromatic Theory  3 types of cones, each with a
different iodopsin (a photosensitive pigment)
• Each type of iodopsin can absorb and respond to a
range of wavelengths
• Photosensitive pigments 
– Erythrolabe  maximum absorption at 565nm (red)
– Chl l b  maximum absorption at 535
Chlorolabe
i
b
ti
t 535nm (
(green)
)
– Cyanolabe  maximum absorption at 440nm (blue)

124
Visible light
Hue

Wavelength (nm)

Indigo
g

400-450

Blue

450-480

Cyan-Blue

480-510

Green

510-550

Yellow-Green

550-565

Yellow

565 590
565-590

Orange

590-630

Red

630-700
125
Chromatic aberration
• The type of error in an optical system in which the
formation of a series of colored images occurs, even
though only white light enters the system.
system
• Chromatic aberrations are caused by the fact that the
refraction law determining the path of light through an
optical system contains the refractive index which is a
index,
function of wavelength.
• Thus the image position and the magnification of an
optical system are not necessarily the same for all
wavelengths, nor are the aberrations the same for all
wavelengths
126
Chromatic aberration
• Short wavelength light focused
more anterior than long
wavelength li ht
l
th light
• Violet focused more anterior
than Red
127
Spherical aberration
• A blurred image that occurs when
light from the margin of a lens or
g
g
mirror with a spherical surface comes
to a shorter focus than light from the
central portion.
• Also called dioptric aberration
128
Spherical aberration
•
•
•

•

A perfect lens (top) focuses all
incoming rays to a point on the
optic axis
A real lens with spherical
surfaces (bottom) suffers from
spherical aberration
It focuses rays more tightly if
they enter it far from the optic
axis than if they enter closer to
the axis
It therefore does not produce a
perfect focal point

129
Spherical aberration
• Mirror spherical
aberration
• Reflective Caustic
generated f
d from a
circle and parallel
rays

130
Accommodation table
Age (years)

Rate of Accommodation (Diopters)

8

13.8

25
5

99
9.9

35

7.3

40

5.8
58

45

3.6

50

1.9

55

1.3
Vaughan DG

131
Refractive index (Helium D Line)
•
•
•
•
•
•

Air
Water
Cornea
Aqueous and vitreous
Spectacle crown glass
PMMA

1.000
1.333
1.376
1.336
1 336
1.523
1.492
1 492

American Academy of Ophthalmology

132
Refracting power (D)
• Corneal system

43.05

– Anterior surface
– Posterior surface

48.83
- 5.88

• Lens system
– Relaxed
– Maximum accommodation

19.11
33.06
33 06

• Complete optical system
– Relaxed
– Maximum accommodation

58.64
70.57

American Academy of Ophthalmology

133
DIOPTER CONVERTION - MILIMETER
K

K

Reading
(D)

Radius
(mm)

Reading
(D)

Radius
(mm)

47.57
47.50
47 50
47.25
47.00
47 00
46.75
46.50

7.07
7.11
7 11
7.14
7.18
7 18
7.22
7.26

46.25
46.00
46 00
45.75
45.50
45 50
45.25
45.00

7.30
7.34
7 34
7.38
7.42
7 42
7.46
7.50
134
Pinhole visual acuity measurement
• If visual acuity improves  refractive error
usually present
• Disease of macula 
– Unable to adapt to amount of light through the
pinhole
– Visual acuity can decrease markedly

• M t useful  1 2 mm
Most
f l
1.2
– Refractive error – 5.00 to + 5.00 D
American Academy of Ophthalmology

135
Refraction
Common
Disorder

Moderate

Severe

-1.00 t – 4 00
1 00 to 4.00
Diopters

-4.00 t – 6 00
4 00 to 6.00
Diopters

-6.00 and above
6 00 d b
Diopters

Hyperopia

+1.00 to +2.00
Diopters

+2.00 to +4.00
Diopters

+4..00 and above
Diopters

Astigmatism

-1.00 to –2.00
Diopters

-2.00 to -4.00
Diopters

-4.00 and above
Diopters

Myopia

Mild

136
Refraction
• Myopia (Nearsightedness)
– Pathophysiology
• Axial Curvature Increased index of refraction
Axial, Curvature,

– Severity
• Mild Moderate High
Mild, Moderate,

– Clinical
• Simplex/Stationary, Progressive, Malignant

Deborah Pavan-Langston, 2008

137
Myopia
y p
•
•

Children born myopic  small percentage  not become
emmetropic by age 6-8 years
Previously emmetropic children or h
P i
l
t i hild
hyperopic may b
i
become myopic
i
– Hyperopes greater than +1.50 D rarely become myopic and may
become more hyperopic

•
•

Prevalence of myopia begins to increase at about age of 6 y
y p
g
g
years
Juvenile-onset myopia
– 7-16 years of age
– Primarily due to growth in globe axial length
– L
Largest i
t increase i girls at age 9 10 years and i b
in i l t
9-10
d in boys at age 11 12
t
11-12
years
– Usually stops in middle teen years, 15 for girls and 16 for boys

•
•

Myopia starting after 16 is less severe and less common
y p
g
Adult-onset myopia
– Begins at about 20 years of age
– Risk factor  extensive near work
American Academy of Ophthalmology

138
Significant myopia in childhood
g
y p
•
•
•
•

Cycloplegic refraction are mandatory
Full refractive error, including cylinder, should be corrected
Young children tolerate cylinder well
On theory  prolonged accommodation increase development of
myopia
– Some  undercorrection myopia
– S
Some use bif
bifocal, with or without At i
l ith
ith t Atropine

•

Parents should be educated about
– Progression of myopia
– Need for frequent refraction
– Possible prescription changes

•
•
•

Contact lenses  older children  avoid problem of image
magnification by high minus lenses
Intentional undercorrection f myopic esotrope  d
I t ti
l d
ti for
i
t
decrease th
the
angle of deviation  well tolerated
Intentional overcorrection for myopic error  controlling
(
)
exodeviation (some value)
American Academy of Ophthalmology

139
Refraction
• Hypermetropia (Farsightedness)
– Structural
• Axial, Curvature, Index of refraction

– Accommodative
• Latent, manifest, total

– Severity

Uncorrected can causes
• Strabismus  Esotropia
• Ambliopia
Deborah Pavan-Langston, 2008

140
Correcting hyperopia in childhood
• No esodeviation and reduced vision  NOT
necessary correcting low hyperopia
• Significant astigmatic error must be fully
corrected
d
• Hyperopia coexists esotropia  full correction of
the cycloplegic refractive error
• In a school age child  full correction may
cause b u ed vision
blurred s o
– Because inability to relax accommodation fully
– A short course of cycloplegia may help
American Academy of Ophthalmology

141
Clinical refraction
• Refraction approach  ARK
• Subjective  Trial and error by trial optical
lenses
• Objective  Streak retinoscopy
– Characteristic of reflex
• Speed
• Brilliance
• Width

– Four characteristic of STREAK reflex
•
•
•
•

Break
Width
Intensity
Skew
American Academy of Ophthalmology

142
Streak retinoscopy

Neutralization
With
Against
ga s
143
Finding Neutrality
•
•
•
•

•
•
•

In against movement, the far point is between the examiner and the
perfect therefore, to bring the far point to the examiner’s pupil, minus,
lenses should be placed in front of the patient’s eye.
patient s
Similarly, in the case of with movement plus lenses should be placed in
front of the patient’s eye.
Similarly, in the case of with movement, plus lenses should be placed in
front of the patient s eye
patient’s eye.
This leads to the simple clinical rule: if you see with motion, add plus
lenses (or subtract minus); if you see against motion, add minus lenses
(or subtract plus). Lens power should be added (or subtracted) until
neutrality is reached
y
Since it is considered easier to work with the brighter, sharper with image, it
is preferable to overminus the eye and obtain a with reflex and then reduce
the minus (add plus) until neutrality is reached.
,
Be aware that the slow, dull reflex and then reduce the minus
refractive errors may be confused with the pupil-filling neutrality reflex
or with dull reflexes (as seen in patients with hazy media).
Place high-power plus and minus lens over the eye and look again.

American Academy of Ophthalmology

144
Finding Neutrality
g
y

145
Finding the cylinder axis
g
y
• Before retinoscope is used to measure the powers in
each of the principal meridians, the axes of the
p
p
meridians must be determined.
• Characteristics of the streak reflex can aid in determining
axis.
– Break. A break is seen when the streak is not parallel to one of
the meridians. The are projecting the line is discontinuous, or
broken. The break disappears (ie, the line appears continuous)
g
when the streak is rotated on to the correct axis. The correcting
cylinder should be placed at this axis.
– Width. The width of the streak varies as it rotated around the
correct axis. It appears narrowest when the streak aligns with
the axis
– Intensity. The intensity of the line is brighter when the streak is
on the correct axis. (This is a subtle finding, useful only in small
cylinders)
American Academy of Ophthalmology

146
Finding the cylinder axis
g
y

American Academy of Ophthalmology

147
Finding the cylinder axis
g
y

148
Finding the cylinder axis
g
y

American Academy of Ophthalmology

149
Finding the cylinder axis
g
y

American Academy of Ophthalmology

150
Finding the cylinder axis
g
y

American Academy of Ophthalmology

151
Finding the cylinder power
•
•

Once the two principal meridians are identified, the axis separately
in turn.
With two spheres
spheres.
– Neutralize one spherical lens. If the 90º axis is neutralize with a +1.50
sphere and the 180º axis is neutralized with a +2.25 sphere, the gross
retinoscopy would be +1.50 + 0.75 x 180. The examiner’s working
distance should be subtracted from the sphere to obtain the refractive
correction.

•

With a sphere and cylinder.
– Neutralize one axis with spherical lens. To continue working using with
reflexes,
reflexes neutralize the lens plus axis first Then with this spherical lens
first. Then,
in place, neutralize the axis 90º away by adding a plus cylindrical lens
directly from the trial lens application. The spherocylindrical gross
retinoscope can be read directly from the trial lens application.

•

It is also possible to use two cylinders at right angles to each other
for this gross retinoscopy ; however, this variant does not seem to
provide any advantages over the other methods.

American Academy of Ophthalmology

152
Aberrations of the Retinoscopic Reflex
•
•
•
•

•

With irregular astigmatism, almost any type of aberration may
appear in the reflex.
Spherical aberration tend to increase the brightness at the center or
periphery of the pupil, depending on whether the aberrations are
positive or negative.
As the point of neutrality is approached one part of the reflex may
approached,
be myopic while the other is hyperopic relative to the position of the
retinoscope. This will produce the scissors reflex.
Sometimes a marked irregular astigmatism or optical opacity
produces confusing, distorted shadows that can markedly reduce
confusing
the precision of the retinoscopic result. In such as subjective
refraction should be used.
All of these aberrant reflexes become more noticeable with larger
papillary di
ill
diameters. I these cases, considering the central portion
In h
id i
h
l
i
of the light reflex yields the best approximation.

American Academy of Ophthalmology

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Summary of retinoscopy
1.

2.
3.

4.

5.

The steps below summarize how to performing streak retinoscopy using
a plus cylinder phoropter. Set the phoropter to 0 D sphere and 0 D
cylinder.
cylinder Use cycloplegia if necessary Otherwise fog the eyes or use a
necessary. Otherwise,
non accommodative target.
Hold the sleeve of the retinoscope in the position that produces a
divergent beam of light. (If the examiner can focus the linear filament of
the retinoscope on a wall, the sleeve is in the wrong position)
wall
position).
Sweep the streak of light (the intercept) across the pupil perpendicular to
the long axis of the intercept and watch the papillary light reflex. Sweep in
several different meridians. Use the right eye to examine the patient’s
right eye, and use the left eye to examine the patient’s left eye.
patient s
Add minus sphere (dial up on a phoropter) until the retinoscopic reflex
shows with motion in all meridians. Add a little extra minus sphere if
uncertain. If the reflex are dim or indistinct, consider high refractive errors
and make large changes in sphere ( D, -6 D, -9 D, etc).
g
g
(-3
)
Add plus sphere (dial down on a phoropter) until the retinoscopic reflex
neutralizes or shows a small amount of residual with motion in one
meridian. If all meridians neutralizes simultaneously, the patient’s
refractive error is spherical. Proceed to step 9.
American Academy of Ophthalmology

154
Summary of retinoscopy
y
py
6.

7.

8.

9.
10.

Rotate the streak 90º and set the axis of the correcting plus cylinder
parallel to the streak. Sweep this meridian to reveal additional with
motion. Add plus cylinder power until the remaining with motion is
neutralized.
neutralized Now the retinoscopic reflex should be neutralized in all
meridiens simultaneously.
Refine the correcting cylinder axis by sweeping 45º to either side of it.
Move in slightly closer to the patient to pick up with motion. Rotate the
axis of the correcting plus cylinder a couple of degrees toward the “guide”
guide
line, the brighter and narrower reflex. Repeat until both reflexes are
equal.
Refine the cylinder power by moving in closer to the patient to pick up
with motion in all directions. Back away slowly, observing how the
reflexes neutralize. Change sphere or cylinder power as appropriate to
make all meridians neutralize simultaneously.
Subtract the working distance. If working at 67 cm, subtract 1.5 D. if the
examiner’s arms are short or the examiner prefers working closer, the
p
g
,
appropriate dioptric power for the distance chosen should be subtracted.
Record the streak retinoscopy findings and, if possible, check the
patient’s visual acuity after he or she has had time to wear the
prescription and readjust to ambient room light.
American Academy of Ophthalmology

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Retinoscopy: Final correction
•
•

If we use working lenses  Another
correcting lenses  Final correction
If for example in 50 cm working distance,
we use S +2.00 working lenses, and we
2.00
get: Horizontal S -6.00 and Vertical S 3 00, t e
3.00, the Final correction:
a co ect o
– S -6.00 C +3.00 A 90 or,
– S -3 00 C +3 00 A 180
3.00 +3.00
156
Lenses
• Meniscus Lens or Curve Lens  Lens with
one spherical convex surface and the other
spherical concave. Meniscus lenses often have
a base of 6 D for the surface of lesser curvature.
• Polarizing Lens A lens that transmits light
waves vibrating in one direction only. In the
other direction perpendicular to it, the light
waves are absorbed In this way reflected glare
absorbed.
is reduced.
157
The Basic Lenses

(A), biconvex; (B), biconcave; (C), planoconvex; (D), plano concave;
(E),concavoconvex, periscopic convex, converging meniscus;
(F), convexoconcave, periscopic concave, diverging meniscus;
(G, H), cylindrical lenses, concave and convex.
MedDict 2007

158
Sphere lenses

159
Sphere Lens

Biconvex Lenses

CaF2 Lenses

Plano Concave Lenses

Biconcave Lenses

Meniscus Sphere
Lenses

Changch Jixiang 2006
hun
g,

Plano Convex Lenses

160
Spheric correction
• Least minus for myopia
– More minus forces contraction of cilliary
muscles for unnecessary accommodation 
Fatigue

• Most plus for hyperopes
– Less plus retains accommodation

161
Spherical aberrations
• More peripheral rays focused anteriorly
• Exacerbates myopia in low light (night
myopia) about – 0.50 D
• Increase as fourth power of pupil diameter
– Small pupil can cause better vision

• Can also occurs following refractive
surgery
– Aspheric cornea becomes more spherical
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Achromatic lenses
•
•
•
•
•

Achromatic Lenses consist of two or more elements, usually of
crown and flint glass that have been corrected for chromatic
aberration with respect to two selected wavelengths.
Most company provides achromatic lenses consisting of two
elements.
These lenses have considerably reduced not only chromatic
aberration bust also spherical aberration and coma aberration.
These are designed with respect to three wavelength 480nm,
546.1nm
546 1nm and 643 8nm
643.8nm.
They are best used in replacing singlet where improved
performance is required.
– Positive Achromatic Lenses
– Negative Achromatic Lens

Changchun Jixiang, 2006

163
Achromatic lenses

Positive Achromatic Lenses

Negative Achromatic Lenses

Changchun Jixiang, 2006

164
Astigmatism
g
• Classified as
– Sh
Shape
• Regular astigmatism
– With the rule
» Common in children
» Vertical meridians is steepest
» A i near 90º
Axis
– Against the rule  opposite
» Older adult

• Irregular astigmatism
– Rigid contact lenses may be useful
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Circle of least confusion

Conoid of Sturm

166
Cylinder lenses
y

167
Cylinder lenses

Plano Convex Cylindrical Lenses

Plano Concave Cylindrical Lenses

Biconvex Cylindrical Lenses

Biconcave Cylindrical Lenses

Changchun Jixiang, 2006
Meniscus Cylindrical Lenses

168
Cylinder axis

American Academy of Ophthalmology

169
Astigmatic dial technique
• Obtain best visual acuity using SPHERES only
y
g
y
• FOG the eye to about 20/50 by adding PLUS
sphere
• Note the BLACKEST and SHARPEST line of
the astigmatic dial
• Add MINUS CYLINDER with axis
PERPENDICULAR to the blackest and sharpest
line (Rotate minus cylinder if necessary) until all
lines APPEAR EQUAL
es
QU
• REDUCE plus sphere or ADD minus until best
acuity is obtained with the visual acuity chart
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Astigmatic correction
g
• For children  full correction with correct axis
• For adult  adaptable full correction
• Reduce distortion
–
–
–
–

Use minus cylinder
y
Minimize vertex distance
Rotate axis toward 180º or 90º
Reduce cylinder power and use spherical equivalent

• Spatial distortion is binocular phenomenon 
occlude one eye to verify
• If fail to reduce distortion  use contact lenses
or iseikonic corrections
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Toric lenses

American Academy of Ophthalmology

172
Toric lenses
• Shaped like a section through a rugby ball
• P
Prescribed t correct astigmatism 
ib d to
t ti
ti
contact lenses and IOLs
• Toric lenses can be plus, minus, one
principle meridian plus with the other
minus
p
y
• Referred as Spherocylinder lenses
173
Prism lenses

174
Prisms aberration
• In addition to chromatic aberration
• Producing colored fringes at the edges of
objects viewed through the prism
• Other aberration
– Asymmetrical magnification of field
– Asymmetrical curvature of field

• Usually insignificant but  produce
symptoms even with low-power
p
prisms.
ophthalmic p
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Prismatic effect of decentred lens
• Convex lens  two
prisms cemented
together at their
BASEs
BASE
• Concave lens  two
prisms cemented
together at their
APEXs
• Decentred lens 
Prism effect  Base
in or Base out

Decrease convergence

Increase convergence
Bifocals
• A lens having one
section that
corrects for distant
vision and another
section that
corrects for near
vision.
vision

177
Bifocals

The dot indicates the optical centre of the near portion
A, executive-type segment; B, flat-top segment; C, round segment;
D,
D curved segment
d

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178
Trifocals

•

Three prescription powers: a distance power, a mid-range power, and a
near power.

•

The distance power helps to see things at a distance, the mid-range
power helps to see things at intermediate distances and the near power
distances,
corrects vision close up.

•

Tri-focal lenses are available in a variety of options, including thin and
light lenses, impact resistant lenses and transition lenses (lenses that
change from light to dark).

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179
Progressive Lens
•

Characterized by a gradient of
increasing lens power added to
power,
the wearer's correction for the
other refractive errors.

•

The gradient starts at a
minimum, or no addition power,
at the top of the lens and
reaches a maximum addition
power, magnification, at the
bottom of the lens.

•

The length of the progressive
power gradient on the lens
surface is usually between 15
and 20 mm with a final addition
power between 1 00 to 3 00
1.00 3.00
dioptres.
MedDict 2007

180
Transposition

181
S - 6.00 C + 3.00 A 90º
0.00

- 6.00

- 6.00

- 6.00

+3.00

+3.00

0.00

- 6.00

- 6.00

Make the
transposition
of it

- 3.00

- 3.00

- 6.00
182
Transposition
• New sphere is the ALGEBRAIC SUM of old sphere and
cylinder
• New cylinder is same value with old cylinder but with
cylinder,
OPOSITE sign
• Change axis of cylinder by 90º

S - 6 00 C + 3 00 A 90º
6.00
3.00 90
S - 3.00 C - 3.00 A 180º
IS IT SAME OR EQUAL ???

183
S - 3.00 C -3.00 A 180º
- 3.00

- 3.00

0.00

0.00

- 3.00

- 3.00

- 3.00

- 3.00

- 6.00

EQUAL

- 3.00

- 3.00

- 6.00
184
Is your correction correct?
y
• Duke Elder  add + 0.25 or – 0.25 D
– I it bl
Is i blurred or still clear ?
d
ill l
– Smaller, darker, farther away or any such change

• Duochrome test  RAM-GAP
– Red add minus, green add plus

Binocular balance
• Fogging
• Prism dissociation
• Cycloplegics
American Academy of Ophthalmology

185
Refraction : Correction
•
•
•

Spectacle / glass
Contact lenses
Keratorefractive surgery
–
–
–
–
–
–
–
–

RK  Radial keratotomy
PRK  Photo Refractive Keratotomy / Keratectomy
Laser Thermal Keratoplasty
LASIK (Laser-assisted in-situ Keratomileusis), EpiLASIK
SBK  Sub-Bowman Keratomileusis
LASEK  Laser-assisted Sub-Epithelial Keratomielusis
LaserACE  Restoring accommodative ability
CK  Conductive Keratoplasty  Radio-frequency-based Collagen
shrinking procedures
– Arcuate keratotomy
– Intrastromal corneal ring

•

IOL
– AC Lens, Claw lens (25-6)  Artisan (Ophtec), Verisyse (
,
(
)
( p
),
y (Abbott
Medical Optics), STAAR Visian ICL and Toric ICL
– Posterior lens by CLE / RLE (>13)

186
Corneal Collagen Cross-Linking
g
g
• Corneal thermal remodeling  (also) can be induced by
Microwave Keratoplasty
Micro a e Keratoplast  treat Keratocon s and
Keratoconus
Refractive Errors
• UV radiation  accelerates corneal stiffening by
riboflavin
• Cross-linking occurs between collagen helix,
aminoglycans and other substances in corneal substrate
• D li i “Controlled I
Delivering “C t ll d Insult” t St
lt” to Stromal C ll
l Collagen Fib
Fibers
bellow epithellium and Bowman’s layer  change shape
without cutting.
• Fatten the cornea  after Lasik or incisional surgery
• Achieve corneal rigidity equivalent to 600 years of
natural ageing
Marshall J, 2010

187
Corneal Collagen Cross-Linking
g
g

•
•

Older procedure  30 minutes riboflavin soaks and 30 minutes UV
p
exposure  potential endothelial damage, complication to lens and retina
Newer procedure  2 minutes riboflavin soaks and 3 minutes UV exposure
with mask-covered protection at peripheral and central of the cornea 
protecting endothel, corneal stem cells, lens and retina  Keraflex KCL
(Avedro)
(A d )
Marshall J, 2010

188
Contact Lenses Fitting

189
Contact lenses : Materials
1.
1 HEMA (Hydroxyethyl methacrylate)
2. Non HEMA  Hydrogel lenses  Hydrophyllic
3. HEMA + PVP (Polyvinylpyrrolidone)
( y y py
)
- To increase water holding ability ,
- PVP  Yellowing by age / heat disinfection
4.
4 HEMA + MMA (Methylmethacrylate)
(M th l th
l t )
- To increase stiffness.
- Lens more durable
durable.
- The pores are smaller than any known
bacterium or virus
190
Contact Lenses Fitting
•

Base curve
–
–
–
–
–

•

Radius of curvature to be cut on the posterior surface of the lens
Minimal apical clearance
Guided by the K measurements along two principal meridians
Selected to ensure a comfortable and healthy fit for patients
Range from 8.40 mm (40.25 D) to 7.00 (48.25 D)

Diameter
– Optical zone range between 6.0 – 8.0 mm
– Central thickness  less than 0.10 mm

•

Peripheral curve
– Curve radii range between 8 40 – 13 00 mm
8.40 13.00
– Curve width  0.10 – 0.45 mm

•
•

Power
Lens surface design
–
–
–
–

Spherical lens
Back surface toric lens
Front surface toric lens
Bitoric
Bit i
American Academy of Ophthalmology

191
The Contact Lenses

Peripheral curve width

Optic zone

Base curve

Peripheral curve radii

Peripheral curve width

Center thickness

192
VERTEX DISTANCE CORRECTION
Vertex Distance (mm)
Spectacle
Power (D)

10

11

12

13

10

12

13

Contact Lens Power
Minus Lenses

4.00
4.50
5.00
5.50
6.00
6.50
7.00
7.50
8.00

11

3.87
4.25
4.75
5.25
5.62
6.12
6.50
7.00
7.37

3.87
4.25
4.75
5.12
5.62
6.00
6.50
6.87
7.37

3.87
4.25
4.75
5.12
5.62
6.00
6.50
6.87
7.25

Plus Lenses
3.75
4.25
4.75
5.12
5.50
6.00
6.37
7.25
7.62

4.12
4.75
5.25
5.75
6.37
7.00
7.50
8.12
8.75

4.12
4.75
5.25
5.87
6.37
7.00
7.62
8.12
8.75

4.25
4.75
5.25
5.87
6.50
7.00
7.62
8.25
8.87

4.25
4.75
5.37
5.87
6.50
7.12
7.75
8.25
8.87
193
FITTING STEPS
Good fit
1. Sufficient movement
2. Proper centration
3. Stable vision
4.
4 Sharp retinoscopic reflex
5. Clear keratometry mires
194
FITTING STEPS
Tight fit
1.
1 Vision fluctuates (clears briefly after blink)
2. Bubbles trapped under the lens
3. Declining comfort over a span of hours as the lens is worn
4. A burning sensation following by redness or an indication
appearing around the corneal circumference
5. Restricted or no movement of the lens
6. Keratometry mires that are distored, but clear on blinking
7. A fuzzy retinoscope reflex that clears on blinking
195
FITTING STEPS
Loose fit
1. Variable vision (briefly clears after blinking)
2.
2 Bothersome lens awareness
3. Lack of centration
4. Too much movement
5. Lens edge stand off l
5 L
d
t d ff lens d
decenter onto th sclera
t
t the l
7. Bubbles forming under the lens edge
8. Keratometry mires that are clear, but blurs on blinking,
and than clear
9. A clear retinoscopic reflex, that blurs after blinking
196
197
Toric contact lenses
• An astigmatic eye is not perfectly round (like a
soccer ball) but more shaped like a rugby ball.
• O i f
One-in-four people with l
l
i h low amounts of
f
astigmatism can get away with wearing normal
(spherical) contact lenses
lenses.
• A person with higher amounts of astigmatism
needs to wear special contact lenses called
toric lenses
198
What makes a to c co tact lens d e e t
at a es toric contact e s different?
• If you think of the eye as a rugby ball, that ‘rugby ball’ is
y
y
g y
,
g y
positioned at a certain angle in the eye socket.
• In order for the contact lens to correct astigmatism, it
needs to lie at that same angle in front of the eye
eye.
• Usually contact lenses rotate on the eye with each blink.
A toric contact lens is designed in such a way, that it
won t
won’t rotate on the eye
eye.
• Most toric lenses are made slightly thicker at the bottom
of the lens.
• The thicker part will weigh the lens down at the bottom,
preventing it from turning on the eye.
199
Radial Keratotomy

200
Laser Thermal Keratoplasty

201
Laser assisted
Laser-assisted in situ Keratomileusis

202
Laser-assisted Sub-Epithelial Keratomileusis

203
Arcuate Keratotomy

204
Intrastromal Corneal Ring

205
Aniseikonia
• Translated from Greek aniseikonia means
"unequal images".
• It is a binocular condition so the image in
condition,
one eye is perceived as different in size
compared to the image in the other eye
eye.
• Two different types of aniseikonia can be
differentiated: static and dynamic
diff
ti t d t ti
dd
i
aniseikonia
206
Aniseikonia
• Static aniseikonia or
aniseikonia in short means that
in a static situation where the
eyes are gazing in a certain
direction
• The perceived (peripheral)
images are different in size
207
Aniseikonia : Static

208
Aniseikonia
• Dynamic aniseikonia or (optically
induced) anisophoria means that
the
th eyes h
have t rotate a different
to t t
diff
t
amount to gaze (i.e. look with the
sharpest vision) at the same point in
space
p
• This is especially difficult for eye
rotations in the vertical direction
209
Aniseikonia : Dynamic

210
Aniseikonia

Schematic presentation of the different steps to get to a perceived
image size and the visualization of a field angle α
211
Aniseikonia

Features : a) Example of a single aniseikonia test image, b) same aniseikonia
test image as on the left, but now with an (exaggerated) vertical fixation
g
,
(
gg
)
disparity compensation (click on image to enlarge).
212
Anisophoria
• Is a condition in which the balance of the
vertical muscles of one eye differs from
that of the other eye  the visual lines do
not lie in the same horizontal plane
• Eye muscle imbalance  the horizontal
visual plane of one eye is different from
that of the other

213
Amblyopia
y p
Type :
• St bi i amblyopia
Strabismic
bl
i
– Frequently  in esotropia patients

• A i
Anisometropic (R f ti ) amblyopia
t i (Refractive)
bl
i
– Difference in refraction greater than 2.50 D

• Isoametropic amblyopia
– Bilateral refractive error grater than + 5.00 or – 10.00 D

• Deprivation amblyopia
– Caused by such as media opacities
Deborah Pavan-Langston, 2008

214
CyberSight, 2003
215
216
Strabismus

217
Position of gaze
g
• Primary position
– Straight ahead

• Secondary position
– Straight up, straight down
– Right gaze, left gaze

• Tertiary position  Four oblique position
– Up and right, up and left
– Down and right, down and left

• Cardinal position
American Academy of Ophthalmology

218
Cardinal position and Yoke muscles
RSR
LIO

Right Gaze

LSR
RIO

RLR
LMR

LLR
RMR

RIR
LSO

LIR
RSO

Left Gaze

American Academy of Ophthalmology

219
Eye movement
• Agonist
– Primary muscle moving the eye in a GIVEN direction

• Synergist
–
–
–
–
–

Muscle in the same eye
As the agonist
That can act with agonist
Produce a GIVEN movement
E.g Superior rectus with I f i oblique  elevate the eye
E :S
i
t
ith Inferior bli
l
t th

• Antagonist
–
–
–
–

Muscle in the same eye
As the
A th agonist
i t
That can act with in the direction opposite
E.g : Medial rectus and lateral rectus
American Academy of Ophthalmology

220
Basic
• Sherrington’s law for reciprocal innervation
– Increased innervation and contraction of GIVEN
EOM 
– Accompanied by reciprocal decrease of innervation
and contraction of its antagonist EOM
f
O
• Yoke muscle
– Two muscle (one in each eye)
– Are Prime mover of their respective eyes
– In GIVEN position gaze
– E.g : right gaze  RLR and LMR simultaneously
innervated and contracted  to be “yoked” together
yoked
American Academy of Ophthalmology

221
Basic
• Hering’s law of motor correspondence
Hering s
– The state  equal and simultaneous
innervation flow to Yoke muscle
– Concerned with the desired direction of the
gaze

American Academy of Ophthalmology

222
EOM : Functions
Muscle

Primary

Secondary

Lateral rectus

Abduction

None

Medial rectus

Adduction

None

Superior rectus

Elevation

Adduction
Intorsion

Inferior rectus

Depression

Adduction
Extorsion

Superior oblique

Intorsion

Depression
Abduction

Inferior oblique

Extorsion

Elevation
Abduction
Vaughan DG

223
EOM : Origin
g
Muscle

Origin

Functional
origin
i i

Lateral rectus

Annulus of Zinn

Annulus of Zinn

Medial
M di l rectus
t

Annulus of Zi
A
l
f Zinn

Annulus of Zi
A
l
f Zinn

Superior rectus

Annulus of Zinn

Annulus of Zinn

Inferior rectus

Annulus of Zinn

Annulus of Zinn

Superior oblique

Orbit apex above
Annulus of Zinn

Trochlea

Inferior oblique

Behind lacrimal fossa

Behind lacrimal fossa

American Academy of Ophthalmology

224
EOM : Insertion from limbus

•
•
•
•

Medial rectus
Lateral rectus
Superior rectus
Inferior rectus

5.5
5 5 mm
6.9 mm
7.7 mm
6.5 mm

American Academy of Ophthalmology

225
EOM : Wide and Length
•
•
•
•
•

Superior Rectus  5.0 mm and 41.8 mm
Inferior Rectus  4.2 mm and 40 mm
Lateral Rectus  6 5 mm and 40.6 mm
6.5
40 6
Medial Rectus  4.0 mm and 40.8 mm
Superior Oblique  1 2 mm and 
1-2
– Muscle part 40 mm
– Tendineus part 20 mm

• Inferior Oblique  1-2 mm and 37 mm
Kumar SM 2007

226
EOM : Gazes
Up and right

RSR - LIO

Up and left

LSR – RIO

Right

RLR – LMR

Left

LLR - RMR

Down and right

RIR - LSO

Down and left

LIR - RSO
Vaughan DG

227
Eye movement
• Versions
– Eyes move in the same direction

• Vergences  Disconjugate binocular eye
movement
–
–
–
–
–

Convergence  15-20 ∆ distance and 25 ∆ for near
Divergence  6-10 ∆ distance and 12-14 ∆ for near
Incyclovergence  2-3º
Excyclovergence
y
g
Vertical vergence  2-3 ∆

American Academy of Ophthalmology

228
Eye movement : Supranuclear control system
•

Saccadic system
– G
Generates all fast eye movements or refixation
t
ll f t
t
fi ti
– Up to 400-500º/sec

•

Smooth pursuit
– Generates all following, or pursuit eye movements
following
pursuit,
– Pursuit latency is shorter than for saccades
– Maximum velocity 30-60º/sec

•

The vergence system
– Controls disconjugate eye movements

•

The position maintenance
– Maintains a specific gaze position
– Allowing an object to interest to remain on the fovea

•

The non optic reflex
– Integrated eye movement with the body movement
– Most important system is Labyrinthine system
American Academy of Ophthalmology

229
Variation of deviation
With gaze position or fixating eye
• Comitant (Concomitant)
– Deviation doesn’t vary in size with direction of gaze or
fixating eye

• Incomitant (Noncomitant)
– Deviation varies in size with direction of gaze or
fixating eye
– Most  paralytic or restrictive
– In acquired condition  may indicate neurologic or
orbital problems or diseases
American Academy of Ophthalmology

230
Grades of binocular vision
• 1st Grade
– Simultaneous perception

• 2nd Grade
– Fusion

• 3rd Grade
– Stereopsis

Kanski JJ, 2007
231
Fusion
•
•

Cortical unification of visual object into a single percept
Made by simultaneous stimulation of corresponding retinal areas

Sensory fusion
– Relationship between retina and visual cortex
– Corresponding retinal points project to same cortical locus
– Corresponding adjacent retina points have adjacent cortical
representations

Motor fusion
–
–
–
–

Vergence movement
Causes similar retinal i
C
i il
i l image
Fall and be maintained on corresponding retinal areas
Disparities can be induced by, E.g : phoria, etc

American Academy of Ophthalmology

232
Stereopsis and Depth perception
• Stereopsis
p
– Binocular sensation
– Relative or subjective ordering of visual objects in
depth or 3 dimensions

• Depth perception
–M
Monocular clues i l d
l
l
include
•
•
•
•
•

Object overlap
Relative object size
Highlight and shadow
Motion parallax
Perspective
American Academy of Ophthalmology

233
AC/A Ratio
•

Accommodative Convergence / Accommodation Ratio
– Normal is between 3:1 to 5:1

– AC/A = PD +

∆n – ∆o
D

Gradient method
– PD = pupil distance (millimeter)
– ∆n = near deviations (prism diopter)
– ∆o = distance deviations (prism diopter)
sign convention :
– Esodeviation +
– Exodeviation -

– D = diopter of accommodation
– Distance 6 m
– Near 0.33 m

American Academy of Ophthalmology

234
ESODEVIATION
• Esodeviation
– Esophoria
• Controlled by fusion under condition of normal
y
binocular vision

– Intermittent esotropia
• C t ll d b f i under condition of normal
Controlled by fusion d
diti
f
l
binocular vision
• Spontaneous becomes manifest
• Particularly with fatigue or illness

– Esotropia
American Academy of Ophthalmology

235
Esotropia
•
•

Pseudoesotropia
Congenital esotropia
– Classic essential
– Nystagmus and esotropia
y g
p

•

Accommodative esotropia
– Refractive (Normal AC/A ratio)
– Non refractive (High AC/A ratio)
– Partially accommodative

•

Non-accommodative acquired esotropia
–
–
–
–
–
–

•

Basic
Acute
Cyclic
Sensory depriviation
Divergence insufficiency and divergence paralysis
Spasm of near synkinetic reflex

Incomitant esotropia
– Sixth nerve paresis
– Medial rectus restriction  Thyroid and trauma
y
– Duane’s syndrome and Möbius syndrome
American Academy of Ophthalmology

236
Pseudoesotropia
• Infant often have a wide, flat nasal bridge
with prominent medial ep ca a folds a d
po
e
ed a epicanthal o ds and
a small interpupillary distance.
• May appear esotropic
• I fact their eyes are straight.
In f t th i
t i ht
• No real deviation exists
• Both corneal light reflex and cover testing
results are normal.

237
Congenital Esotropia
•
•
•
•

Large constant esotropia (usually > 40 PD)
Onset birth to 6 months of age
Amblyopia common (50%-60%)
Associated motor phenomenon (
p
(usually
y
present after 1 year of age) :
– Inferior Oblique Over Action (IOOA)
– Dissociated Vertical Deviation (DVD)
– Latent nystagmus

238
Non-surgical treatment
Congenital esotropia
•
•
•
•
•
•
•

Abduction should be full or only slightly limited. Mild (-1) limitation of
abduction is common and does not necessarily indicate a lateral rectus
paresis.
Try the dolls head maneuver or spinning the child (vestibular stimulation) to
elicit full abduction in infants
Check for inferior oblique overaction and V-pattern
Check fixation preference: strong fixation preference for one eye indicates
amblyopia in the fellow eye.
Cross-fixate  fixing with right eye for objects in the left visual field and with
left eye for objects in the right visual field
Cross-fixate  indicate no significant amblyopia.
Measure deviation :
– Prisms Alternate Cover Test (PACT) is the BEST.
– KRIMSKY test  if PACT i unobtainable
t t
is
bt i bl

•

Cycloplegic refraction
– Use cyclopentolate 0.5% in infant < 24 year of age and 1% for older children
– If cycloplegic refraction shows > 3 D  prescribe full hyperopic correction.
– If ET > 10 to 15 PD persist after prescribe full hyperopic correction 
SURGERY is required

239
Accommodative esotropia
• CLINICAL FEATURES
– Usually acquired around 2 to 4 years of age
– Moderate to large esotropia (20 to 50 PD)
– Variable angle that is often intermittent
– Associated with hyperopia usually +2 to +6 D
– Classify as
• R f ti (Normal AC/A ratio)
Refractive (N
l
ti )
• Non refractive (High AC/A ratio)
• Partially accommodative
240
Non surgical treatment
•

Refractive accommodative esotropia
– Corrective lenses
• Full amount of hyperopia as determined under cycloplegia
• Full time spectacle wear  instill Atropine 1% at bed time to make initial
compliance
• Esotropia fully corrected distance and near
–
–
–
–

Full hypermetropic correction
ET < 8 to 10 PD
Single vision spectacle (without bifocal)
Surgery is not needed.
needed

• Distance corrected, but there is residual esotropia at near (high AC/A ratio)

–
–
–
–
–

Full hypermetropic correction
Distance deviation resulting fusion (i.e, < 10 PD ET)
Residual ET at near that can not be fused (i e > 10 PD ET)
(i.e
Prescribe a flat-top bifocal add. (start : + 2.50 to + 3.00 D)
Prescribe the least amount of near add to obtain fusion while leaving a
small near esophoria (E < 5 PD)

• Residual esotropia distance and near (
p
(Partially Accommodative esotropia)
y
p )

– With full hypermetropic correction
– Distance esotropia persist can not be fused (usually > 10 PD).
 SURGERY is INDICATED

– Miotic agent  subtitutes for glasses
American Academy of Ophthalmology

241
Non surgical treatment
• Non-refractive accommodative esotropia
– Bifocals
•
•
•
•
•

Flat-top design preferred
+2.50 to +3.00 D
Top of the segment should CROSS the pupil
Vertical height not exceed distance portion of the lens
Progressive lens must be fitted higher of 4 mm than adult fitting
with maximum bifocal power of +3.50 D
• Give detail to opticians
• Acceptance value 
– Fusion at distance
– L
Less th 10 ∆ residual esotropia at near
than
id l
t i t

– Long-lasting cholinesterase inhibitors  0.125% echothiophate
iodide both eye one time daily for 6 weeks
American Academy of Ophthalmology

242
Bifocal for Deviations

243
Order for surgery
• Surgery between 6 months and 2
years of age (most reference
recommend)
• Surgery between 6 months and 1 year
of age (standard approach).
• Early surgery between 3 and 5 months
of age (controversial, but may improve
sensory outcome)
outcome).
244
Surgical Approach
• The procedure of choice  bilateral medial
rectus muscle recession
g
g
• Near deviation as the target angle.
• In older patients with irreversible amblyopia
 recession medial rectus and resection
lateral
l t l rectus t amblyopic eye
t to
bl
i
• The surgical goal  not to operate the
patients out of glasses but to achieve
glasses,
alignment and fusion with full hypermetropic
correction
245
Non accommodative
Non-accommodative esotropia
• CLINICAL FEATURES :
–
–
–
–
–

Usually emmetropic, may be myopic
Onset after 2 years, even in late adulthood
Full duction
Late onset ET of unknown etiology
Surgery is the treatment of choice
• Bilateral lateral rectus recession
• Often undercorrection increase the amount of recession
• Try using prism adaptation to determine the full target angle
angle,
especially if there is a disparity between the distance and
near deviation.
• Operate for the full prism adapted angle
246
Sensory Esotropia
• Associated with a monocular blindness
or dense amblyopia
amblyopia.
• Treatment : recession lateral rectus
and resection medial rectus muscle is
performed on the eye with poor vision
• To obtain Cosmetic appearance of
straight eyes.
247
EXODEVIATION
• Exodeviation
– Pseudoexotropia
• An appearance of exodeviation when in fact the
pp
eyes are properly aligned
• Positive angle kappa
• Wide interpupillary distance

– Exophoria
• Controlled by fusion u de co d o o normal
Co o ed
us o under condition of o a
binocular vision

– Intermittent exotropia
American Academy of Ophthalmology

248
Intermittent exotropia
•

Classified by
– Difference distance and near between alternating prism and cover test
measurement
– Change in near measurement by unilateral occlusion or +3.00 D lenses

•

Clinical features
–
–
–
–
–
–

Most common form of exotropia
Usually present after 1 year of age
Large exophoria that spontaneusly becomes to a tropia
g
p
p
y
p
High grade stereopsis when fusing; suppression when tropic
Squint one eye to bright sun light
The exotropia is typically manifest when the patient is fatigued,
daydreaming or ill
– Symptoms  blurred vision, asthenopia, visual fatigue and rarely
diplopia in older children and adults

American Academy of Ophthalmology

249
Intermittent exotropia
• Basic type
– Same at near and distance

• Divergence excess
– Greater at distance
– True divergence excess
• Greater at distance even after a periods of monocular occlusion
• High gradient AC/A ratio at near by +3.00 D lenses

– Simulated divergence excess
• Greater than distance
• Same after one eye is 1 hour occluded  to remove the effect of
tenacious proximal fusion

• Convergence insufficiency
– Greater at near than distance
– Excludes isolated convergence insufficiency
American Academy of Ophthalmology

250
Non surgical treatment
•

Corrective lenses
– Improve retinal image clarity

•

Additional minus lens power
– Usually 2-4 D beyond refractive error correction
– Temporarily stimulate accommodative convergence

•

Part time patching
– Passive orthoptic treatment
– 4-6 hours per day or alternate daily patching
– Treatment for small to moderate-sized deviation

•

Active orthoptic treatment
–
–
–
–

•

Anti suppression therapy / diplopia awareness
Fusional convergence training
Alone or in combination with patching, minus lenses and surgery
Good for deviations of 20∆ or less

Base in prism
– Promote fusion
– Not recommended for long term treatment  cause a reduction in
fusional vergence amplitudes
f i
l
lit d
American Academy of Ophthalmology

251
Surgical treatment
•
•
•
•
•

Deviation of 15 ∆ or more
Nearly constant exotropia
Still i t
intermittent
itt t
Before 7 years of age
Before 5 years of strabismus duration

American Academy of Ophthalmology

252
NOTE
• Children under 4 years of age are at
risk f d
i k for developing postoperative
l i
t
ti
amblyopia and losing binocular vision.
• It is probably best to postpone surgery
until 4 years of age unless the patient
demonstrates progressive loss of
fusion control.
253
Another exodeviation
• Constant exodeviation
– Congenital exotropia
– Sensory exotropia
– Consecutive exotropia
– Exotropia Duane’s retraction syndrome
– Neuromuscular abnormalities
– Di
Dissociated h i
i t d horizontal d i ti
t l deviation

American Academy of Ophthalmology

254
A-V Patterns in horizontal strabismus
A V P tt
i h i
t l t bi
• A Pattern
– Eyes closer together in up gaze
– 10 PD difference compares to down gaze

• V P tt
Pattern
– Eyes closer together in down gaze
– 15 PD difference compares to up gaze

Deborah Pavan-Langston, 2008

255
A Pattern
• Etiology
– Most f
frequent  overaction of SO
f
– With or without underaction of IO
– As SO acts abduction in downward gaze
• Esotropia decreases
• Exotropia increases

– If no overaction of SO  suspect underaction of LR

• Treatment
– Deviation more than 10 PD
– Bilateral weakening  Tenotomy with silicone expander
– Horizontal surgery
g y
• With upward displacement of MR
• With downward displacement of LR

– Bilateral SO surgery  avoided in patient with foveal bifixator
Deborah Pavan-Langston, 2008

256
V Pattern
•

Etiology
– Most frequent  overaction of IO
– Primary underaction of SO
– As IO acts abduction in upgaze
• Esodeviation decreases
• Exodeviation increases

– Overaction of LR  V exotropia

•

Head position
– V esodeviation  chin held down close work
– V exodeviation  chin held up

•

Treatment V esotropia
– Recession or disincertion of overacting IO
– Recession or downward the MR if obliques are normal

•

Treatment V esotropia
– Recession or disincertion of LR if IO overacts
Deborah Pavan-Langston, 2008

257
Strabismus : Position test
Measurement of deviation
• Hiscberg test
• C
Cover t t
test
• Cover uncover test
• Krimsky test
• Prisms Cover test
• Prisms Alternate Cover Test (PACT)
American Academy of Ophthalmology

258
259
260
261
262
263
Strabismus : Sight test
• WFDT
• Maddox’s rod

264
265
266
267
268
Approach to Recession surgery
Minimal (mm)

Average
maximum (mm)

Maximum
ever (mm)

LR

4

8 - 10

MR

2.5

7 adult
6 children
5 - 5.5

6-7
14 for nystagmus

SR

2.5

5

IR

2.5

10

5
Eugene M. Helvestone

269
Approach to Resection surgery
Minimal (mm)

Average
maximum (mm)

Maximum
ever (mm)

LR

5

8 infant
10 children and adult

-

MR

5

8 infant
10 children and adult

-

SR

2.5 - 3

5

-

IR

2.5 - 3

5

-

Eugene M. Helvestone

270
Prisms Muscle
Prisms-Muscle length conversion

• 5 ∆ Di t f 1 mm MR recession
Diopter for
i
• 2.5 ∆ Diopter for 1 mm LR recession
• 2.5 ∆ Diopter for 1 mm MR and LR
resection

271
Both eye surgery for Esodeviation :
Angle of esotropia (∆)

Recess MR OU (mm)

OR

Resect LR OU (mm)

10

3.0

4.0

20

3.5
35

5.0
50

25

4.0

6.0

30

4.5

7.0

35

5.0

8.0

40

5.5

9.0

50

6.0

9.0

American Academy of Ophthalmology

272
Monocular surgery for Esodeviation
Angle of esotropia (∆)

Recess MR OU (mm) AND Resect LR OU (mm)

10

3.0

4.0

20

3.5
35

5.0
50

25

4.0

6.0

30

4.5

7.0

35

5.0

8.0

40

5.5

9.0

50

6.0

9.0

American Academy of Ophthalmology

273
Both eye surgery for Exodeviation :
Angle of exotropia (∆)

Recess LR OU (mm)

OR

Resect MR OU (mm)

15

4.0

3.0

20

5.0
50

4.0
40

25

6.0

5.0

30

7.0

6.0

40

8.0

6.0

American Academy of Ophthalmology

274
Monocular surgery for Exodeviation :
Angle of exotropia ( )
g
p (∆)

Recess LR OU (mm) AND Resect MR OU (mm)
(
)
(
)

15

4.0

3.0

20

5.0

4.0

25

6.0

5.0

30

7.0

6.0

40

8.0

6.0

50

9.0

7.0

60

10.0
10 0

8.0
80

70

10.0

9.0

80

10.0

10.0

American Academy of Ophthalmology

275
Strabismus : Exercise

Synophthophore

Holme’s stereoscope

276
Glaucoma

277
Glaucoma : Basic
• Definition
– Optic neuropathy
– Visual field defect
– Rise of IOP as major risk

278
279
Glaucoma : Basic
•
•
•
•
•
•
•
•

IOP measure
Angle examination
Optic nerve head examination
Vascular change
RNFL examination
i ti
Visual field examination
Central corneal thickness and rigidity
General eye examination*
280
IOP : Basic
•
•
•
•
•
•
•

Normal IOP  10-20 mmHg
10 20
Average  15 mmHg
Fluctuation
Fl t ti  2 56 mmHg
2.56
H
Diurnal Variation  3-6 mmHg
Peak period  Morning
Decrease during the night
Hypotony < 5-6 mmHg
Gumansalangi MNE, 2003

281
IOP : Determining factors
F = C (P – P )
(Po Pe)
• F
• C

= rate of aqueous outflow (normal 2 µl/min)
= facility of aqueous outflow (normal 0.2
µl/min/mmHg
• Po = IOP in mmHg
• Pe = episcleral venous pressure (normal 10 mmHg)

Kanski JJ, 2007

282
How to measure the IOP
• First line
– Applanation tonometer  Nowadays Gold standard  AT 900D
(Haag-Streit International)
– Dynamic contour tonometer  E g : PASCAL (Ziemer)
E.g

• Second line
– Air-puff non-contact tonometer
– Corvis ST Air-puff non-contact tonometer with Scheimpflug
Camera Cornea Monitoring (OCULUS)
– Tono-Pen, The Pachmate DGH 55, Diaton, Schiotz tonometer
– iCare ONE tonometer, SOLX IOP sensor*  IOP monitoring

283
IOP : Flow
•
•
•
•
•

Cilliary body
Posterior chamber
Pupil
P il
Anterior chamber
Delivery
– Trabecular pathway (85-95%)
(85 95%)
– Uveo-scleral pathway (5-15%)
– Iris (Kanski)
284
IOP : Flow
• Aqueous come in to eye by :
– Diff i
Diffusion
– Ultrafiltration
–C
Carbonic Anhydrase II activity
– Active secretion

American Academy of Ophthalmology

285
Glaucoma: Vascular dysregulation
y g
• Endhotelial dysfunction
– Impaired endothelium-derived nitric oxide
activity
– Abnormalities of the endothelin system 
altered Endothelin-1 (ET1) vasoreactivity

• Defective auto regulation of ocular blood
flow
• Instable blood supplies to the tissue
Henry E, 2006; Araie M, 2010

286
Glaucoma : Angle
•
•
•
•
•
•
•

Torch
Von Herrick Slit-lamp
Gonioscopy
Ultrasound Biomicroscopy (UBM)
Anterior
A t i OCT
Scheimpflug Camera Pentacam
Very high frequency (VHF) ultrasound eye
scanner  Artemis (ArcScan, Inc)
287
Angle : Observation

288
Angle Examination : Torch

289
Angle Examination : Van Herick

Von Herrick and Shaffer grades
Grade

Ratio of aqueous gap/cornea

Clinical interpretation

Shaffer angle degrees

4

>½/1

Closure impossible

45-35

3

½-¼ /1

Closure impossible

35-20

2

¼/1

Closure possible

20

1

<¼/1

Closure likely with full dilation

10 or less

0

Nil

Closed

0

290
Angle Examination : Gonioscopy

291
Identification of Schwalbe’s Line
Schwalbe s

Thomas R, 2006

292
Shaffer’s Intepretation

Classification

Angle Width

Visible Structure

Clinical Intepretation

Grade 0

Closed

Schwalbe’s line is not visible

Totally closed angle

Grade I

10°

Schwalbe’s line visible

Considerable risk of closure

Grade II

20°

Anterior trabeculum is visible

Bear watching

Grade III

30°

Scleral spur is visible

No risk of angle closure

Grade IV

40°

Ciliary body is visible

No risk of angle closure

293
PAS look alike

Thomas R, 2006

294
Rubeosis

Thomas R, 2006

295
Angle Recession
g

Thomas R, 2006

296
Angle Examination : UBM

297
Angle Examination : UBM

Normal eye’s angle

Angle : Pupillary block

298
Angle Examination : Anterior OCT

Visante OCT (Carl Zeiss Meditec AG)
299
Scheimpflug Camera Pentacam

300
Artemis ( Ultralink)
50 MHz ArcScan

301
The Angle

302
Shaffer s
Shaffer’s Intepretation
Classification
Cl
ifi ti

Angle
A l Width

Visible St
Vi ibl Structure
t

Clinical I t
Cli i l Intepretation
t ti

Grade 0

Closed

Schwalbe’s line is not visible

Totally closed angle
y
g

Grade I

10°

Schwalbe’s line visible

Considerable risk of closure

Grade II

20°

Anterior trabeculum is visible

Bear watching

Grade III

30°

Scleral spur is visible

No risk of angle closure

Grade IV

40°

Ciliary body is visible

No risk of angle closure

303
Optic disc
A. Surface
B. Pre Laminar
C. Laminar
D. Retro Laminar

304
GON : Evaluation
• Indirect ophthalmoscope*
• Direct ophthalmoscope
• Slit lamp : stereoscopic view
• H b or El B
Hruby
Bayadi l
di lens
• 60, 78, 90 D
• Contact lens

Thomas R, 2006

305
GON : Evaluation
•
•
•
•
•
•
•

Disc  Generally
Cup
Neuro R ti l Ri (NRR)
N
Retinal Rim
Peripapillary hemorrhage
Circum Linear Vessels (CLV)
Para Papillary Atrophy (PPA)
Retinal Nerve Fiber Layer (RNFL)
306
GON : Evaluation
Generalized
Large optic cup
L
ti
Asymmetry of the cup
Progressive enlargement
of the cup

Focal
Narrowing ( t hi ) of th rim
N
i (notching) f the i
Vertical elongation of the cup
Cupping to the rim margin
Regional palor
Splinter hemorrhage
S li t h
h
Nerve fiber layer loss

Less specific
Exposed l i cribosa
E
d lamina ib
Nasal displacement of vessels
Baring of circumlinear vessels
Peripapillary crescent

(TJ et al, 2003)
al

307
Cup and Disc

308
Disc Excavasion

309
Definition of Cup : Disc Ratio
• Disc Diameter
• Cup Diameter
• CDR = c / d

c d

• Horizontal > Vertical

Thomas R, 2006

310
Thomas R, 2006
R
311
a. Normal C/D Ratio 0.2
b. Same Disc 1 year later with C/D
Rasio 0 5
R i 0.5
c. Cup enlarge to Infero Temporal
and Splinter Hemorrhages
d. Cup enlarge to Superior and show
Inferior Bayoneting Sign
e. Advance Cupping Oval Disc
enlarge to superior and inferior
f. Pale Papil with deep excavasion

312
CDR Asymmetry

Thomas R, 2006

313
Asymmetric cupping

314
Cup Depth
•
•
•
•

Not of much importance
In normal : depends on disc area
In glaucoma : type & level of IOP
Deepest with high IOP
– Juvenile POAG
– Angle recession

Thomas R, 2006

315
Neuro Retinal Rim (NRR): Shape
• Sloping rim in small and intermediate discs
• Steep or over hanging with oblique insertion
• Supero nasal tilt in normal
• Nasal tilt in myopes
Thomas R, 2006

316
NRR in Glaucoma
• Loss of physiological shape
• ISNT rule i b k
l is broken
• Vertical cup enlarges
Thomas R, 2006

317
Jonas ISNT Rule
•

Less marked in large discs

•

Rim more evenly distributed

•

Punched out well defined
cup in large discs

•

p
Also compare Inferior &
Superior to temporal rim

•

Inferior to Temporal 2 : 1

•

Superior to Temporal 1.5 : 1

Thomas R, 2006

318
NRR : I S N T
• Partially depends on exit of central retinal
vessels
l
• Rim furthest away is more affected
• May explain unusual configuration of rim

Thomas R, 2006

319
Temporal Portion of Rim
• Papillo macular bundle
• Preferential cupping temporally with field
loss near fixation
• POAG with Myopia and NTG

Thomas R, 2006

320
Glaucoma & Contour of Rim
• May cause a backward bowing of the rim
tissue
• Deep extension of the cup in one meridian
• Gentler sloping backward : Saucerization

Thomas R, 2006

321
Rim contour : Normal

Thomas R, 2006

322
Saucerization
• Slight backward
bowing : like
saucer
• Periphery or a
portion
ti
• Or whole disc
• May be first
change
Thomas R, 2006

323
Shelving : No Field Defect ?

Thomas R, 2006

324
Excavation : Field Defect

Thomas R, 2006

325
Excavation : Field Defect

Thomas R, 2006

326
Excavation : Superior and Inferior

Thomas R, 2006

327
Notching

Thomas R, 2006

328
Disc Hemorrhage
• Rare in normals (1%)
• 4 -7 % in glaucoma
7
• > In “NTG”
• Lasts 10 weeks (1035)

Thomas R, 2006

329
Disc Hemorrhage
• Splinter or flame
shaped
• Border of disc
• Inferior or superior
temporal region
• RNFL defects,
Notching, Focal
perimetric loss
Thomas R, 2006

330
Circum Linear Vessels (CLV)
• Vessel hugging
gg g
the NRR
• Exits disc for
macula
• Normally present
in 50 % of eyes
Thomas R, 2006

331
Circum Linear Vessels (CLV)

Thomas R, 2006

332
Circum Linear Vessels “Bared” in Glaucoma
• N
Normal CLV
l
• As rim is lost : gap
between vessel and
rim
– Implies loss of rim

• F i l specific
Fairly
ifi
• Superficial or deep

CLV normally present in 50 % of eyes

Thomas R, 2006

333
Para Papillary Atrophy (PPA)
• Central beta zone
• Peripheral alpha zone
• Rare nasally or
circumferential
• Correlate with myopia
and age

Thomas R, 2006

334
Para Papillary Atrophy In Normals

• Beta zone : 20 %
• Alpha zone : 95 + %

Thomas R, 2006

335
PPA : Alpha Zone
•
•
•
•

Peripheral to beta or disc margin
Irregular Hyper and Hypo pigmentation
Thinning of RPE
Relative scotoma

Thomas R, 2006

336
PPA : Beta Zone
•
•
•
•
•

Central to alpha
Peripheral to disc margin
Marked atrophy of RPE
Visible choroidal vessels & sclera
Absolute scotoma

Thomas R, 2006

337
PPA in Glaucoma
• Central beta zone
more important

• Peripheral alpha
zone

Thomas R, 2006

338
PPA in POAG
• B t larger in hi h
Beta l
i high
myopic POAG
• Next in age
related POAG
• Less in SOAG
• ? NTG and POAG

Thomas R, 2006

339
Disc Hemorrhage a d Para Papillary Atrophy
sc e o age and a a ap a y t op y

• PPA associated
with h
ith hemorrhages
h
• PPA  marker for
old hemorrhages

Thomas R, 2006

340
Axonal distribution

341
Glaucoma : RNFL Defect

342
Normal RNFL :
Axons Bundled by Mueller Cell Processes
Bright fine striations

• Best seen 
Inferior and
superior temporal
p
p
(Inferior > Superior)
• Bright Dark Bright
• Fans off the disc to
periphery
Thomas R, 2006

343
RNFL Visibility
•
•
•
•

Clear media
Without yellowing of lens
Deeply pigmented RPE
Decreases with age
D
ith
– Loose 4000 - 5000 per year

Thomas R, 2006

344
RNFL : Normal ?
• “Obscures”
normal vessels
• Slit like or groove
like defects
• Narrower than
retinal vessels

Thomas R, 2006

345
Localized RNFL Defects
•
•
•
•
•

Dark wedge
Larger than vessel
Touching disc
Fan out
Broad at temporal
raphe

Thomas R, 2006

346
Localized RNFL Defects
• Not seen in normal
• 20% of Glaucoma eyes
– Less with early glaucoma
– Touch the disc

• Other causes of atrophy
– Drusen, Toxoplasmosis,
Ischemia, Papiledema,
Optic Neuritis

Thomas R, 2006

347
Localized RNFL Defects a d Disc Hemorrhage
oca ed
e ects and sc e o age

• Disc hemorrhage
• Localized defect
– 6 - 8 weeks

• Localized type of
disc damage : Notch

Thomas R, 2006

348
Diffuse RNFL Defects
• I f i less visible
Inferior l
i ibl
than Superior
• Bright Dark, Bright
Bright, Dark
pattern lost
g
• Macula as bright
as Superior and
Inferior
• “N k d” vessels
“Naked”
l

Thomas R, 2006

349
Frequency of RNFLD in Glaucoma

• More with focal NTG
• Less with
– Age related POAG
– Highly myopic OAG
–J
Juvenile OAG
il

Thomas R, 2006

350
Importance of Localized RNFL
p
Defects in Early Diagnosis
• E
Eyes with normal
ith
l
IOP and Visual
Fields
• Show field loss on
follow up
• “Pre perimetric”
Glaucoma
• J t’ R l # 2
Jost’s Rule
Until proved otherwise, all glaucoma (suspects) have a RNFL defect
Thomas R, 2006

351
Subtle Retinal Nerve Fib L
S btl R ti l N
Fiber Layer D f t
Defect

Thomas R, 2006

352
With Experience :

Thomas R, 2006

353
With More Experience :

Thomas R, 2006

354
Re check
Re-check !

Thomas R, 2006

355
Many Optic Disc Changes Have
Been Described in Glaucoma
Loss of ISNT pattern
Localized notch in the rim
Acquired Pit
Disc Hemorrhage
Wedge / diffuse loss of retinal
nerve fibers
 Absent rim inferiorly,
superiorly, temporally & or
nasally
 Increase in cupping over time










•
•
•
•
•
•

Asymmetry in CDR > 2
y
y
Cup large for disc size
Vertically oval cup
Baring of CL vessels
Over pass phenomenon
Large CDR
CDR of > 0.7
Deep cup
Laminar dot sign
g
Thinned retinal arterioles

Don t
Don’t Just Use The Cup : Disc Ratio !
Thomas R, 2006

356
Once more

357
RNFL Examination
• Ophthalmoscope (Red free light)
• R dF
Red Free Ph t
Photographs
h
• HRT, OCT, GDxVCC
Slit lamp (Green light)

358
SLP, OCT and CSLO/T
•
•
•

Pre Perimetric Glaucoma Detection
Non Perimetric Glaucoma Progression Analysis
RNFL analysis over Optic disc analysis

359
Scanning laser polarimetry
– GD VCC (Carl Zeiss Meditec AG)
GDxVCC (C l Z i M dit

360
GDxVCC

361
OCT

Normal retina OCT

Glaucomatous retina OCT
362
OCT : Symmetric optic discs with C/D ratio of 0.3
Optic Nerve Head Analysis Results
Vert. Integrated Rim Area (Vol.)
Horiz. Integrated Rim Width (Area)
Disk Area
Di k A
Cup Area
Rim Area
Cup/Disk Area Ratio
Cup/Disk Horiz. Ratio
p
Cup/Disk Vert. Ratio

.321 mm3
1.717 mm2
2.53
2 53 mm2
2
.938 mm2
1.592 mm2
0.371
0.647
0.593

Optic Nerve Head Analysis Results
Vert. Integrated Rim Area (Vol.)
Horiz. Integrated Rim Width (Area)
Disk Area
Cup Area
Rim Area
Cup/Disk Area Ratio
Cup/Disk Horiz. Ratio
Cup/Disk Vert. Ratio

.313 mm3
1.706 mm2
2.217 mm2
.764 mm2
1.453 mm2
0.345
0 345
0.622
0.586

RNFL analysis demonstrates a typical p
y
yp
pattern in the OD and flattening of the RNFL p
g
pattern in the OS.
Thinning of the superior RNFL is consistent with the visual field defect and the diagnosis of glaucoma.
This was later confirmed by visual field with infero-nasal defect, OS

363
OCT : OD appears within normal limits with a C/D ratio of 0.5. OS has
large cup with C/D ratio of 0.7. Visual fields within normal limits
Optic Nerve Head Analysis Results
Vert. Integrated Rim Area (Vol.)
Horiz. Integrated Rim Width (Area)
Disk Area
Di k A
Cup Area
Rim Area
Cup/Disk Area Ratio
Cup/Disk Horiz. Ratio
p
Cup/Disk Vert. Ratio

.327 mm3
1.578 mm2
1.998
1 998 mm2
2
.646 mm2
1.352 mm2
0.323
0.538
0.58

Optic Nerve Head Analysis Results
Vert. Integrated Rim Area (Vol.)
Horiz. Integrated Rim Width (Area)
Disk Area
Cup Area
Rim Area
Cup/Disk Area Ratio
Cup/Disk Horiz. Ratio
Cup/Disk Vert. Ratio

.188 mm3
1.597 mm2
2.973 mm2
1.766 mm2
1.207 mm2
0.594
0 594
0.775
0.791

Anatomic large nerve head with normal RNFL. Only distinguished with Stratus OCT Crossg
y
g
sectional imaging is vital in the analysis of RNFL thickness in vivo, particularly in differentiating
healthy RNFL from glaucomatous RNFL
364
Glaucoma RNFL scanning on Cirrus OCT
NEW Optic Disc cube 200 X 200 scan pattern

365
Optic Disc Cube 200 X 200 scan pattern
Auto Center™
Center of ONH automatically identified.
Measurement of TSNIT graph thickness is
automatic. Less operator dependant and crucial
for
f repeatibility
tibilit

366
Cirrus HD-OCT
Normal OU RNFL
printout
i t t
Similar to Stratus OCT RNFL
thickness reporting format
thi k
ti f
t
RNFL thickness map
RNFL thickness
deviation map (
p (LSO
fundus)
RNFL thickness values
ISNT and Average

Multi-ethnicity (Including
Asian Eye) NDB

367
Cirrus HD-OCT
RNFL thickness report

OS RNFL
loss at 6
o’clock

368
Cirrus HD-OCT
OU nerve loss
RNFL printout
p

369
RTVue
3D SD-OCT
with Ganglion
Cells Analyzer

370
Confocal scanning laser topography
– HRT3 (Heidelberg Engineering GmbH)  provides
objective measurements of the optic nerve head and
surrounding RNFL
– High quality stereo photographs of the optic disk

371
HRT

372
The Moorfields Regression Analysis

HRT measurements have been shown to have high diagnostic accuracy for
detecting glaucoma.
glaucoma
The Moorfields Regression Analysis had a sensitivity and specificity of 84% and
96% respectively.
An analysis based on the shape of the optic disc and surrounding RNFL resulted
in a sensitivity and specificity of 89% and 89%.
A sophisticated type of neural network analysis called a Support Vector Machine
373
resulted in a sensitivity and specificity of 91% and 90%
VISUAL FIELD (VF)
( )
• Isopter /isop·ter/ (i-sop´ter) a curve
/isop ter/ (i sop ter)
representing areas of equal visual acuity in
the field of vision
• A curve of equal retinal sensitivity in the
visual field
– Designated by a fraction
– The numerator being the diameter of the test
object
– The denominator being the testing distance
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374
Indication of Visual field test
•
•
•
•
•
•
•
•
•
•

Raised IOP
Suspected GON
Asymmetric C/D Ratio  > 0.3
3 mmHg IOP difference on both eyes
H
diff
b h
Glaucoma on other eye
Previous retinal detachment
Unexplained low visual acuity
Discomfort “perfect” vision
sco o t pe ect s o
Unexplained headache and migraine
Injured eye
Gumansalangi MNE, 2003

375
Visual field : Normal
• The field of vision is defined as the area that is perceived
simultaneously by a fixating eye.
• The limits of the normal field of vision are 60° into the superior
60
field, 75° into the inferior field, 110° temporally, and 60°
nasally.
• An island of vision in the sea of darkness
• The island represents the perceived field of vision, and the
sea of darkness is the surrounding areas that are not seen.
• In the light-adapted state, the island of vision has a steep
light adapted state
central peak that corresponds to the fovea, the area of
greatest retinal sensitivity.
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376
THE NORMAL VISUAL FIELD

377
THE NORMAL VISUAL FIELD
• The contour of the island of vision relates to both
the anatomy of the visual system and the level of
retinal adaptation.
• The highest concentration of cones is in the
fovea, and most of these cones project to their
own ganglion cell.
• This one-to-one ratio between foveal cone and
ganglion cell results i maximal resolution i the
li
ll
l in
i l
l i in h
fovea.
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378
KINETIC PERIMETRY
• In kinetic perimetry a stimulus is moved from a nonseeing
perimetry,
area of the visual field to a seeing area along a set meridian.
• The procedure is repeated with the use of the same stimulus
along other meridians usually spaced every 15°.
meridians,
15
• In kinetic perimetry, one attempts to find locations in the
visual field of equal retinal sensitivity.
• By j
y joining these areas of equal sensitivity, an isopter is
g
q
y,
p
defined.
• The luminance and the size of the target is changed to plot
other isopters.
• In kinetic perimetry, the island of vision is approached
horizontally.
• Isopters can be considered the outline of horizontal slices of
the island of vision.
vision
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379
STATIC PERIMETRY
• In static perimetry the size and location of the test
perimetry,
target remain constant.
• The retinal sensitivity at a specific location is
determined by varying the brightness of the test
target.
• The shape of the island is defined by repeating the
threshold measurement at various locations in the
field of vision.
MedWeb, 2008

380
STATIC PERIMETRY

381
MANUAL PERIMETRY: THE GOLDMANN VISUAL FIELD

• The Goldmann perimeter is the most widely
used instrument for manual perimetry.
• It is a calibrated bowl projection instrument with
a background intensity of apostilbs (asb), which
is
i well within th photopic range.
ll ithi the h t i
• The size and intensity of targets can be varied to
plot different isopters kineticall and determine
kinetically
local static thresholds.
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382
THE GOLDMANN VISUAL FIELD
•
•
•
•

First in 1945 by Hans Goldmann
Photopic background ( 10 cd/m² )
Moving and static circular targets
The stimuli used to plot an isopter are identified by a
Roman numeral, a number, and a letter.
p
j
• The Roman numeral represents the size of the object,
from 0.05º Goldmann size 0 (1/16 mm2) to 1.7º
Goldmann size V (64 mm2) .
• Each size increment equals a twofold increase in
diameter and a f f ld i
di
d fourfold increase i area
in
• Visual angle + 90º
MedWeb, 2008

383
GOLDMANN VISUAL FIELD

MedWeb, 2008

384
GOLDMANN VISUAL FIELD
• The number and letter represent the
intensity of the stimulus.
5 db
• A change of one number represents a 5-db
(0.5 log unit) change in intensity, and each
letter represents a 1-db (0.1 log unit)
change i i t
h
in intensity.
it
• The dynamic range of the Goldmann
perimeter from the smallest/dimmest target
(01a) to the largest/brightest target (V4e) is
greater than 4 log units, or a 10,000-fold
change.
h
MedWeb, 2008

385
GOLDMANN VISUAL FIELD
• The number and letter represent the intensity of
p
y
the stimulus. A change of one number
represents a 5-db (0.5 log unit) change in
intensity,
intensity and each letter represents a 1 db (0 1
1-db (0.1
log unit) change in intensity.
• The dynamic range of the Goldmann perimeter
from the smallest/dimmest target (01a) to the
largest/brightest target (V4e) is greater than 4
log it
l units, or a 10 000 f ld change.
10,000-fold h

MedWeb, 2008

386
GOLDMANN VISUAL FIELD
• Isopters in which the sum of the Roman numeral (size) and
number (i t
b (intensity) are equal can b considered equivalent.
it )
l
be
id d
i l t
For example, the I4e isopter is roughly equivalent to the II3e
isopter.
• A change of one number of intensity is roughly equivalent to a
change of one Roman numeral of size.
• The equivalent isopter combination with the smallest target
size usually is p
y preferred because detection of isopter edges is
p
g
more accurate with smaller targets.
• One usually starts by plotting small targets with dim intensity
(I1e) and then increasing the intensity of the target until it is
maximal before increasing the size of the target
target.
• The usual progression then is I1e (ARW1) I2e (ARW1) I3e
(ARW1) I4e (ARW1) II4e (ARW1) III4e (ARW1) IV4e (ARW1)
V4e
e
MedWeb, 2008

387
GOLDMANN VISUAL FIELD

388
AUTOMATED PERIMETRY
• The introduction of computers and automation
heralded a new era in perimetric testing.
• St ti testing can be performed in an objective
Static t ti
b
f
di
bj ti
and standardized fashion with minimal
p
perimetrist bias.
• A quantitative representation of the visual field
can be obtained more rapidly than with manual
testing.
testing
• The computer allows stimuli to be presented in
a pseudorandom, unpredictable fashion.
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389
AUTOMATED PERIMETRY
• Patients do not know where the next stimulus will
appear, so fixation is improved, thereby increasing
the reliability of the test.
• Random presentations also increase the speed
with which perimetry can be performed by
bypassing th problem of l
b
i the
bl
f local retinal adaptation,
l ti l d t ti
which requires a 2-second interval between stimuli
if adjacent locations are tested
tested.

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390
Static suprathreshold and threshold testing
• Is processes to determine sensitivity of the retina to light
stimulus
• In addition to plotting isopters kinetically, static
suprathreshold and threshold testing can be performed
manually.
ll
• Once an isopter is plotted, the stimulus used to plot the
isopter is used to statically test within the isopter to look
for localized defects.
• In this way, it acts as a suprathreshold stimulus.
• Static thresholds also can be determined along set
meridians to obtain profile plots of the visual field, but like
any multiple thresholding task, it is time consuming.
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391
Visual Fields : Advanced Concepts
•

The Threshold Strategy
– The threshold strategy defines the threshold as being that level of light intensity
that the patient responds to 50% of the time
– Th most common example i th H
The
t
l is the Humphrey Vi
h
Visual A l
l Analyzer 24 2 th h ld
24-2 threshold
strategy for glaucoma.
– In this strategy, a grid of 54 points is tested in the central 24 degrees

•

Swedish Interactive Thresholding Algorithm (SITA)
– Designed to reduce testing time while still providing an adequate test of visual
sensitivity.
– Reduced test time should increase attentiveness and result in a more reliable
test
– There are two different SITA programs :
• SITA Standard  designed to replace the Full Threshold program
(e.g. Full Threshold 30-2  a grid of 76 test points).
• SITA Fast  designed to replace Fastpac, which is a simplified Threshold program

•

The Suprathreshold or Screening Strategy
– Screening strategies use knowledge of the normal threshold values to present
only suprathreshold stimuli that are just above the normal threshold values.
– If the patient misses a significant number of these stimuli then the program is
stimuli,
considered to have detected a defect that warrants further testing
392
Visual Field Analyzer
y
• Standard Achromatic Automated Perimetry (SAP)
–
–
–
–
–
–
–
–

White-on-white perimetry
Whit
hit
i t
First established 1972 by Franz Frankhauser et al
Mesopic to Photopic background (1.27 cd/m² or 10 cd/m²)
Static test targets with 0.43º Goldmann size III for Standard test
1.7º Goldmann size V for low vision testing
Standardized-high availability-wide dynamic range
Feasible visual range usually ± 30º, theoretically up to ± 90º
SAP :
• Humphrey Visual Field Analyzer II (Carl Zeiss Meditec AG),
program 24 2 software version 3 4 and the SITA testing
24-2, f
i 3.4.7, d h
i
algorithm
• Centerfield 2 Compact Perimetry (Oculus Optikgeräte GmbH)
Survey of Ophthalmology, 2007

393
Automated perimetry : Indicator
• Fixation errors: the number of times the patient looks
away from the central target. This is a key indicator of
patient cooperation or fatigue
fatigue.
• False positives: the number of times the patient pushes
the button when, in reality, a light source is not illuminated.
• False negatives: the number of times the patient fails to
push the button when, in reality, there is a light source
illuminated. These spots can be repeat tested by the
onboard computer at exactly the same spot to best
understand the patient's ability to produce an accurate fi ld
d
d h
i ' bili
d
field
test.
• Points tested: indicates the total number of separately
illuminated testing points and therefore data points
points,
presented to the patient for testing. Reliable patients can
produce a very useful field with a limited number of test
po ts
points.
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394
Automated perimetry : Indicator
• Reliability index : the overall reliability of the patient's
testing for each eye. Poor reliability may indicate patient
fatigue,
fatigue insufficient understanding of the test or poor
test,
vision for other reasons such as cataracts. Visual field
tests can also be used to ferret out malingerers.
• Standard deviation: the difference in peripheral field
acuity when compared to a normative data base, or
simply put, a large group of similar normal patients. This
tells the doctor whether or not a particular p of the
p
part
peripheral field is normal, depressed, or absent.
• Visual field map: the final basic report indicating the
patient's visual field anywhere from the central 10
degrees all the way out to the farthest reaches of the
field at 90 degrees. Altered patterns in the field map from
reliable patient testing are often extremely useful in the
diagnosis of ocular or neurological disorders
disorders.
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395
ASSESSING RELIABILITY
False-Positive Catch Trials
• A sound cue is given before each stimulus is presented in automated
tests.
• Periodically, the sound cue is given but no test stimulus is presented.
• Af l
false-positive result occurs if th patient responds t th sound cue
iti
lt
the ti t
d to the
d
alone.
False-Negative Catch Trials
• A false-negative catch trial is recorded if a patient does not respond at a
location that had a measurable threshold earlier in the examination.
g
g
y
patient
• A high number of false-negative catch trials may indicate p
inattentiveness and an unreliable visual field.
• The false-negative response rate is higher in eyes with extensive visual
field defects than in those with normal visual fields.
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396
How to Interpret : HFA
Single Field Analysis (
g
y
(SFA) p
) print out :
• Test parameter
• Patient’s data
• Reliability indices
• dB graph
• Gray scale pattern
• Total deviation
• Localized pattern deviation
• Glaucoma Hemifield Test (GHT)
• Global indices
397
HFA Interpretation : Acceptability

• Right test data
• Correct patient’s data
398
HFA Interpretation : Reliability

• Fi ation Loss < 20 %
Fixation
• False positive < 33 %
• False negative < 33 %

399
Normality : dB Graph
• The dB test by HFA
range between “0” and
“50” dB
50
• A typical “normal”
reading is around 30
dB
• A value at or above 40
dB is very unusual

400
Normality : Gray scale
• The actual threshold value
on the dB graph converted
to a Gray scale
• The value less than or equal
to 0 dB represented b solid
d by lid
black
• The value above 40 dB are
represented by total white
• Commonly  we can not
make a diagnosis based on
g y
the gray scale
• The gray scale format quite
useful when the patients to
be explained about their
visual field status
401
Total deviation : Numerical plot
• The numeric plot is the actual decibel
deviation at each point as compared to
normative data
– Zero  Threshold
– Positive  More sensitive
– Negative  Depressed

402
Total deviation : Probability plot
• The probability plot indicates the statistical
significance and predicts the possibility of
such an normality in normal population
• Gray scale pattern
– “ < 5 % “ means l
less th 5 of 100 normal
than
f
l
people (control) have this result
– “ < 0.5 % “ means less than 5 of 1000 normal
05
people (control) have this result
403
Total deviation
• The Total deviation plot
p
highlights any overall
depression of visual field
– Generalized loss
– Localized loss (scotoma)

• The generalized field loss
is caused by
–
–
–
–
–

Cataract
Corneal opacities
Media opacities
Miosis
Refractive errors
404
Pattern deviation
• Shows sensitivity
y
losses after an
adjustment to
remove any
generalized
depression
• Primarily
highlights only
significant
localized visual
l
li d i
l
field loss
• The most
useful analysis
405
Deviation : Normality
Total Deviation

Pattern Deviation Interpretation

No symbol

No symbol

Normal

Some symbols

Same pattern

Pure localized loss

Many symbols

No symbols

Pure generalized loss

Many symbols

Fewer symbols

Mixed loss

No or fewer

Many symbols

Trigger happy
406
Glaucoma Hemifield Test (GHT)
• It compares points on the upper field to
corresponding points on lower one
• The GHT based on :
– The sensitivity of field should be similar on both
hemifield
– In Glaucoma the upper and lower hemifield are often
significantly different

• Sensitivity difference between the upper
and lower hemifield are hallmark of
glaucomatous field loss
407
GHT : Approach

408
GHT : Result
•
•
•
•
•

Outside normal limits
Borderline
General Reduction of sensitivity
Abnormally hi h sensitivity
Ab
ll high
iti it
Within normal limits

409
Global indices

• Mean Deviation (MD)
• Pattern Standard Deviation (PSD)

410
Mean Deviation (MD)
• Th average measure of how much elevation or
The
fh
h l
i
depression the patient’s visual field compared to
a normal person of the same age
• Derived from the Total deviation
• Shows how much the whole field departs from
normal
• Very sensitive to generalized loss
• A small defect will not affect MD significantly
411
Pattern Standard Deviation (PSD)
• It is a measure of th d
i
f the degree t which th
to hi h the
shape of the patient’s field differs from the
normal age-corrected reference fi ld
l
t d f
field
• An index of localized non uniformity of the
surface of the hill of vision
f
f th
f i i
• Strongly sensitive to the localized defect
• I not affect by purely generalized d f t
Is t ff t b
l
li d defect
• Very helpful in diagnosing early glaucoma
412
Global indices : Summary
MD

PSD

Interpretation

Normal

Normal

Probably Normal
y

Abnormal Normal

Generalized loss

Normal

Abnormal Small localized defect

Abnormal Abnormal Large defect with significant
Localized component
413
Normality : Definitively Abnormal

• GHT  Outside normal limits
• PSD  p < 5 %

414
Visual Field Loss : Indicator

• Mean Deviation  < - 5 dB
• Mean Deviation  p < 10%

415
Defect identification
•
•
•

Type
Pattern
Tendency

416
Defect identification : Type
•G
Generalized
li d
• Localized
• Mixed

417
Defect identification : Pattern
•
•
•
•
•
•
•

Paracentral scotoma
Nasal step
Arcuata
Temporal wedge
T
l
d
Altitudinal
Hemianopsia
Etc
418
Defect identification : Tendency
•
•
•
•

Glaucoma
Retinal disorders
Neurological problems
Artifact

419
Anderson s
Anderson’s criteria
It must be Glaucoma
• GHT  Outside normal limits
• PD  Cluster of 3 or more non-edge
points p < 5% with one of p < 1%
• PSD  p < 5 %

420
GLAUCOMATOUS VISUAL FIELD DEFECTS

• Any clinically or statistically significant
deviation from the normal shape of the
hill of vision can be considered a visual
field defect.
• In glaucoma, these defects are either
diffuse depressions of the visual field
or localized defects that conform to
p
nerve fiber bundle patterns.
MedWeb, 2008

421
Glaucomatous VF Defect
Most appearances
• Paracentral
• Arcuate
• Nasal step
• Temporal wedge
• Altitudinal defect

American Academy of Ophthalmology

422
GON and VF Defect Progression

Community Eye Heath 2012

423
PARACENTRAL DEFECTS
• Circumscribed paracentral defects are an early
sign of localized g
g
glaucomatous damage.
g
• The defects may be absolute when first
discovered, or they may have deep nuclei
,
y
y
p
surrounded by areas of less dense involvement.
• The dense nuclei often are numerous along the
course of the nerve fiber bundle
MedWeb, 2008

424
PARACENTRAL DEFECTS

MedWeb, 2008

425
ARCUATE SCOTOMAS
• More advanced loss of arcuate nerve fibers
leads to a scotoma that starts at or near the
blind spot, arches around the point of fixation,
and terminates abruptly at the nasal horizontal
meridian .
• An arcuate scotoma may be relative or
absolute.
• In the temporal portion of the field, it is narrow
because all of the nerve fiber bundles converge
onto the optic nerve.
nerve
• The scotoma spreads out on the nasal side and
may be very wide along the horizontal meridian.
MedWeb, 2008

426
ARCUATE SCOTOMAS
•

•

•

A notch at the inferior pole of
the optic disc (A) reflects
damage to retinal nerve fibres
projecting in an arcuate pattern,
(B) resulting in an arcuate field
defect.
Section through the optic disc
(C) illustrates that nerve fibres
from peripapillary areas (red
arrow) are located centrally in
the optic nerve while fibres from
peripheral areas (green arrow)
are located near the nerve
sheath.
Damage occurring midway
between sclera and cup yields a
paracentral d f t (blue arrow).
t l defect (bl
)
427
Differential Diagnosis of Arcuate Scotomas

MedWeb, 2008

428
NASAL STEP DEFECTS
• Because of the
anatomy of the
horizontal raphe, all
complete arcuate
scotomas end at the
nasal horizontal
meridian.
• A steplike defect along
the horizontal meridian
results from
asymmetric loss of
nerve fiber bundles in
the superior and
inferior hemifields.
MedWeb, 2008

429
NASAL STEP DEFECTS
• Nasal step defects may be evident in some
isopters but not in others, depending on which
nerve fiber bundles are damaged.
• The width of the nasal step also varies. Nasal
f
steps frequently occur in association with
arcuate and paracentral scotomas, but a nasal
p
,
step also may occur in isolation.
• Approximately 7% of initial visual field defects
are peripheral nasal step defects
defects.

MedWeb, 2008

430
TEMPORAL WEDGE-SHAPED DEFECTS
WEDGE SHAPED
• Damage to nerve fibers on the nasal side of the
optic disc may result in temporal wedge-shaped
defects.
• These defects are much less common than
defects in the arcuate distribution.
• Occasionally, they are seen as the sole visual
field defect.
• Temporal wedge defects do not respect the
horizontal meridian.
MedWeb, 2008

431
TEMPORAL WEDGE-SHAPED DEFECTS
WEDGE SHAPED

Community Eye Heath 2012

432
Altitudinal Scotoma
Altit di l S t
• A more extensive arcuate defect
• Involving 2 quadrants in either the superior
or inferior field

American Academy of Ophthalmology

433
Altitudinal Scotoma: Causes
•

RETINAL CAUSES
– B
Branch R ti l A t
h Retinal Artery O l i
Occlusion
– Branch Retinal Vein Occlusion
– Retinal Coloboma

•

OPTIC NERVE LESION
– Ischemic optic neuropathy (both arteritic and non-arteritic types)
– Papil edema
– Optic disc coloboma

•

LESION IN CEREBRAL CORTEX
–
–
–
–

Superior or Inferior calcarine cortex lesion
Temporal lobe lesion
Parietal lobe lesion
Tumors affecting both occipital lobe may produce bilateral superior or
inferior ltit di l field defect.
i f i altitudinal fi ld d f t
434
GLOBAL INDICES
• The mean deviation (HFA) or mean defect
(
)
(Octopus) reflects the overall depression or
elevation of the visual field.
• The deviation from the age-matched normal
value is calculated at each location in the visual
field.
• Th mean deviation i simply th average
The
d i ti is i l the
(Octopus) or the weighted average (HFA) of the
deviation values for all locations tested.
• Like the mean sensitivity, the mean deviation is
most sensitive to diffuse changes and is less
sensitive to small localized scotomas
scotomas.
MedWeb, 2008

435
GLOBAL INDICES
• Pattern standard deviation (HFA). Such
(
)
irregularities can be due to a localized visual
field defect or to patient variability.
• Th corrected l
The
d loss variance or corrected pattern
i
d
standard deviation provides a measure of the
irregularity of the contour of the hill of vision that
is not accounted for by patient variability (shortterm fluctuation).
• It is increased when localized defects are
present
MedWeb, 2008

436
INTEREYE COMPARISONS
• The difference in the mean sensitivity between a
patient s
patient's two eyes is less than 1 dB 95% of the
time and less than 1.4 dB 99% of the time.
• Intereye differences greater than these values
are suspicious if they are unexplained by non
g
glaucomatous factors, such as unilateral
,
cataract or miosis.
MedWeb, 2008

437
New opinions in VF analyzing
• Nowadays SAP armed by Visual field
progression software, E.g :
i
ft
E
PROGRESSOR GPA software package
for
f HFA (C l Z i M dit AG)
(Carl Zeiss Meditec

438
Glaucoma Progression Analysis (GPA)
• Advancing the Science of Progression Analysis with
improved GPA d i  d t
i
d
design
determine th stage of disease
i the t
f di
and the rate of progression, and assess your patient’s
risk of future vision loss  all at a glance
• N
New single-page G id d P
i l
Guided Progression A l i (GPA)
i Analysis
report delivers current exam results, trends the entire
visual field history and projects future vision loss.
• New Visual Field Index (VFI)  an improved measure of
a patient’s visual function status and is optimized for
glaucoma progression analysis.
• New software reporting offers guidance for severely
depressed visual fields
• New GPA algorithm allows GPA analysis to be run on
more patients right away by allowing a mix of Full
Threshold and SITA exams.

439
New opinions in VF analyzing
• But still SAP can only detect the visual
field defect after about 50% loss of the
ganglion cells

• How to detect earlier ?

440
Weinreb’s Structural/ Functional Relationship
in Glaucoma as the Disease Progresses
g
VF
Early
% Loss
s

As compared to
GCC, RNFL is still
most widely used
and accepted by
thought leaders and
Drs worldwide
orld ide

Moderate

Severe
Time

Adapted f
Ad t d from Professor Robert N. Weinreb
P f
R b tN W i
b
Hamilton Glaucoma Center, University
California San Diego

441
442
Latest generation :
g
Ganglion cell VF Analyzer
• Short-Wavelength Automated Perimetry (SWAP)
–
–
–
–

First 1986 by Pam Sample et al
Photopic background
Static test targets with 1.7º Goldmann size V and 440 nm Blue color
In SWAP, a 440-nm, narrow-band, 1.8° target is presented at 200ms duration on a bright 100 cd/m2 yellow background and
selectively tests the short-wavelength–sensitive cones and their
connections
– Selecti e test for Koniocell lar path a  Bl e sensitive cones
Selective
Koniocellular pathway
Blue sensiti e
– Feasible visual range + 30º
– Detecting glaucoma 5 years earlier than white on white perimetry
Survey of Ophthalmology, 2007

443
Latest generation :
Ganglion cell VF Analyzer
• F
Frequency-Doubling Technology Perimetry
D bli
T h l
P i t
(FDT)
– First 1966 by Don Kelly et al
– FDT was measured with the frequency-doubling
visual field instrument (Carl Zeiss Meditec AG) using
Welch-Allyn technology (Skaneateles Falls, NY) and
the N-30 program, software version 3.00.1
– Magnocellular  Motion detecting sensitivity
– The targets consist of a 0.25-cyc/deg sinusoidal
g
grating that undergoes a 25-Hz counterphase flicker
g
g
p
Survey of Ophthalmology, 2007

444
Latest generation :
Ganglion cell VF Analyzer
• Frequency Doubling Technology Perimetry
Frequency-Doubling
(FDT)
– The test involves a modified binary search staircase
y
threshold procedure with stimuli presented for a
maximum of 720 ms. FDT measures the contrast
needed for detection of the stimulus
– Each grating target is a square subtending
approximately 10° in diameter.
– Targets are presented in one of 18 test areas located
within the central 20° radius of the visual field
temporally and 30° nasally
Survey of Ophthalmology, 2007

445
Latest generation :
Ganglion cell VF Analyzer
• High-Pass Resolution Perimetry (
g
y (HPRP)
)
– First introduced 1987 by Lars Frisen
– In HPRP, ring-shaped vanishing optotypes which vary
in size are used to assess resolution ability in the
central 30° of the visual field
– The optotypes used in HPRP are high-spatialfrequency filtered targets where the inner and outer
portions of the rings are darker (15 cd/m2), whereas
the
th center portion of the rings i b i ht (25 cd/m2)
t
ti
f th i
is brighter
d/
– Parvocellular Color, Form, Long wavelength
sensitivity
446
Latest generation :
Ganglion cell VF Analyzer
• Hi h P
High-Pass R
Resolution Perimetry (HPRP)
l ti P i t
– The space-averaged luminance of the entire ring is equal to the
luminance of the photopic background (20 cd/m2)
– Th f
Therefore, when the edges of the ring cannot b resolved, th
h th d
f th i
t be
l d the
rings blend into the background, that is, the targets are either
resolved (seen) or they are invisible
– The target consists of rings of different sizes presented at 50
sizes,
locations within the central 26-30°
– No stimuli are presented within the central 5° of the visual field
– The subject responds when the target is large enough to resolve
– E.g : HPRP is with the Ophthimus High-Pass Resolution
Perimeter, version 2.0, software version 2.51 (HighTech Vision,
Malmö, Sweden).
447
Examples of visual field pattern deviation display for SAP, SWAP, FDT, and the small and deep
dent display for HPRP in a patient with GON. Each plot shows the location and number of stimulus
test locations as designated by either a box or a dot Dot: within normal limits The shading in the
dot.
limits.
boxes denotes the probability of abnormality relative to the internal normative database of each
device. Probabilities are shown in the corresponding key.
448
VF Defect :
Charts and Facts

449
Source of error in VF Analyzing
•
•
•
•

Miosis
Lens or media opacities
Uncorrected refractive error
Spectacles
S
l
– Decrease of sensitivity up to about 1.2 dB per Diopter
– Boundary scotoma caused by the frame

• Ptosis
• Inadequate retinal adaptation
• Fatigue
Kanski JJ, 2007

450
Another VF Analyzer
•
•
•
•
•
•
•

Matrix
PULSAR
Flicker Perimetry
Fli k P i t
Motion Detection Perimetry (MDP)
Motion Automated Perimetry (MAP)
Motion Coherence Perimetry (MCP)
Rarebit Perimetry
Survey of Ophthalmology, 2007

451
Endothelial
cell loss
Trabecular
damage /
PAS

Iris atrophy

Primary
angle
closure
Lens damage

Ischemic
Optic
Glaucomatus

Neuropathy

Optic
Neuropathy

Damage to ocular tissue in angle-closure glaucoma
angle closure
Foster PJ 2001

452
CLASSIFICATION OF GLAUCOMA
(JAPAN GLAUCOMA SOCIETY, GUIDELINES FOR GLAUCOMA)
ANTERIOR CHAMBER ANGLE
NORMAL OPEN ANGLE

GON

NO

GVFD

NO

YES

IOP
NORMAL

ELEVATED

NORMAL

YES

IOP

IOP
NORMAL

ELEVATED

NORMAL-TENSION
GLAUCOMA (SUSPECT)

NORMAL

ELEVATED

NORMAL-TENSION
GLAUCOMA

OCULAR HYPERTENSION
PRIMARY OPEN-ANGLE
GLAUCOMA (SUSPECT)

PRIMARY OPEN-ANGLE
GLAUCOMA

453
Steroid-induced glaucoma
g
• Uncertain
• Steroid  excessive deposit of acid
mucopolysaccharide or
glycosaminoglycan (GAG)
• It present in trabecular meshwork 
ti t b
l
h
k
abnormal function

Trans Am Ophthalmol Soc,1977
454
Newest term of POAG and NTG
• Developmental and degenerative ocular
problems
– Degenerative of entire ocular vascular and trabecular
meshwork*
– Regression failure of hyaloid artery in third trimester
of gestation  facilitating the high IOP to directly hits
the optic nerve head
– Previously “ fragile “ optic nerve head and RNFL
y
g
p
* Does not occur in NTG
455
Glaucoma : T t
Gl
Treatment
t
•
•
•
•
•

Causes  Trauma, New vessels etc
Medical
Laser
Surgery
Others
Others*

456
Gaucoma : Medical
Class

Dosage

IOP
decrease

Time to peak effect/ washout

1.  blockers
Timolol Maleat

bid

20-30%
20 30%

2-3
2 3 hours/1 month

Betaxolol

bid

15-20%

2-3 hours/1 month

bid, tid

20-30%

2 hours/7-14 days

2. Alpha 2 adrenergic agonist
Brimonidine

3. Carbonic Anhidrase inhibitor
Dorzolamid
D
l id

bid,
bid tid

15-20%
15 20%

2-3 hours/48 h
23h
/48 hours

Brinzolamide

bid, tid

15-20%

2-3 hours/48 hours

4. Prostaglandin analogues & Prostamides
ostag a d a a ogues
osta des
Latanoprost

qd

25-32%

10-14 hours/4-6 weeks

Travoprost

qd

25-32%

10-14 hours/4-6 weeks

p
Bimatoprost

q
qd

27-33%

10-14 hours/4-6 weeks

Unoprostone
Tafluprost

bid
qd

13-18%
18-22%

Unknown
Unknown

457
Glaucoma : Pathways to IOP reduction

458
Target IOP
g
Target IOP may be defined as a pressure, rather a
range of intraocular pressure levels within which
the progression of glaucoma and visual field
loss will be delayed or halted

• Advanced POAG  12 mmHg
• Early g
y glaucoma  17 mmHg
g
• NTG  11 mmHg
Gumansalangi MNE, 2002

459
AAO GUIDELINES: TARGET IOP
GUIDELINES
• Open angle glaucoma with IOP in the
mid to high 20s  Target IOP range 1418 mmHg
• Advanced Glaucoma  Target IOP is
< 15 mmHg
• OHT whose IOP > 30 mmHg with no
sign of optic nerve damage  Target
IOP < 20 mmHg
Survey of Ophthalmology, 2003

460
Factors to be considered
•
•
•
•
•
•
•
•

Efficacy: Maximal IOP reduction
Minimum required drug
Easy to use and compliance
Giving flat diurnal curve
Ocular tolerability
Systemic safety
Cost effective
Quality of life
Gumansalangi MNE, 2002

461
Glaucoma : Laser
• Argon laser trabeculoplasty
p
y
y
• Selective laser trabeculoplasty  Primary
Glaucoma Therapy?
• Laser gonioplasty
• Nd:YAG laser iridotomy
y
• Diode laser cycloablation
• Endoscopic cyclo laser photocoagulation
462
Glaucoma : Surgery
•
•
•
•
•
•
•
•
•
•
•

Inflow procedures
p
Vitrectomy
Lens extraction
Pupil
P il reconstruction
t ti
Iridectomy
Trabeculectomy
Tubes and Shunting
Canaloplasty
Viscocanalostomy
Deep sclerotomy
Crosslinked NaHA  surgery enhancer
enhancer*
463
Glaucoma: Surgery

464
Glaucoma Devices, Tubes and Shunting
•
•
•
•
•
•
•
•
•
•
•
•

Molteno Implant
Pressure Ridge Molteno Implant
Ahmed Valve
Baerveldt Tube Shunt
SOLX Gold Shunt
iScience Microcatheter Canaloplasty
GLAUCOLIGHT C
Canaloplasty D i (DORC)
l l t Device
ExPress Mini-Shunt (Alcon Inc)
iStent (Glaukos)
Hydrus (Ivantis)
Stegmann Canal Expander
AqueSys Collagen Tube Implant
465
Glaucoma : Cilliary body ablation
• Cyclocryo therapy
• Ultrasound
• Diode laser

466
467
Is there more to glaucoma
treatment than l
h lowering IOP ?
i
• Inhibition of activation of Astrocytes
• Inhibition of Nitric-Oxide-Syntase 2 (NOS-2)
• Reduces nocturnal overdipping
– Fludrocortisone 0.1 mg 2 times per week

•
•
•
•
•

Improvement of vascular regulation and autoregulation
Combat of oxidative stress
Inhibition of Metalloproteinase-9 (MMP-9)
Stimulation of Heat Shock Protein (HSP) production
Neuroprotection
– Memantine  N-Methyl D-Aspartate (NMDA) receptor
g
antagonist
Survey of Ophthalmology, 2007

468
Lens and cataract
L
d t
t

The Pioneer
Prof. dr. Istiantoro Sukardi, Sp.M(K)
Sukardi, Sp.M(K)

469
Lens fluid dynamics

470
Lens Opacities Classification System III
(LOCS III)

471
Opt ca o et y ased Cata act C ass cat o
Optical Biometry Based – Cataract Classification
• No Cataract (NC) 
• For Refractive Lens Extraction (RLE)
Phacoemulsification Plan
• Optical Biometry Examinable Cataract (OBEC) 
• For Low Energy Phacoemulsification Plan
• For learning Phacoemulsification and for transition to
MICS and Femtosecond Laser Cataract Surgery
• Optical Biometry Un-examinable Cataract (OBUC) 
• For High Energy and More Maneuver
Phacoemulsification Plan
Pardianto G ESCRS 2010
472
Paradigm of lens surgery
• Avoid advanced cataract complications 
prevents avoidable bli d
t
id bl blindness
• Restores visual function
• Nowadays  refractive surgery 
p
improves visual function 
Phacoemulsification or more*
Eurotimes, 2009

473
Refractive Surgery
• Optical synergy  Sharper vision
– Zero spherical aberration
– Reduced chromatic aberration
– Full visible light transmission
– Glistening free
– Limited Lens Epithelial Cells (LEC) migration

Eurotimes, 2009

474
Cataract surgery : State of the Art
• More comfort, faster and reliable
,
advanced examination
• Minimal invasion
• Minimal manipulation
• Minimal complication
• Better result
• Better outcome
• More improved visual function
475
Intraocular materials
•
•
•
•
•
•

Sterile
Inert
I t
Non toxic
Non allergenic
pH Balanced
Long lasting stable
476
Crystalline Lens vs IOLs
•
•
•
•

200 250
200-250 vs 20 mm3 volume
11 vs 12-13 mm overall diameter
4.5
4 5 vs 1 mm thi k
thickness
10 vs 5-6 mm front surface radii of
curvature
• 6 vs 5-6 mm back surface radii of
curvature
Eurotimes, 2010

477
Spherical vs Aspheric Lens
Spheric

478
Spherical vs Aspheric Lens
Aspheric

479
Spherical vs Aspheric Lens

Changchun Jixiang, 2006

480
IOL : Biometry
• A Scan biometry
– Very dense cataract
– Use different keratometry analyzer

• 3rd and 4th generation formulated biometry  Phakic IOL
and post refractive surgery biometry
– Partial Coherence Laser Interferometer or Non-contact Optical
Coherence Biometry or Laser Interferometry Technique
C h
Bi
t
L
I t f
t T h i
• IOL Master 5.0 (Carl Zeiss Meditec AG),
• Lenstar LS 900 (Haag-Streit International)
• Pentacam HR (OCULUS Optikgeräte GmbH)
(
p g
)
• IOL Station (NIDEK)

– Advanced Immersion A Scan biometry
• Aviso (Quantel Medical)
481
Aviso (Quantel Medical)

IOL Master 500 (Carl Zeiss Meditec AG)

Lenstar LS 900 (Haag Streit International)
(Haag-Streit
482
IOL Calculation Formulas
• 1st Generation
– SRK  Sanders, Retzlaf and Kraff

• 2nd Generation
– Binkhort, Hoffer, SRK II, Holladay

• 3rd Generation
– SRK/T, Hoffer-Q

• 4th Generation
– Holladay 2, Haigis, Camellin-Calossi
– Double K technique  Post LASIK
483
IOL calculation formulas
• SRK  P = A - (2.5L) - 0.9K
– L in millimeter
– K in Diopter

• Older guidance (Axial length approach)
– > 26 mm
– 24.4 – 26 mm
– 22 – 24 5 mm
24.5
» or 

– < 22 mm

SRK-T, Optimized Haigis
Holladay
Holladay 2 Haigis
2,
Average of SRK/T, Holladay,
Hoffer-Q

Hoffer-Q, Optimized Haigis
484
Reevaluated IOL Calculation :
• Less than 22 mm or more than 25 mm
axial length
• Less than 40.00 D or more than 47.00 D of
K Reading
• Difference in both eyes :
– More than 1.00 D K Reading
– More t a 0 3 mm a a length
o e than 0.3
axial e gt
– More than 1 D IOL Power in target of
emmetropia
485
The IOLs

•
•
•
•
•

360
360º barrier edge
Corrects spherical aberration to essential zero
Increases contrast sensitivity
Reduces harmful blue lights
g
p
Significant improvement of visual function

486
IOL: Spheric vs Aspheric

IOL Spherical aberration correction by Spherical IOL vs Aspheric IOL

Alcon, 2010

487
Lens and Cataract : IOLs
Aberration counter
Aberration-counter Aspheric IOLs
• Acrysof IQ Aspheric Natural IOL (Alcon, Inc)
• enVista Glistening-free Aspheric IOL (
g
p
(Bausch & Lomb
Incorporated)

• Akreos MI60 Microincision Lens with Aspheric Aberration-Free
Optics IOL (Bausch & Lomb Incorporated)

•
•
•
•

TECNIS 1-Piece Aspheric IOL (Abbott Medical Optics)
C-flex and Superflex Aspheric IOL ( y )
p
p
(Rayner)
HOYA’S Aspheric ABC Design IOL (HOYA)
Afinity Collamer Aspheric IOL (Staar)
y
488
Multifocal IOL : Refractive
• Designed with several optical zones on the
intraocular l
i t
l lens.
• These zones provide various focal points,
allowing for an improvement in distance,
intermediate, and near vision.

489
Multifocal IOL : Diffractive
• Gradual diffractive steps on the intraocular
lens implant that create a smooth
transition between focal points.
• Th IOL also b d i
The
l bends incoming li ht t th
i light to the
multiple focal points to increase vision in
various lighting sit ations
ario s
situations.

490
Apodization
• Is the gradual reduction or blending of diffractive
step heights.
• Distributes the appropriate amount of light to
pp p
g
near and distant focal points  regardless of the
lighting situation.
• The apodized diffractive optics are also
designed to improve image quality and minimize
visual di
i
l disturbances – a significant i
b
i ifi
improvement
over traditional multifocal technologies
Alcon, 2010

491
Multifocal :
Multifocal*: Accommodative
• An accommodative intraocular lens implant only
p
y
has one focal point, but it acts as if it is a
multifocal lenses.
• Th IOL was designed with a hi
The
d i
d i h hinge similar to the
i il
h
mechanics of the eye’s natural lens.
• Using the eye’s muscles the single focal point of
eye s muscles,
an accommodative intraocular lens can shift to
bring objects at varying distances into focus.
– Change in SHAPE of the lens in the eye
– Change in POSITION of the lens in the eye
492
Multifocal, Accommodating IOLs
,
g

493
Multifocal IOLs
• AcrySof ReSTOR Diffractive Apodization
Aspheric IOL
(Alcon Inc)
(Alcon,
• ReZoom TECNIS Multifocal IOL (Abbott
Medical Optics)
• TECNIS 1 Diffractive Aspheric 1-piece
Multifocal IOL (Abbott Medical Optics)
• Acriva Reviol Multifocal IOL (VSY
Biotechnology)
• AT Lisa (Carl Zeiss Meditec AG)
• MF4 (Ioltech  Carl Zeiss Meditec AG)
• M-flex (Rayner)
( y )
• Versario (CROMA)

494
Accommodating IOLs
• Crystalens AT-45 Accommodating IOL
(C&C Visions)
• KH-3500 (Lenstec)
• Bi C
BioComFold 43A (M h )
F ld
(Morcher)

495
Toric IOLs
• AcrySof Toric Natural IOL (Alcon, Inc)
• Acri.LISAToric IOL (Acri.Tec  Carl Zeiss
(
Meditec AG)
• AA4203TF (Staar)
• MicroSil (H manOptics)
(HumanOptics)
• T-flex (Rayner)
• M-flex-T  Toric Multifocal (Rayner)
M flex T

496
Photochromic IOLs
•
•
•
•
•

Colorless UV-Blocking at night
Changes to a yellow outdoor during the day
Does not compromise scotopic vision at night
Provides additional protection from blue light
E.g : MATRIX Acrylic AURIUM (Medennium)

497
MICS IOL
•
•
•
•

MI60 (Bausch and Lomb)
AT Lisa (Carl Zeiss Meditec AG)
AT S
Smart 48S (C l Z i M dit AG)
t
(Carl-Zeiss-Meditec
ThinLens UltraChoice 1.0 (Technomed
GmbH)
• Lentis L-303 (Oculentis GmbH)
(
)
• CareFlex (w2o Medizintechnik AG)
498
Hydrophilic vs Hydrophobic IOL
• Hydrophilic IOL
–
–
–
–

Less Uveitis
Less Anterior Capsule Contraction
Less Glaucoma
Less Capsular Block

• Hydrophobic IOL
– More adhesiveness to posterior capsule
– Less PCO

• New design  Anterior surface hydrophilic and
posterior surface hydrophobic  Bi Flex 1.8
(Medicontur)
(M di
t )
499
Haptic
• Three-piece
Three piece
– Less PCO  if square-edged optic IOL
– Less space  if in posterior chamber / sulcus
fixation  less glaucoma

• One piece
One-piece
– Less PCO  if design as 360-degree squareedged IOL
– Not recommended fixated in the sulcus
500
Hi-end Operating microscope
•

Excellent in
–
–
–
–
–
–
–
–

Bright illumination
Red reflex
Depth perception
Outstanding Beam splitter  Assistance, Teaching and Recording
Smooth X-Y-(Z)
Great i
G t in zoom and focus maneuver
df
UV barrier
Blue filter

•
•
•
•

Carl-Zeiss OPMI Lumera i and Lumera T
MÖLLER Hi-R 900 and Hi-R 1000
Leica M844 F40
Alcon LuxOR™ Surgical Microscopes with Q-VUE™ 3-D assistant

•

Do not forget : How to adjust your microscope
microscope.
501
Cataract surgery : Phacotechnique
• 1st Generation
– Kelman tecnique 
• Can-opener capsulotomy
• Anterior chamber

• 2nd Generation
– Can-opener capsulotomy
p
p
y
– Posterior chamber Phaco
– Sculpting

• 3rd Generation
– Continuous Curvilinear Capsulorrhexis (CCC)
– In-situ Phaco  Endo-capsular
– E.g : Divide and Conquer, Sheperd’s Phaco Fracture
Technique, Fine’s Chip and Flip Technique, Fine and
colleagues’ Crack and Flip Technique, Nagahara’s
Phaco C
Ph
Cop, Pf iff ’ Q i k Ch and K h’ St
Pfeiffer’s Quick Chop d Koch’s Stop
and Chop
502
Cataract surgery : Phacotechnique
• 4th Generation
– CCC
– Supracapsular
– E.g : Fine, Parker and Hoffman’s Choo Choo Chop
and Flip
– Revolution in
•
•
•
•
•

Micro incision  1 7 - 1 8mm
1.7 1.8mm
Cooler Phaco
Phaco-tip
IOLs
Improvement in uncorrected post-operative day one visual
acuity
503
Cataract surgery : Anesthesia
• Nowadays trend  Topical, and some  add
y
p
,
by Viscoelastic-borne intra cameral anesthesia
• But please do not forget and keep your ability to
perform
f
–
–
–
–
–

Akinesia  the absence (or poverty) of movement
Retrobulbar
Peribulbar
Sub-tenon
Sub-conjunctiva

• In special case  General anesthesia
504
Cataract surgery : Incision
•
•
•
•
•

Clear Corneal Incision recomended
Small to Micro
(
)
Micro to 1.6 - 1.8 mm incision (MICS)
But  size is not everything
Factors to be considered
–
–
–
–
–

Shape and contour of incision
Well sealed and water tight
Depend on cataract density and hardness
Depend on instruments to perform
Depend on surgeon ability
p
g
y
505
Avoid incision leak
•
•
•
•
•
•
•
•

Square incision
Proper size
2-3
2 3 steps direction
Avoid incision burns
Good t h i
G d technique phaco and IOL i
h
d
insertion
ti
Good tip and cartridge
Checking incision at end of surgery
Stromal hydration
506
Limbal relaxing incision
• With the rule  CCI and superior limbal
relaxing i i i
l i incision
• Against the rule  temporal CCI and
limbal relaxing incision

Vajpayee RB 2005
RB,
507
Cataract surgery : “Peri-phaco”
Peri phaco
• CCC  Continuous Curvilinear
Capsulorrhexis
Caps lorrhe is
• Tools:
– N dl
Needle
– Forceps
–F t
Femtosecond Laser 
dL
•
•
•
•

Alcon LenSx (Alcon LenSx Laser Inc)
LensAR Laser System (LensAR Inc)
Catalys Precision Laser System (OptiMedica)
CUSTOMLENS TECHNOLAS (Perfect Vision)
EuroTimes, 2010; EyeWorld, 2010

508
Cataract surgery : “Peri-phaco”
Peri phaco
• Hydrodissection  Injection of a small
amount of fluid into the capsule of the lens
to separate the nucleus from cortex
• H d d li
Hydrodelineation  I j ti of fl id
ti
Injection f fluid
between the layers of the nucleus of the
lens using a bl t needle  G ld Ri
l
i
blunt
dl
Golden Ring

509
Hydrodissection : Be careful
•
•
•
•

Posterior pole cataract
Traumatic cataract
Hard brown cataract
Post vitrectomy cataract

Rajan M, Mehta C, 2009
510
Phacomachine and instrumentation
•
•
•
•
•
•
•
•

Well contour micro incision
Surge free anterior chamber maintenance
Cooler phaco tips
Smoother vacuum and phaco power
Endothelial friendly
E d th li l f i dl
Reduce dropping nucleus
Less edema, less astigmatism
Better outcome
511
Phacomachines
a. Peristaltic Pump
A pump which fluid is forced along by waves of
contraction produced mechanically on flexible
tubing

512
Phacomachines
b. Venturi Pump
This pump is driven by compressed gas (nitrogen or
air) that is directed through chamber B

513
Phacomachines
c. Diaphragm Pump
A flexible diaphragm A is alternately pushed in and
pulled out by a rod connected to an electric motor
rotating as indicated

514
Comparison of p p
p
pumps
Peristaltic

Venturi

Flow based

Vacuum based

Vacuum created on occlusion of phaco tip

Vacuum created instantly via pump

Flow is constant until occlusion

Flow varies with vacuum level

Drains into a soft bag

Drains into a rigid cassette

Devgan U, 2008

515
Phaco Pump Comparison
Pump

Pro

Contra

Vacuum
e.g. Venturi

Less posterior occlusion surge
Better for vitreous removal
Material comes to tip easily

Need source of compressed gas
Need rigid cassette

Flow
Fl
e.g. Peristaltic

Better f
B tt for sculpting
l ti
No need for compressed air

Post
P t occlusion surge
l i
Need occlusion for vacuum to build

Siebel BS, 2008
516
Lens and Cataract : Phacomachines
Newest phacomachines :
• WHITESTAR SignatureTM System with FusionTM
Fluidics and ELLIPSTM Transversal Ultrasound
(Abbott Medical Optics)
• Th Stellaris MICSTM Vi i E h
The St ll i
Vision Enhancement S t
t System
with EQ FluidicsTM Technology (Bausch & Lomb
Incorporated)
• INFINITI Vision S
System with INTREPIDTM Fluidics
Management System and the OZil® IP Intelligent
Phaco Torsional Handpiece (Alcon, Inc)
• The CENTURION® Vision System (Alcon, Inc)
• Qube Smart System (CROMA)
• Faros OS3 and CataRhex3 (Oertli)
517
Micro Incision Sleeve Development

Support smaller incisions
– Reduce shaft diameter

Optimize performance
– Maximize chamber
stability
– Wound protection
– Minimize wound leakage

Alcon Inc

518
Infusion Sleeve Technology
Translucence
– Maximize visualization

Thin Walls
– Maximize Flow
– Minimize bulk

Large Holes
– Maximize Flow

Smooth Profile
– Ease of insertion
– MicroSmooth Technology

Tight Tolerances
– Consistency
– Quality

Alcon Inc

519
Older Footswitch Positions

1. Irrigation
2.
2 Irrigation
Aspiration + Vacuum

3. Irrigation
Aspiration + Vacuum
U/S Power

520
Footswitch Positions
1.
1 Irrigation can set
always ‘On’

2. Irrigation
g
Aspiration + Vacuum

3. Irrigation
Aspiration + Vacuum
U/S Power

521
Phacodynamics : Fundamentals
• Ultrasound (U/S): Repulsive forces  Power (percent)
and also  Ph
d l
Phaco ti
time (
(second)  A
d)
Average U/S,
U/S
Effective U/S and Absolute U/S
• Aspiration Flow Rate: (cc/min); is the magnetic action
Rate:
in system to ATTRACT lens material at a specific speed.
• Vacuum: (mmHg) is negative pressure in system used
to HOLD the pieces
• Bottle height: (cm)  Estimate IOP (mmHg) = Bottle
height X 0.74  now automated by compressor
gy
technology
522
Ultrasound: Phaco power
• Absolute phaco time (APT) and Effective
phaco time (EPT)
• Equivalent phaco time at 100% power
• APT = total phaco time (seconds)
• EPT = phaco time (seconds) X average
phaco power (percents)

Devgan 2004

523
Power Delivery
• Duty cycle: The ratio of working time to
total time of U/S  usually expressed as a
percent
• P l per second (PPS) A
Pulse
d (PPS): Amount of pulse
t f l
those are delivered in one second.

524
Power modulation

Devgan 2004

525
AFR and Vacuum
• Aspiration Flow Rate (Attracts)
• Vacuum (negative holding pressure)

Alcon Inc

526
ASPIRATION FLOW RATE (AFR)
• What does it do?
– Attracts material to the tip
– Determines how fast material is
drawn to the phaco tip

Alcon Inc

527
ASPIRATION FLOW RATE (AFR)
• Fluid moving through the tubing toward the
collection b i referred t as A i ti Fl
ll ti bag is f
d to
Aspiration Flow,
or Aspiration.
• Aspiration starts when the pump starts .
ASPIRATION
FLOW

-Pump rotation pushes fluid out

TO DRAIN BAG

PERISTALTIC PUMP

-More fluid moves in
-That is Aspiration Flow
-Speed of flow is Aspiration Flow Rate
-Pump speed controls AFR

Alcon Inc

528
AFR: FOLLOWABILITY
• WHAT DOES THIS TERM APPLY TO?
– The ability to attract material to the tip

• WHAT CONTROLS IT?
– Aspiration Flow Rate

Alcon Inc
529
VACUUM
–Negative Pressure or
Negative
Holding Force
–Measured in mmHg
–Holds material onto the tip
–The higher the vacuum the
greater the holding force
Alcon Inc

530
Vacuum: OCCLUDE
• Occlusion refers to an obstruction of the
phaco tip

Alcon Inc

531
Vacuum: Purchase
• The grip of the vacuum on the occluding
material.
• The higher the vacuum the greater the
vacuum,
purchase.

Alcon Inc

532
Rise Time
• WHAT IS IT?
– The measurement of how fast
vacuum builds upon occlusion
– Rise Time is directly related to AFR
– The faster the AFR the shorter the
Rise Time
Alcon Inc

533
COMPLIANCE
• WHAT IS IT?
“The ability of an object
to yield elastically
when a force is
applied”
• WHAT IMPACT DOES
IT HAVE?
The more compliance,
the slower the
responsiveness and
performance

Alcon Inc

534
NON-COMPLIANCE
Non-Compliance is “the ability
of an object to maintain
rigidity when a force is
applied”.

The more Non-compliant a
p
fluidic system is, the more
responsive it’s performance
will be (ie: “True Control”)
Alcon Inc

535
Vacuum: VENTING

Vacuum  Back to neutral

Alcon Inc

536
Vacuum: REFLUX
V
• Push fluid flow
•R l
Release material that attached on th
t i l th t tt h d
the
phacotip after complete venting
process

Alcon Inc

537
Vacuum: SURGE

FLUIDIC
IMBALANCE

• Outflow

• Exceeds

• Inflow
Alcon Inc

538
Vacuum: SURGE

539
ULTRASOUND (U/S)
(
)
• Refers to frequencies above the range of
human audibility, or above 20,000 vibrations
per second
second.
• In phacoemulsification, the term “ultrasound” is
used because the phaco needle moves back
and forth in excess of 20,000 times per second
 MICS is in 28,500 times per second
,
p
• There are no “sound waves” associated with
phacoemusification.
Alcon Inc

540
U/S: FREQUENCY
•How

FAST the phaco needle moves back and forth
Frequency
q
y

WHAT IS THE FREQUENCY RANGE?
•The frequency of ultrasonic handpieces is between
27,000 d 60,000
2 000 and 60 000 cycles per second
l
d
Alcon Inc

541
U/S: STROKE
• WHAT IS IT?

The tip travels 3.5 mils at maximum power

Stroke

How FAR the phaco tip moves back and forth
p
p
Alcon Inc

542
U/S POWER
• U/S Power is the percent of the maximum
stroke length traveled b th phaco ti
t k l
th t
l d by the h
tip.
• Phaco tip moves in and out in linear fashion.
• Some handpieces have a maximum
excursion (Stroke) of 3.2 mils , or 3.2
thousands of an inch (0 001 inch) which
(0.001 inch),
would represent 100% power.
• Lower power settings are some portion of the
maximum stroke, e.g., 60% would be 1.92
mils of travel.
Alcon Inc

543
PIEZOELECTRIC HANDPIECE
• The forward and back linear (in a straight
line) motion of a U/S handpiece is
generated by piezoelectric crystals.
• Th
These crystals, which are l
t l
hi h
located i th
t d in the
handpiece, vibrate at a known frequency
when electricit r ns thro gh them
hen electricity runs through them.

Alcon Inc

544
PIEZOELECTRIC HANDPIECE
•

Motion is generated when a tuned, highly refined crystal is deformed
by the electrical energy supplied from the console.
t l
i il to the
t h
• Th
These crystals are similar t th ones i a watch.
in
• The phaco tip is attached to the vibrating crystals.

Alcon Inc

545
CHATTER
• WHAT IS IT?
– Fragments rebounding from the tip

WHAT CAUSES IT?
• Chatter occurs when stroke overcomes Vacuum and AFR
Alcon Inc

546
•
•
•
•
•

U/S: LOAD

WHAT IS IT?
Occurs when the tip encounters nuclear material
WHAT HAPPENS?
Requires more power to maintain stroke
Load is constantly changing

No Load

Load
Alcon Inc

547
CAVITATION
WHAT IS IT?
• The formation of vacuoles in a liquid by a swiftly moving solid
body (an ultrasonic tip)
• The collapse of the vacuoles produces energy which will
erode solid surfaces

Alcon Inc

Boat Propeler Example of Cavitation

548
CAVITATION
Kelman tip

Implosion f
I l i of vacuoles produces:
l
d
Nine (9) ATA of pressure
l

5000° F destructive energy release

This takes place on a microscopic scale

Alcon Inc

549
TUNING
• The method used to match up the driving
frequency of the console with the operating
frequency of the phaco handpiece and tip.

Alcon Inc

550
U/S: Power modulation
• Continuous
– Continuous delivery of power
– Phaco is on in position three
– Usually increasing ultrasound power with
depth into foot position
– Used for partial-occlusion sculpting

Chang DF, 2004; Oetting T, 2005

551
U/S: Power modulation
• Pulse
– Allows surgeon to vary the power with linear control
with a fixed number of pulse per second (pps)
– Ranges from 1 to 20 pps
– With a 50% duty cycle and linear control of power
– Phaco pulses with duty cycle on and off
– Usually with equal on and off time or 50% duty cycle
(time on/cycle time)
– Usually the rate (or inverse of duty cycle) is fixed (Hz)
– Usually increasing ultrasound power with depth into
foot positi
Chang DF, 2004; Oetting T, 2005

552
U/S: Power modulation
• Burst
– Allows surgeon to vary the number of burst of power
per unit time
– With Constant amount of power
– Duration  varied widely  5-600 ms
– Reduce in thermal and exposure time of energy
– Bursts of power come with off time that decreases
with depth into foot position
– Usually when floored in position 3 -- ultrasound power
becomes continuous
b
i
– Ultrasound power is fixed
Chang DF, 2004; Oetting T, 2005

553
U/S: Power modulation
• Hyperpulse
– Uses short on time pulses e.g. 25% on; 75%
off
– Fixed duty cycle; fixed pulse rate
– Usually increasing ultrasound power with
depth into foot position

Oetting T, 2005

554
Advantages & Disadvantages
of Various U/S Modes
Mode

Advantages

Disadvantages

Applications

Continuous

Simple

- Repels nuclear
material
- Hot

Sculpting

Pulse

Less hot

- Can repel nuclear
material

- Choo choo chop
- Segment removal

Burst
B t

- L
Less h t
hot
- Holds material
well

Chopping
Ch
i

Hyperpulse

- Followability with
long off cycle
- Cool with long off
y
cycle

- Sculpting
- Bimanual small
incision

Siebel BS, 2008

555
U/S: Amount of Power
• Early phacomachine
– Available in pedal position 3
– Power level was set on the machine panel

• Over a decade
–S
Surgeon able to vary the power
– In LINEAR fashion
– By modulating pedal travel in position 3
Chang DF, 2004

556
Laws of Phaco Physics
 Smaller tips occlude easier
 The smaller the tip, the more precise
p,
p



ultrasonic control
The smaller the tip, the easier to
p
maneuver
The larger the tip, the better it holds

Alcon Inc

557
Laser Phacoemulsification
• 2940 nm Erbium:YAG Laser
– Erbium:YAG Phacolase (Carl Zeiss Meditec AG)

• Neodymium:YAG Laser
– Neodymium:YAG Photon Laser PhacoLysis System (Paradigm
Medical)
– Dodick Q-Switched Neodymium:YAG laser (ARC GmbH)

• Femtosecond Laser
– Vi t (TECHNOLAS P f t Vi i )
Victus
Perfect Vision)
– Alcon LenSx (Alcon Inc)  Rhexis, Incision, Nuclear
fragmentation, Limbal Relaxing Incision (LRI)
– L
LensAR
AR
– Catalys (OptiMedica)
– Femto LDV Z Models (Ziemer-S)*
Kohnen T, Koch DD, 2005; Auffarth G, 2010; EyeWorld 2010; Salz JJ, 2010

558
Femtosecond Laser Cataract Surgery
•
•
•
•

Data collection
Docking
OCT or S h i fl S
Scheimpflug Scan
Laser works:
– CCC
– Lens softening
g
– Clear corneal incision
– Limbal relaxing incision
g
559
Docking and OCT guide scan
• Diagram of the optical
and mechanical
interface between the
laser system and the
y
eye.
• The femtosecond laser
and OCT beam share
the same optical path,
p
providing an exact
g
co-registration of the
OCT image with the
laser segmentation
patterns.
560
Femtosecond Laser Cataract Surgery

561
Tips in Zonular weakness
p
• Full dilated pupil
• M i t i d b BSS d
Maintained by BSS-adrenaline (1 1 000 or 0 5
li (1:1,000 0.5
ml in 500 ml)
• Viscoadaptive ophthalmic viscosurgical devices
(OVD)
• 2 4 to 2.75 mm incision
2.4 2 75
• Large capsulorhexis ( 5mm or more)
• Cortical cleaving hydrodissection*
• Use a Capsular tension ring (CTR)
Chee SP 2009; Kim WS 2009; Pangputhipong P 2009

562
Tips in Zonular weakness
p
•
•
•
•

Groove long, wide and deep or triangular groove
Bevel ti d
B
l tip downward
d
Long horizontal chop
Utilize Triangular cracking technique  chop
both distal corner without any nuclear rotation*
• I i ti pole as l
Irrigation l
low as possible ( b t 70mm –
ibl (about 70
75 mm)  reduce any BSS misdirection
• Implant Three piece foldable IOL with PMMA
Three-piece
haptics
Chee SP 2009; Kim WS 2009; Pangputhipong P 2009

563
Small Pupil Management Devices
• Malyugin’s Ring Pupil Expander
• Behler’s Iris Retractor
• Iris Hooks

564
Viscoelastic materials
•
•
•
•
•
•
•
•

Maintains space
Spreads and protects tissues
Coats tissues and instruments
Non-toxic
Non-inflammatory
N i fl
t
Optically clear but visible
Neutral effect on IOP
Protects the endothelium
American Academy of Ophthalmology

565
Viscoelastic : Rheology
•
•
•
•
•

Viscosity
Pseudo plasticity
Elasticity
Cohesion and Dispersion
Rigidity

Kohnen T, Koch DD, 2005

566
Viscoelastic materials
• Sodium Hyaluronate (SH)
– Healon Healon GV Healon 5 (Abbott Medical
Healon,
GV,
Optics)
– Provisc (Alcon, Inc)
(
,
)
– AmVisc Plus (Bausch & Lomb Incorporated)
– VisThesia (Ioltech – Carl Zeiss Meditec AG) 
Plus 2% Lidocain HCl

• Chondroitin sulfate (CS)
– Vi
Viscoat (Al
(Alcon, I )
Inc)
– DisCoVisc (Alcon, Inc)
Kohnen T, Koch DD, 2005

567
Viscoelastic materials
• Hydroxypropyl methyl cellulose (HPMC)
– Ocuvis (CIMA Technology)
– OcuCoat (Bausch & Lomb Incorporated)

• Colagen IV
– Removed from market  world-wide fear of possible
prior contamination of human-sourced protein

• Polyacrylamide
– Formation of microgel  clogged the trabecular
meshwork  could not b eliminated  idl
h
k
ld
be li i
d rapidly
removed from the market in Europe and USA
Kohnen T, Koch DD, 2005

568
569
Cohesive vs Dispersive
• C h i  Vi
Cohesive
Viscoadaptives, Vi
d ti
Viscouscohesive viscoelastics
–
–
–
–
–
–
–

Heavy molecular weight
High concentration
Create and preserve space
Displace and stabilize tissues
Pressurize the anterior chamber
Clear view of posterior capsule
Easy to remove

– E.g : 2.3% SH  Healon 5 (Abbott Medical Optics (Abbott
Medical Optics), SH 1 6%  Amvisc (Bausch and Lomb)
Optics)
1.6%
Lomb),
1.4% SH  Healon GV (Abbott Medical Optics), SH 1.2% 
StaarVisc II (Staar Surgical), and SH 1%  ProVisc (Alcon,
)
Inc)
Kohnen T, Koch DD, 2005

570
Cohesive vs Dispersive
• Dispersive  Medium viscosity, Very low
viscosity Very-low
viscosity
– Coating tissues
– Partition spaces
– Prolonged retention
– E.g : 3.0% SH  Viscoat (Alcon, Inc), Healon D (Abbott Medical
g
(
,
),
(
Optics), HPMC 2%  Ocucoat (Bausch and Lomb)

• Dual Characters  Viscous-Dispersive
Viscous Dispersive
– Cohesive and Dispersive in one
– E.g :
• Healon D + G ( bbott Medical Opt cs)
ea o
GV (Abbott ed ca Optics)
• Duovisc (Alcon, Inc)

– The proven protection of Viscoat
– The ease to removal of ProVisc
Kohnen T, Koch DD, 2005

571
Rojanapongpun P, 2010

572
Soft shell technique
– Protects compromised
corneal endothelium and
posterior capsular bag
– Injects dispersive
viscoelastic materials
– Followed by cohesive
viscoelastic materials
injection
– P h di
Push dispersive viscoelastic
i
i
l ti
materials anteriorly 
coating the endothelium
– Or  also push dispersive
viscoelastic materials
i
l ti
t i l
posteriorly  coating the
posterior capsular bag 
safer in-the-bag IOL
implantation
573
Vasavada A, 2009

574
Steroid cataract formation
• Glucocorticoids are convalently bound to
lens proteins
• Resulting in  destabilization of the
protein structures
• All i f th modification, i : oxidation
Allowing further
difi ti
ie
id ti
• Leading to cataract
Experimental Eye Research, 1997
575
Vitreoretina

577
Retinal Layers

American Academy of Ophthalmology

578
Retinal Layers

American Academy of Ophthalmology

579
Retina : Basic
• Strongest j
g
junction
– Ora serrata
– Optic nerve head

• Retinal vessel
– Inner 2/3 by Central retinal artery
– Outer 1/3 by Choriocapillaris  also supply
• Fovea
• RPE

– Cilioretina artery
• In 50% of persons it supplies 30% parts of inner retina
• In 15% of persons it contributes to some of macular
circulation
580
Retinal vessels

581
Retina : Blood Ocular Barrier
• Blood Retinal Barrier
– Retinal Blood Vessel  analogous to Cerebral Blood
Vessels  maintain Inner Blood-Retina Barrier
–I
Inner Blood-Retina B i performed b
Bl d R ti Barrier
f
d by
• Single Layer of Non Fenestrated Endothelial Cells  TightJunction (zonulae occludens)
• Basement Membrane, pericytes (Interupted layer)
• Internal Elastic Lamina & Smooth Muscle (Near Optic Head )

– Outer Blood-Retina Barrier performed by RPE in
RPE,
which adjacent cells are similarly joined by zonulae
occludens
American Academy of Ophthalmology

582
Retina : Blood Ocular Barrier
• Blood Aqueous Barrier
–I
Inner non-pigmented cilliary epithelium
i
t d illi
ith li
– Tight-junctions between epithelial and
endothelial cells

American Academy of Ophthalmology

583
RPE : Function
•
•
•
•
•
•
•
•

Vitamin A metabolism
Maintenance of outer blood-retina barrier
g y
photoreceptor outer segment
p
g
Phagocytosis of p
Absorption of light (reduction of scatter)
Heat exchange
Formation of basal lamina
Production of mucopolysaccharide matrix
Active transport of material in and out of the
RPE
American Academy of Ophthalmology

584
Clinical Facts
• The outer Blood retinal barrier the RPE
barrier,
RPE,
and the retinal vascular endothelium utilize
the same receptor-ligand pairing to control
receptor ligand
lymphocyte traffic into the retina
• The outer Blood retinal barrier is a
common site for inflammatory attack, often
resulting in breakdown of barrier functions
and choroidal neovascularization
Penfold PL, Provis JM, 2005

585
Blue Light toxicity to RPE
• Over time  RPE accumulates Fluorescent
material  Lipofuscin
• Lipofuscin absorbs blue light  Lipofuscin
Fluorophore A2E  in presence of Oxygen 
generate A2E Epoxides
• A2E Epoxides toxic to RPE and induces
Apoptosis
poptos s
• RPE can no longer nourish photoreceptor cells
 adversely affect the vision
586
Fundus : Examination
•
•
•
•

Optic nerve head
Retinal appearance
Vascular shape
Macula

587
Fundus : Optic nerve head
•
•
•
•
•
•
•
•

Margin
Color
Disc, Cup,
Disc Cup Rim shape
Para papil
Vascular change
V
l
h
Hemorrhage
Myeline
Membrane
588
Fundus : Retina
• RNFL
• Hard exudates
– Intra retinal lipoprotein deposits

• Soft exudates  Cotton Wool Spot (
p (CWS)
)
– Fuzzy or ill-defined edges as retinal ischemia to infarction 
cotton-wool spot

• Microaneurysm  around areas of capillary non perfusion
• Hemorrhage
–
–
–
–

Pre-retinal
Retinal  Flame-shaped
Sub-retinal  Fluids level
Roth spot  hemorrhages with white center  Leukemia

• Degeneration
589
Fundus : Vascular
• AV ratio
• AV crossing
– Sallus
– Gunn
– Banking

• Axial reflect
– Copper wire
– Silver wire

• Malformation
590
Fundus : Macula
• Reflect
• Malformation :
– Edema
– Hole
– Drusen  deep or dull yellow deposit
• Located in the outer retina of posterior pole
• Histologically corresponds to abnormal thickening of the inner
aspect of Bruch’s membrane
• Basal laminar deposits  long-spacing collagen between the
plasma membrane and basement membrane of the RPE
• B
Basal li
l linear d
deposits  d
it
deposits of electron-dense granules and
it f l t
d
l
d
phospolipid vesicles in the inner parts of Bruch’s membrane

– Pigment
– Cicatrix
American Academy of Ophthalmology

591
American Academy of Ophthalmology

592
The 1.5 mm Macula

Penfold PL, Provis JM, 2005

The central human retina or macula,
with an idealized view of its bl d vessels.
ith
id li d i
f it blood
l
The optic disc (OD) is to the left. The
macula is subdivided into the central-most
foveola, which is surrounded in turn by the
,
y
0.35 mm fovea, parafovea and wider
perifovea in 5.5 mm of posterior pole. Each
is indicated by concentric circles. Blood
vessels form a ring outlining the foveal
avascular zone, which marks the inner
593
limits of the foveal pit
Drusen
•

•
•
•
•
•
•

Drusen
– Hard drusen  appear clinically as small yellow punctate
small, yellow,
deposits
– Soft drusen  paler, larger deposits
Is presence of cellular debris
Located in the outer retina of posterior pole, underneath the RPE
Histologically corresponds to abnormal thickening of the inner
aspect of Bruch’s membrane
Consist of extracellular deposit  that aggregate between RPE and
Bruch’s membrane
Basal laminar deposits  long-spacing collagen between the
plasma membrane and basement membrane of the RPE
Basal linear deposits  deposits of electron-dense granules and
phospolipid vesicles in the inner parts of Bruch’s membrane

Penfold PL, Provis JM, 2005 ; Eurotimes 2009

594
Macula : HRA OCT Spectralis (Heidelberg E i
M
l HRA-OCT S
li (H id lb
Engineering)
i )
595
Simple test for macular function
•
•
•
•

Colour test
Photostress Recovery test
Amsler grid
g
Heyne Retinoscopy

596
Distribution of photoreceptor
cells and ganglion cells on the
g g
macula

Penfold PL, Provis JM, 2005
597
The cone cells
• Sharp photoreceptor
• A human eye can see wavelengths in the range of 380 to
760nm. This range is called the visible region
• Trichromatic Theory  3 types of cones, each with a
different iodopsin (a photosensitive pigment)
• Each type of iodopsin can absorb and respond to a
range of wavelengths
• Photosensitive pigments 
– Erythrolabe  maximum absorption at 565nm (red)
– Chlorolabe  maximum absorption at 535nm (green)
– Cyanolabe  max. absorption at 440nm (blue)
598
Color test
•
•
•
•

Color naming
Yarn test
Lantern test
Plate test
– Hardy-Rand-Rittler plates  Red/Green and Bleu/Yellow
– Ischihara’s Polychromatic or Pseudoisochromatic plates 
Ischihara s
Red/Green

• Arrangement test  Hue discrimination test
• Anomaloscopes test
• Panel test  Farnsworth Panel D-15 and FarnsworthMunsell 100-Hue test
599
Deficient Color Vision
• Dichromacy (Color blindness)
– Red / Green deficiencies
• Protanopes
– Confusion  at a point at the red end (right end) of the
spectrum l
locus
– Reds also appear darker to protonopes than to normals

• Deuteranopes
– Confusion lines  an extraspectral point (off the chart to the
lower right, in these coordinates) and their brightness vision is
more like that of color-normals

– T it
Tritanopia and T it
i
d Tritanomaly  Y ll
l
Yellow / Bl
Blue
deficiencies
– The third class  Achromacy
Birch, 2001

600
Ischihara’s Pseudo-isochromatic plates
p
• Standard illumination
– Daylight
y g
– 20-60 foot candles

• 75-100 cm reading distance
75 100
• 3-5 seconds observation time per plate
• N color contact l
No l
t t lens wear
Deborah Pavan-Langston, 2008

601
Dark-adaptation test
p
• The Goldman-Weekers machine
• Used to plot the dark-adaptive curve
• In bright light 10 minutes and then all lights are
extinguished
• Interval 30 seconds  make a measurement of light
threshold in one area of visual field
• By presenting a gradually increasing light stimulus
• U til b l visible t th patient
Until barely i ibl to the ti t
• The graph of decreasing retinal threshold against time :
– Initial steep slope  cone adaptation
– Subsequent gradual slope  rod adaptation

• Depression of the dark-adaptation  affecting outer
retina and RPE, E.g : Retinitis pigmentosa
Deborah Pavan-Langston, 2008

602
Retina : How to draw the retina
• Central  Macula
• Ora Serrata
– Temporal
– Nasal  Thinner

• Color :
–
–
–
–
–

Red
R d
Blue
Red with blue margin
Brown
Black
603
RD : Basic
• RETINAL DETACHMENT (RD) :
A SEPARATION OF THE SENSORIC RETINA
FROM THE RETINAL PIGMENT EPITHELIUM

• RETINAL BREAK :
A FULL-THICKNESS DEFECT IN THE
SENSORY RETINA
604
RD : Classification
I. RHEGMATOGENOUS R.D. (RRD)
( PRIMARY R D )
R.D.
II. NON-RHEGMATOGENOUS R.D.
( SECONDARY R D )
R.D.
1. TRACTIONAL R.D.
2.
2 EXUDATIVE R D
R.D.

605
RD : Classification
•

MINIMAL
– Vitreous haze
– Vitreous pigment clumps
pg
p

•

MODERATE
–
–
–
–

•

Wrinkling of inner retinal surface
Rolled edge of retinal breaks
Retinal stiffness
Vessel tortousity

MARKED full thickness fixed retinal folds
– C1, C2, C3 (1,2,3 quadrant(s))

•

MASSIVE fixed retinal folds in four quadrant
q
– D1 wide funnel shape
– D2 narrow funnel shape
– D3 closed funnel  invisible optic disc
American Academy of Ophthalmology

606
RD : Rhegmatogenous

Kanski JJ, 2007

607
RRD : Principle of management
• First : find all breaks
• Second : create a chorioretinal irritation
surrounding each breaks
• Finally : bring the retina and choroid into contact
for sufficient time  produce chorioretinal
adhesion  permanently close the breaks

American Academy of Ophthalmology

608
RD : Management
• Break only : Laser Photocoagulation
• With Detachment
– Si l
Simple
•
•
•
•

Scleral buckle  Local and Encircling
Sub retinal fluid drainage
Pneumoretinopexy
Cryoretinopexy  Limited due to PVR formation

– Vitrectomy
609
Buckle vs Vitrectomy
• Vitrectomy
– More expensive*
– More equipments and technology
– Longer learning curve to perform
– Induce more complication
– Need specific positioning
– S l more diffi lt case
Solve
difficult

610
Buckle vs Vitrectomy
y
• Buckle
– Cheaper and faster
– Less equipments and technology
– Longer learning curve to perform
– Less complication
– Better mobilization
– Need more skill to identifying break location
and placing buckle precisely on it
– More painful
– Myopic shift

611
Vitrectomy is prefer : When?
•
•
•
•
•
•
•
•

Unclear media
Unsolved traction
Not indented breaks by buckle
Posterior breaks
Need of membrane peeling
PVR
Multiple or spreading breaks
Combined with anterior segment surgery
612
Buckle
• Make indentation to close and prevent
breaks
• Silicone
– Band
– Tire
– Sponge

• Sleeve for adjust the tightening
• Suture to sclera with non absorbable
material
613
Vitrectomy
•

Machines  1,000 up to 7,500 cuts per minute  face to Microincision Vitroretinal Surgery (MIVS)
– Examples :
• CONSTELLATION Vision System (Alcon, Inc)
• Stellaris PC Phacoemulsification and Vitrectomy System (Bausch & Lomb
Incorporated)

• Oertli OS3 and Faros Ophthalmic Micro-incision Surgery System (Oertli
Instruments)

• The Associate 6000 Ophthalmic Microsurgical System (DORC)
g
y

• eva Ophthalmic Microsurgical System (DORC)
• The VersaVIT and Core Essentials Vitrectomy Machine System and
Vitrectomy Packs (Synergetics)

•

New  Vitreoretinal Endoscopic
– Micro endoscopy for vitrectomy and endophotocoagulation
– Examples :
p
• Endo Optiks
• 23 g tapers to 27 g probe and 25 g tapers to 30 g probe IRIDEX EndoProbe
614
Vitrectomy
• Microscope enhancement system 
Retinal wide angle observation tools
– Examples :
•
•
•
•
•
•

RESIGHT Fundus Viewing System (Carl Zeiss)
MERLIN Surgical Viewing System (Volk)
Oculus SDI 4 (OCULUS Optikgeräte GmbH)
Oculus BIOM 5 (OCULUS Optikgeräte GmbH)
EIBOS 200 (Platinum Medical)
SUPER VIEW Wide Angle (Insight Instruments)
615
Vitrectomy
y
• Endo Laser
– Example :
p
• PUREPOINT Laser (Alcon, Inc)

• Instruments
– Example :
• 23 and 25+ gauge Micro-Incision Vitrectomy Surgery 
MIVS (Alcon, Inc)  ULTRAVIT® High Speed Vitrectomy
Probes with Duty Cycle Control
• 25+ and 27+ Probe TotalPLUS Paks (Alcon Inc)  7,500
cpm Ultra-High Speed Cutting
• Hi-speed 23 and 25 g g NovitreX3000 and
p
gauge
OertliKatalyst (Oertli Instruments)
• Intraocular pressure stabilizer  Autoseal PMS (Oertli
Instruments)
• 27 gauge MIVS system pack (DORCH and Synergetics)
• GRIESHABER® Instrumentation (Alcon Grieshaber AG)

616
Vitrectomy : Illumination
•
•
•
•
•
•

Halogen  Yellow Dimmer Light
Xenon  Bright White
Metal Halide  Bright Natural
Photon
Ph t  G
Green Yellow
Y ll
Light-Emmiting Diode (LED)
29/30 g Chandelier Fiber Optics
(Synergetics)
617
Gas d Liquid
G and Li id
Purpose :
p
1. MECHANIC MANIPULATION OF RETINA
2. TEMPORARY INTERNAL TAMPONADE OF RETINAL BREAK
3.
3 TO FLATTEN RETINAL DETACHMENT
4. TO MAINTAIN  CLEAR VIEW- RETINA
5. TO MAINTAIN OCULAR TONE

618
The Gas
NONEXPANSILE GASES
–
AIR (NOT PURE GAS)  20% OXYGENE +
80% NITROGENE  < 5 DAYS
–
OXYGENE ( O2 )
–
CARBON DIOXIDE (CO2 )
EXPANSILE GASES
–
SULFUR HEXAFLUORIDE (SF6)  2x
 10 – 14 DAYS
–
PERFLUOROPROPANE (C3F8)  4x
55 – 65 DAYS
619
The Liquid
q
BSS – PLUS
GLUTATHIONE  ANTI OXIDANT
SILICONE OIL
VISCOSITY  1,000 – 5,300 cSt
HEAVY LIQUIDS
- PERFLUORODECALIN (C10F18)
- SURFACE TENSION 16 – 21.6 dyne/cm
- VISCOSITY  2.6 – 8.03 cSt
HEAVY SILICONE OIL
- MIXTURE OF :
- ULTRAPURE POLYDIMETHYLSILOXAN
(CH3)3SiO-n-Si(CH3)3 AND
- PERFLUOROHEXYLOCTANE (C6F8)
620
Heavy Liquid

621
The Laser
TO MANAGE THE BREAKS
– ARGON GREEN (532 nm)
• PREFFERED

– KRIPTON RED (647 nm)
• HAZY MEDIA
• DEEP BURNS
• LESS CHANCE OF RNFL DAMAGE

– DIODE (810 nm)
• VITREORETINAL TRACTIONS
622
Precaution
• Excessive cryoretinopexy  Risk of PVR
• Heavy laser burn 
– Iatrogenic break
g
– Pain and inflammation
– Retinal ede a
et a edema

• Long time heavy fluid  Toxic to retina
• Long time silicone oil  More difficult to
manage  Risk of inferior PVR
• St id i oil fill d eye  N
Steroid in il filled
Necrotic retina
ti
ti
623
PVR : Classification
•

Grade A
– Vitreous haze
– Vitreous pigment clumps
– Pigment cluster on inferior retina

•

Grade B
–
–
–
–
–

•

Wrinkling of inner retinal surface
Rolled and irregular edge of retinal breaks
Retinal stiffness
Vessel tortousity
Decreased mobility of vitreous

Grade CP 1-12
– Posterior to equator : focal, diffuse or circumferential full thickness folds
– Sub retinal strands

•

Grade CA 1-12
–
–
–
–

Anterior to equator : focal, diffuse or circumferential full thickness folds
Sub retinal strands
Anterior di l
A t i displacement
t
Condensed vitreous with strands
American Academy of Ophthalmology

624
Diabetic Retinopathy (DR)
Basic of disease
– Hyperglicemia  EPO, IGF  PKCβ, VEGF
– Basal membrane thickening
– Pericyte death
– Mild endothel proliferative (Microaneurysm)
with plasma leakage

Ong SG, 2009

625
Diabetic Retinopathy (DR)
Basic of disease
– Lost of intramural pericytes
– Compromised blood-retinal barrier by defect in the
p
y
junction between abnormal vascular endothelial cells
– Increased vascular permeability  dot and blot
hemorrhages,
hemorrhages edema and hard exudates
– Extensive capillary closure in tripsin-digest flat
p p
preparations of the retina
– Retinal rendered ischemic by capillary closure
elaborates VEGF  stimulates neovascularization
American Academy of Ophthalmology

626
Diabetic Retinopathy (DR)
Muller cells
–
–
–
–
–
–

Uptake glutamate  toxic to neurotransmitter
Maintain the synaps  release of neurotrophic agents
y p
p
g
Control extracellular ion concentration
Regulate water transport out of retina  Aquaporin 4
Responsive to VEGF  Express VEGFR1
Responsive to Glucocorticoids  Only one* 
Express Glucocorticoid receptors

Ong SG, 2009

627
DR : Basic
Haematologic and biochemical abnormalities
– Increased platelet adhesiveness
– Increased erytrocyte aggregation
– Abnormal serum lipids
– Defective fibrinolysis
– Abnormal level of growth hormone
– Ab
Abnormal serum and whole blood viscosity
l
d h l bl d i
it

American Academy of Ophthalmology

628
DR : Highlight
1. No Diabetic Retinopathy
2. Non
2 N proliferative Di b ti R ti
lif ti Diabetic Retinopathy
th
A. Background Diabetic Retinopathy
B. Preproliferative Diabetic Retinopathy
3. Proliferative Diabetic Retinopathy
4. Diabetic maculopathy
Deborah Pavan-Langston, 2008

629
DR : Non proliferative
Non-proliferative
•
•
•
•
•

Dilated veins
Dot d blot intra ti l hemorrhages
D t and bl t i t retinal h
h
Microaneurysms
Hard exudates
Edema and CWS

Deborah Pavan-Langston, 2008

630
Progression from NPDR to PDR
• Diffuse intra retinal hemorrhages and
mycroaneurysms in 4 quadrants
y
y
q
• Venous beading in 2 quadrants
• IRMA in 1 quadrant

American Academy of Ophthalmology

631
DR : Pre-proliferative
Pre proliferative
• Intra retinal hemorrhages
• Microaneurysm
• Intra retinal microvascular abnormalities (IRMA)
 dilated vessel within the retina
• Venous beading
• Widespread capillary closure
• 10-50% develop to proliferative within a year
Deborah Pavan-Langston, 2008

632
DR : Proliferative
• New vessel on surface the retina and optic
nerve head  usually attached of
posterior hyaloid of vitreous body
• C
Cycatrical stage  vitreous hemorrhages
ti l t
it
h
h
and traction retinal detachment

Deborah Pavan-Langston, 2008

633
Diabetic maculopathy
• Result from increased vascular
permeability
bilit
• With or without hard exudates
• Less commonly  result from ischemia
due to closure of foveal capillaries
p
• May NOT be seen in early background DR
Deborah Pavan-Langston, 2008

634
DME : Type of Thickening
• Uniform speckled
– Extra cellular fluid  Vasogenic mechanism

• Cystic
– Swollen of Muller’s cells  Toxic mechanism
– Not extra cellular fluids

Ong SG, 2009

635
DME : Clinical variations
• Vasogenic
– Localized leakage from microaneurism

• Toxic - Non vasogenic
– Leakage from poorly identifiable sites
– Massive leakage

• Mechanical
– Vitromacular tractions
– Epiretinal membrane (ERM)

• T id - VEGF mediated
Toxid
di t d
– Perpheral ischemia  VEGF over expression
Ong SG, 2009

636
DR : CSME
Clinically Significant Macular Edema
• Thickening of the retina at or within 500 µm of
center of the macula
• Hard exudates at or within 500 µm of center of
the macula
• A zone of retinal thickening one disc area or
larger  any p of which is one disc diameter
g
y part
of center of the macula

American Academy of Ophthalmology

637
DR : CSME

American Academy of Ophthalmology

638
DR : CSME

American Academy of Ophthalmology

639
DR : CSME

American Academy of Ophthalmology

640
DR : High risk PDR
• Mild Neovascularization on disc (NVD) with
vitreous hemorrhages
• Moderate to severe NVD  larger than ¼ to ⅓
disc area with or without vitreous hemorrhages
• M d t N
Moderate Neovascularization at elsewhere
l i ti
t l
h
(NVE) ½ disc area or more with vitreous
hemorrhages

American Academy of Ophthalmology

641
DR : High risk PDR
• At least 3 of :
– Vitreous or pre retinal hemorrhages
– New vessels (NV)
– Location of new vessel on or near optic disc
– Moderate or severe extent of new vessels

American Academy of Ophthalmology

642
DR : Approach
•
•
•
•
•
•
•

Reduce blood sugar
Monitoring Hba1c
Laser photocoagulation
L
h t
l ti
Steroids
Anti-VEGF
Rapamycin (Sirolimus)*
(Sirolimus)
Surgery
Ong SG 2009; Blumenkranz, 2009; Eurotimes 2009

643
DR & DME: Clinical Trial Update
•
•
•
•
•
•
•

N acetylcarnosine
N-acetylcarnosine Eye Drops
Nepafenac Eye Drops
Fenofibrate Oral
F
fib t O l
Dextromethorphan Oral
Danazol Oral
Ranibizumab (Advance Clinical Trial)
Dexamethasone Implant
Retinal Physician 2013

644
DR : Laser rationale
Retina
•
•
•
•
•
•

Thinning of retina
Destruction of ischemic retina
Reduction of VEGF release
Proliferation f d th li l ll
P lif ti of endothelial cells
Increase blood flow
Improve auto regulation
Ong SG, 2009

645
DR : Laser rationale
RPE
•
•
•
•

Destruction of RPE  new growth
Increase transmission of metabolism
Increase Oxygen transmission
yg
Improve “pump”

Ong SG, 2009

646
DR : Laser rationale
Bruch s
Bruch’s membrane
• Altered permeability
• Lipid destruction

Choriocapillary
• Destruction of choriocapillary

Ong SG, 2009

647
DR : Laser
Grid Laser Photocoagulation
g
• Macular application  500 µm up to 3000 µm from
foveal center
• Excluded  area of PMB
• Grid Lens / +78 and +90 D Lens
• Start at 100mW power  increments of 10-20mW
10 20mW
• 50-100 µm spot size
• 0.100 second or less duration
• Spots spaced at least one burns apart
• Supplemental treatment considered at least 3-4 month
after initial coagulation  up to 300 µm
648
DR : Laser
Focal L
F
l Laser Ph t
Photocoagulation
l ti
• Grid Lens / +78 and +90 D Lens
• Start at 100mW power  increments of 1020mW
• 50-100 µm spot size
• 0.100 second or less duration
• Attempt to whiten or darken microaneurysms

649
Laser : PRP
Pan-Retinal Photocoagulation
/ Scatter Laser Photocoagulation
• NVD or / and NVE
• PRP L
Lens
• Start at 180mW power  increase gradually to achieve
the end point
• 500 µm spot size
• 0.100 to 0.200 second duration
• 1800 total applications
pp
• 1 – 1.5 burns width apart
• 3 sessions complete  10 days to weeks apart
• Usually inferior half of retina coagulated first
Usually,
650
DR : Laser
• Poor visual outcome after
photocoagulation associated with :
– Diffuse macular edema with center involved
– Diffuse fluorescein leakage
– Macular ischemia  extensive perifoveal
capillary non perfusion
– Hard exudates in the fovea
– Marked Cystoid Macular Edema (CME)
American Academy of Ophthalmology

651
DR : Laser
• Side effect and complication
– Paracentral scotomata
– Transient increased edema  decreased
vision
– Choroidal Neovascularization (CNV)
– Subretinal fibrosis
– Scar expansion
p
– Inadvertent foveolar burns
American Academy of Ophthalmology

652
Laser in Retina: Nowadays
•
•
•
•
•
•
•
•

Highly focused
Adjustably patterned
Burn effectively  Speed and accuracy
Surrounding area safety
OCT guided with high transparency
Navigated and tracked
Real time information and comfort for patient
Better result and less side effect
653
DR : IVTA Consideration
• Edema refractory to Laser photocoagulation
treatment
• Proximity of leakage to the fovea
• Difficult to laser or more exacerbate of
edema  High risk PDR, Cataract with DME
• Hard exudates with heavy leak close to
fovea
• Extreme exudation
Ong SG, 2009

654
DR : IVTA to Muller s cells
Muller’s
• M ll ’ cells are t
Muller’s ll
target of St id
t f Steroids
treatment
• Increase in Adenosin mediated fluid
resorption
• Reducing the cystic thickening DME

Ong SG, 2009

655
DR : Steroids
• Slow released injectable non-erodible
non erodible
intravitreal steroids
• Fluocinolone Acetonide  Medidur (Bausch &
Lomb)  18 to 36 months

• Oral treatment
– Danazol  Optina (Ampio Pharmaceuticals)

Cousins SW, 2009; Retina Today 2012
,
;
y
656
Vitreous hemorrhages
• Major cause
– Diabetic retinopathy (39-54%)
– Retinal break without detachment (12-17%)
– Posterior vitreous detachment (7.5-12%)
(
)
– Rhegmatogenous retinal detachment (7-10%)
– Retinal NV following BRVO or CRVO (3.5-10%)
(3.5 10%)

American Academy of Ophthalmology

657
DR: Vitrectomy Indications

American Academy of Ophthalmology

658
Central Serous Chorio-Retinopathy (CSCR)
•

Sensory detachment of the sensory retina, resulting from
S
d t h
t f th
ti
lti f
– Altered barrier function
– Deficient pumping function at level of the RPE and may also involving
the choriocapillaris
p

•
•

Preferentially in 30-50 years old healthy men
Sudden onset of
–
–
–
–

•

Blurred and dim vision
Micropsia
Mi
i
Metamorphopsia
Decreased color vision

FFA
– Expansile dot  most common
• Focal hyperfluorescent leak from RPE
• Appear in early phase
• Increase in size and intensity as angiogram processes

– Smokestack
• Leakage of fluorocein into sub retinal fluid pocket
• Produce a pattern of sub retinal pooling of dye

– Mushrooms Umbrella
Mushrooms,
American Academy of Ophthalmology

659
Infrared CSCR : HRA OCT Spectralis (Heidelberg Engineering)
660
Sub retinal fluid in elderly
CSCR

CNV associated
with AMD

Pin point leak relative to a large
area of sub retinal fluid on FFA

Sub retinal fluid corresponds closely
to area of leakage on FFA

Multifocal RPE abnormalities
- Small serous PED

Large drusen

Absence of blood and significant
lipid

Presence of blood and significant
lipid

American Academy of Ophthalmology

661
CSCR : Laser indication
• Persistent serous detachment 3-4 months
34
• Recurrences in eye with visual deficit from
previous episodes
• Presence of permanent visual deficit from
previous episodes in fellow eye
• Development of chronic signs 
– Cystic changes
– Widespread RPE abnormalities

• Occupational
American Academy of Ophthalmology

662
Retina : AMD
International Classification (1995)
(
)
• Age-related maculopathy (
Ageg
p y (ARM)
)
– Drusen
• Small, intermediate, large
• Hard, soft, confluent
Hard soft

– Hyper or hypopigmentation of RPE

• Age-related macular degeneration (AMD)
Age– Exudative
– N -exudative
NonNon
d ti
Koh A, 2005

663
AMD : Exudative
• Choroidal Neovascularisation (CNV)
• Pigment E ith li l D t h
Pi
t Epithelial Detachment (PED)
t
• Glial/scar tissue (disciform scar)

Koh A, 2005

664
AMD : Non-Exudative
Non Exudative
• RPE hypopigmentation >175 m diameter
(Geographic atrophy)
(G
hi t h )

Koh A, 2005

665
AMD : Signs
•
•
•
•
•
•
•

GreenishGreenish-gray or Yellow-green lesion
YellowPigmented halo around lesion
Subretinal hemorrhage
S b ti l h
h
Hard lipid exudates
Sensory retinal detachment
RPE detachment
Cystoid edema
Koh A, 2005

666
AMD : Symptoms
•
•
•
•
•
•
•

Monocular vision loss
p p
Metamorphopsia
Decreased contrast sensitivity
Scotoma
Decreased color vision
Micropsia
Nowadays level of vision early detection and
monitoring  ForeseeHome (NOTALVISION)
Koh A 2005, Retina Today 2013

667
AMD : RF, IF, AF, FA, ICGA
Red Free

Infrared

Fluorescein
Angiography

Autofluorescence

ICG Angiography

HRA Spectralis (Heidelberg Engineering)

668
AMD : HRT and OCT

HRT3 Heidelberg Engineering

Cirrus HD OCT (Carl Zeiss Meditec AG)
669
CNV : Morphology
• Vascular
• Hypervascular
• Fib
Fibrovascular
l

Cousins SW 2009
SW,
670
CNV : Diverse cell types
•
•
•
•
•
•
•

Endothelial
Smooth muscle cells
Pericytes
Myofibroblasts
RPE cells
ll
CD34 progenitor cells
Macrophages
Cousins SW 2009
SW,
671
CNV : FFA
Classic (Type 1) CNV
•
•

Bright area of fluorescence surrounded
by hypofluorescent margin in early phase
Leakage of fluorescein at boundaries of
bright area in late phase

Koh A, 2005

672
CNV : FFA
Occult (Type 2) CNV
• Fibrovascular PED
– Irregular elevation of the RPE
– Stippled fluorescence within 1 to 2 minutes
– Persistent staining or leakage in late phase frames

• Late Leakage Undetermined Source
– Leakage at level of RPE
–A
Areas of leakage d not correspond t an area of
fl k
do t
d to
f
classic CNV or fibrovascular PED in early or mid
phase frames to account for leakage
Koh A, 2005

673
Occult (Type 2) CNV

Hagerman GS 2008
H
GS,
674
CNV : ICG
• Components
p
– Subretinal fibrovascular complex
– Intrachoroidal “Feeder Artery”
– Intrachoroidal “Draining Vein”

• Patterns
– Capillary pattern
– Arteriolar pattern
p
– Mixed pattern

Cousins SW, 2009

675
Occult CNV
• More than one lesion
• Sub RPE low flow and poor defined
vascularity
• High flow arteriolarized
• Atypical polypoidal choroidal vasculopathy
• Retinal angiomatous p
g
proliferation
Cousins SW 2009
SW,
676
AMD : Major Risk Factor
• Molecular Biology :
– H Gene (Known as CFH of HFI)  Located
(
)
on Human Chromosome Iq31
– Less of Particular Non-Coding SNP Variant
(Allele A)  Found in Intron 6 of the Serping 1
Gene

Eurotime, 2009
E ti
677
AMD : Approach
• Laser photocoagulation
• Signal  Anti VEGF
OSI Eyetech (Pegabtanib)  Selective
y
g
)
VEGF165 Inhibitor
– Lucentis® Genentech (Ranibizumab)
– Avastin™ Genentech (Bevacizumab)
– Macugen®
g

– ALG-1001Allegro Ophthalmic (Anti Integrin Oligo Peptide) 
Signaling and Regulating

Cousins SW 2009; Eurotimes 2009, Retina Today 2013

678
AMD : Approach
• Signaling pathway  Steroids
– Anecortave
– Triamcinolone

• Formation  PDT
– Verteporfin dye (Visudyne)
p
y (
y )
• Liposome-encapsulated Benzoporphyrin
• Maximum absorption  light near 689 nm wavelength

– Others :
• Tin Ethyl Etiopurpurin (SnET2, Purytin)
• Lutetium (Lu-Tex)
Cousins SW 2009; Eurotimes 2009, Retina Today 2013

679
AMD : Approach
• E10030 – A ti PDGF Aptamer (Ophthotech)  Synthetic
Anti
A t
RNA molecules  bind protein similar to antibody

•
•
•
•
•

Implantable Miniaturized Telescope (MT)*
p
p ( )
The Lipshitz Macular Implant (LMI)*
The IOL-VIP System*
Gene Therapy  Small interfering (si)RNA*
Membrane Differential Filtration (MDF)  Rheopheresis
 Dry AMD*
AMD

Eurotimes, 2009, 2011

680
AMD : Approach
• I t
Integrin P tid Therapy
i Peptide Th
• ALG-1001
• Topical Therapies*:
–
–
–
–
–

ATG3 (coMentis)
OT-551 (Othera Ph
OT 551 (Oth
Pharm)
)
TG100801 (TargeGen)
Pazopanib (GlaxoSmithKline)
OC-10X (OcuCure)
Eurotimes, 2010; Retina Today 2012

681
AMD : Approach
pp
• Brachytherapy
• Source of radiation is placed close to the
surface of targeted therapeutic area
• Beta radiation targeted at abnormal or leaking
vessels
• Stereostatic Radiotherapy  Oraya Therapy
(Oraya Inc)
(O
I )
Retina Today, 2011, 2012

682
Dry AMD : Approach
y
pp
• Anti oxidants
– Vitamin C, Vitamin E, Beta-Carotene, Zinc and Copper
– Lutein and Zeaxanthin
– Omega 3 fatty acid

•
•
•
•
•

Visual cycle inhibition
Anti inflammatory agents
Complement inhibitor
Targeting amyloid
Neuroprotector
Retina Today, 2011

683
Response to Anti-VEGF
Anti VEGF
• C ill
Capillary-dominated CNV  W ll
d i t d
Well
response
• Mixed CNV  variable response depends
on  Ratio of feeder artery caliber and
length to capillary area
• Arteriolarized CNV  Poor response
p

Cousins SW, 2009

684
Remember
•
•
•
•

PDT induces hypoxia in tissue
yp
PDT induces formation of oxygen free radical
After 1 day  Strong VEGF expression
After 1 month PDT increases expression of
– CD 34 ( marker of endothelial cell)
– CD 105 ( marker of activated endothelial cell)
– KI-67 ( marker of proliferation )

Eurotimes, 2009

685
PDT : Post procedure
• Inflammatory cells observed
y
–
–
–
–
–

Monocytes
Macrophages
Platelets
Mast cells
Leukocytes

• Release angiogenic factors  VEGF, bFGF
IL 1β, IL-2,
• Release cytokines  IL-1β, IL 2, TNFα
• Release vasoactive mediators  Thromboxane,
TNFα, Histamine
Koh A, 2009

686
Remember
• Fundus fluorescein angiography remains an
g g p y
indispensable tool in diagnosis and
management of AMD
• Indocyanine green angiography is useful in
certain situations
• Optical coherence tomography is very popular
because of ease of use and interpretation,
b
f
f
di t
t ti
particularly useful for follow-up
follow• Newer tec ques suc as S O a g og ap y
e e techniques such
SLO angiography
and autofluorescence not so essential for clinical
practice
Koh A, 2005

687
Wet AMD: Clinical Trial Update
•
•
•
•
•
•
•
•
•
•

Proton Beam Irradiation
Slidenafil
Zeaxanthin Oral (Advance Clinical Trial)
Aflibercept Intravitreal injection
Squalamine Lactate Eye Drops
Ranibizumab (
(Advance C
Clinical Trial)
)
LFG316 Intravitreal injection
AGN-150998
AGN 150998 Intravitreal injection
ESBA 1008 Microvolume injection
E10030 Intravitreal administration
Retinal Physician 2013

688
Occult CNV AF and OCT : HRA OCT Spectralis (Heidelberg Engineering)
689
Polypoidal Choroidal Vasculopathy (PCV)
• Also as "idiopathic p yp
p
polypoidal choroidal vasculopathy")
p y)
• A distinct form of choroidal neovascularization (CNV)
• Disorder characterized by vessel networks and
polypoidal lesions
• Specifically, an inner choroidal vascular abnormality
with two distinct components:
– A network of branching vessels predominantly external to the
choriocapillaris, and
– Aerminal aneurysmal dilatations

Nakashizuka H, 2008; Cousins SW, 2009

690
Polypoidal Choroidal Vasculopathy (PCV)
• Sometimes clinically seen as reddish-orange
y
g
spheroidal, or polypoidal, vascular lesions.
• Location  Peripapillary, Sub foveal,
Juxtafoveal, E
J
f
l Extra f
foveal
l
• Formation  Single, Cluster (more than 2
polyps in a group) or String (more than 3 polyps
in a line )
S e
µ
• Size  in µm
• Area  Single, Multiple
Nakashizuka H, 2008; Cousins SW, 2009

691
Polypoidal Choroidal Vasculopathy (PCV)
•

•

•

(A) Color fundus
photograph showing a
white fibrin-like lesion
(arrow) adjacent to
subretinal h
b ti l hemorrhage
h
(arrowhead) and serous
retinal detachment in the
macula.
(B) Fluorescein fundus
angiography showing
granular hyperfluorescence
in the early phase (arrow).
(C) IGA showing polypoidal
lesions resembling grape
clusters
Nakashizuka H, 2008

692
Polypoidal Choroidal Vasculopathy (PCV)
•

•

•

(A) Color fundus photograph
shows orange lesions (arrow)
surrounded by a white lesion.
These findings are consistent with
PCV (i.e., a polypoidal lesion
accompanied b fib i )
i d by fibrin).
(B) Fluorescein fundus
angiography showing two small
round hyperfluorescent lesions
near the fovea (arrow) and a
hyperfluorescent lesion indicating
pigment epithelial detachment
(arrowhead).
(C) IGA showing polypoidal
lesions corresponding to
hyperfluorescent lesions on
fluorescein fundus angiography.

Nakashizuka H, 2008

693
PCV : Management
• Focal laser photocoagulation
• PDT
• Anti VEGF

Cousins SW 2009
SW,
694
Macular hole

•
•

A, Standard StratusOCT image of the normal human macula. Most of the major
intraretinal layers can be visualized in the Stratus OCT image and correlated with
intraretinal anatomy.
B, Ultrahigh-resolution optical coherence tomography (Cirrus HD OCT?) image of
normal human macula. Ultrahigh-resolution OCT has an improved ability to visualize
smaller structures such as the external limiting membrane (ELM) and ganglion cell
layer (GCL) INL = inner nuclear layer; IPL = inner plexiform layer; IS/OS =
(GCL).
photoreceptor inner and outer segment junction; NFL = nerve fiber layer; ONL = outer
nuclear layer; OPL = outer plexiform layer; RPE = retinal pigment epithelium
695

Fujimoto J, 2006
Macular hole : Lamellar

•

Lamellar hole. A, Fundus photograph depicting the direction of optical
,
p
g p
p
g
p
coherence tomography (OCT) scans. StratusOCT (B) and ultrahighresolution OCT (UHR-OCT) (C) images. D, Two-times magnification of the
UHR-OCT image in the region of the hole. ELM = external limiting
membrane; GCL = ganglion cell layer; INL = inner nuclear layer; IPL = inner
plexiform layer; IS/OS = photoreceptor inner and outer segment junction;
NFL = nerve fiber layer; ONL = outer nuclear layer; OPL = outer plexiform
layer; RPE = retinal pigment epithelium.
696
Fujimoto J, 2006
Macular hole : Stage 1

•

Stage 1 macular hole. A, Fundus photograph depicting the direction of
g
,
p
g p
p
g
optical coherence tomography (OCT) scans. Stratus OCT (B) and ultrahighresolution OCT (UHR-OCT) (C) images. D, Two-times magnification of the
UHR-OCT image in the region of the hole. ELM = external limiting
membrane; GCL = ganglion cell layer; INL = inner nuclear layer; IPL = inner
plexiform layer; IS/OS = photoreceptor inner and outer segment junction;
NFL = nerve fiber layer; ONL = outer nuclear layer; OPL = outer plexiform
layer; PR OS = photoreceptor outer segment; RPE = retinal pigment
697
epithelium. *Henle’s fibers of the OPL.
Fujimoto J, 2006
Macular hole : Stage 2
•

Fujimoto J, 2006

Eccentric stage 2 macular hole.
A, Fundus photograph depicting
the hole before surgery and the
direction of optical coherence
tomography (OCT) scans. B C
t
h
B, C,
Stratus OCT (B) and ultrahighresolution OCT (UHR-OCT) (C)
images of the hole before
surgery. D, Two-times
g
magnification of the UHR-OCT
image in the region of the hole.
E, Fundus photograph depicting
repair of the hole after surgery.
F, G, StratusOCT (F) and UHROCT (G) images of the repair of
the hole after surgery H Twosurgery. H, Two
times magnification of the UHROCT image in the region of the
hole repair. ELM = external
limiting membrane; GCL =
ganglion cell layer; INL = inner
nuclear layer; IPL = inner
plexiform layer; IS/OS =
photoreceptor inner and outer
segment junction; NFL = nerve
fiber layer; ONL = outer nuclear
layer; OPL = outer plexiform
layer; PR OS = photoreceptor
l
h t
t
outer segment; RPE = retinal
pigment epithelium.
698
Macular hole : Stage 3

•

Stage 3 macular hole. A, Fundus photograph depicting the direction of
g
,
p
g p
p
g
optical coherence tomography (OCT) scans. B, C, Stratus OCT (B) and
ultrahigh-resolution OCT (UHR-OCT) (C) images. D, Two-times
magnification of the UHR-OCT image in the region of the hole. ELM =
external limiting membrane; GCL = ganglion cell layer; INL = inner nuclear
layer; IPL = inner plexiform layer; IS/OS = photoreceptor inner and outer
segment junction; NFL = nerve fiber layer; ONL = outer nuclear layer; OPL
= outer plexiform layer; PR OS = photoreceptor outer segment; RPE =
retinal pigment epithelium.
Fujimoto J, 2006

699
Macular hole : Stage 4
•

Fujimoto J, 2006

Stage 4 macular hole. A, Redfree fundus photograph depicting
the direction of optical
g p y (OCT)
)
coherence tomography (
scans. B, C, Stratus OCT (B)
and ultrahigh-resolution OCT
(UHR-OCT) (C) images of the
hole before surgery. D, Twotimes magnification of the UHROCT image in the region of the
hole. E, Fundus photograph
depicting repair of the hole after
surgery. F, G, StratusOCT (F)
and UHR-OCT (G) images of the
repair of the hole after surgery.
H, Two-times
H Two times magnification of
the UHR-OCT image in the
region of the hole repair. ELM =
external limiting membrane; GCL
= ganglion cell layer; INL = inner
nuclear layer; IPL = inner
plexiform layer; IS/OS =
photoreceptor inner and outer
segment junction; NFL = nerve
fiber layer; ONL = outer nuclear
layer; OPL = outer plexiform
layer; PR OS = photoreceptor
outer segment; RPE = retinal
pigment epithelium.
700
Hole Form Factor ‘HFF’
HFF

Pullifiato, 1999; Ullrich S, 2002

701
Hole Form Factor ‘HFF’
HFF

• ‘HFF’ > 0,9
• ‘HFF’ < 0,5
• Higher ‘HFF’





80% success rate
25% success rate
Better visual outcome

Pullifiato, 1999; Ullrich S, 2002

702
Vitreo Macular
Vitreo-Macular Adhesion (VMA)
• Symptomatic VMA is which  the vitreous gel
adheres i an abnormally strong manner t th
dh
in
b
ll t
to the
retina
• VMA can lead to vitreomacular traction (VMT)
and subsequent loss or distortion of visual acuity
• Anomalous posterior vitreous detachment (PVD)
is linked to several retinal disorders including
macular pucker, macular hole, age-related
age related
macular generation (AMD), macular edema, and
retinal tears and detachment
Retina Today 2012; Retina Physician 2012

703
Vitreo Macular
Vitreo-Macular Adhesion (VMA)
• Approach  Pars Plana Vitrectomy (PPV)
is used to surgically induce PVD and
release the traction on the retina for
selected cases
• PPV may result in incomplete separation
separation,
and it may potentially leave a nidus for
vasoactive and vasoproliferative
substances, or it may induce development
of fibrovascular membranes
Retina Today 2012; Retina Physician 2012

704
Vitreo Macular
Vitreo-Macular Adhesion (VMA)
• Approach
pp
– Ocriplasmin 2.5mg/ml, a vitreolysis agent  JETREA
(TromboGenics)
– ALG-1001 (Allegro)
ALG 1001

• Pharmacologic vitreolysis has the following advantages
g
y
g
g
over PPV: It induces complete separation, creates a
more physiologic state of the vitreomacular interface,
prevents the development of fibrovascular membranes
membranes,
is less traumatic to the vitreous, and is potentially
prophylactic
Retina Today 2012; Retina Physician 2012

705
CME
• Intraretinal edema contained honeycomb-like
cystoid spaces
• Abnormal perfoveal retinal capillary permeability
• FFA  because of Henle’s fiber layer  Flowerpetal pattern
• Irvine-Gass syndrome
–
–
–
–

High as 60% after ICCE
Lower when posterior capsule remains intact
Occurs 6-10 weeks post operatively
Uncomplicated cases  95% spontaneous resolution
after 6 months

American Academy of Ophthalmology

706
Hypertensive retinopathy
• Grade 0
• Grade 1
• Grade 2
• Grade 3
• Grade 4

No changes
Barely detectable arterial narrowing
Obvious arterial narrowing with focal
irregularity
Grade 2 plus retinal hemorrhages and
or exudates
Grade 3 plus disc swelling
p
g

American Academy of Ophthalmology

707
CRAO
•
•
•
•

Sudden
Severe
Painless
Retina
R ti  opaque, edematous, thi k t nerve fib l
d
t
thickest
fiber layer
and ganglion cell layer in the posterior pole
• Cerry-red spot  orange reflex  intact choroidal
vasculature beneath the fovea  stands out in contrast
to surrounding opaque neural retina

• Iris neovascularization 18% in 1-12 weeks after
1 12
onset with mean time 4-5 weeks
American Academy of Ophthalmology

708
BRVO

In BRVO, the blockage
occurs in one of the smaller
branch vessels th t connect
b
h
l that
t
to the central retinal vein.

Allergan

709
BRVO : Cause of poor vision
•
•
•
•
•
•

Macular edema
Macular pigmentation
Epi ti l
E i retinal membrane (ERM)
b
Macular ischemia
Vitreous haemorrhage
Tractional retinal detachment
Yeo KT, 2009
710
CRVO
•

Non-ischemic
– Milder form
•
•
•
•
•

Mild dilatation and tortuosity of central retinal veins
y
Dot and flame hemorrhages
Macular edema  decreased visual acuity
Mild optic disc swelling
FFA  prolongation of circulation time with breakdown of permeability but minimal
areas of non perfusion

– Sometimes referred as partial, perfused or venous stasis retinopathy

•

Ischemic
–
–
–
–
–

80% CRVO progress to be
Marked venous dilatation at least 10 disc areas
Cotton wool spot
Decrease visual acuity
FFA 
• Retinal capillary non perfusion on posterior pole  non perfused, complete or
hemorrhagic
• Widespread capillary non perfusion

– Iris neovascularization 60% in 3-5 months after onset

American Academy of Ophthalmology

711
CRVO : Approach

Hypoxia Induced
yp
VEGF

Increased Hydrostatic
y
Pressure

Increased Hydrostatic
Pressure

Rheopheresis*
Grid Laser

Inflammatory Vascular
y
Leak

Increased Hydrostatic
Pressure

Cousins SW, 2009
712
CRVO

In CRVO, the blockage
occurs in the central retinal
vein, which is the main
drainage line for blood
leaving the retina

Allergan

713
Allergan

714
Macular Edema

Allergan

715
CRVO : Anti-VEGF and Steroids
Anti VEGF
• Anti-VEGF*
• Intra Vitreal Injection  Preservative-free
Triamcinolone
• Slow-released Drug Delivery System
– Fluocinolone  Retisert (Bausch & Lomb) 
(
)
30 months
– Dexamethasone 
• Posurdex (Allergan)
• Ozurdex (Allergan)
Cousins SW, 2009; EuroTimes, 2010

716
Retinal Vascular Disease : Surgery
• CRAO  Decompression
• BRVO  Arteriovenous Sheatotomy (AVST) 
Reduce compression artery-venous 
p
y
– Persistent CME
– ERM with Vitreous traction
– Significant retinal ischemia  more than 5 discdiameter of capillary non-perfusion with or without NV
–M
Macular i h i
l ischemia

• CRVO  Radial Optic Neurotomy (RON)
Yeo KT, 2009
717
ROP : Indirect ophthalmoscopy
•
•
•
•

Stage 1: Demarcation line
Stage 2: Ridge : height, width, volume
Stage 3 N
St
3: New vessels growing out of ridge
l
i
t f id
Stage 4: Partial retinal detachment
– 4 a. Extra fovea
– 4 b. Involving fovea
g

• Stage 5: Total retinal detachment with
funnel
American Academy of Ophthalmology

718
Zone and clock hours

719
Stage 1:
St
1
Demarcation
Line

Stage 2 : Ridge

Stage 3: Neo
Vascularization

720
ROP : Screening
g
Indirect ophthalmoscopy
• All infants with a birth weight of ≤ 1500 g
• All infants with a gestational age of ≤ 28 weeks
• Infants over 1500g if unstable clinical co rse
o er
nstable
course
• Timing: 4-6 weeks after birth or 31 to 33 weeks
after conception
• Treat < 72 hours after diagnosis of threshold
disease
New approach  RetCam Di it l I
N
h
Digital Imaging (Cl it )
i (Clarity)
721
ROP : Treatment
• Laser photocoagulation
• C th
Cryotherapy
• Retinal detachment surgery

American Academy of Ophthalmology

722
Intravitreal Antibiotics ( / 0 1 ml )
0.1
•
•
•
•
•
•

Gentamycin
G t
i
Vancomycin
Amikacin
Chlorampenicol
Amphotericin B
Ceftazidime
Cefta idime

0.1
0 1 mg
1.0 mg
0.4 mg
1.0 mg
5.0 µg
2.0-2.25
2 0 2 25 mg

American Academy of Ophthalmology

723
Intravitreal Steroids ( / 0.1 ml )
01
• Dexamethasone
• Triamcinolone

0.4 mg
4 mg

American Academy of Ophthalmology

724
Consideration : Anatomy
• Limbus identification
• Lens existence
– Ph ki  3 5 – 4 mm
Phakic
3.5
– Aphakic / Pseudophakic  3 mm

• Cilliary body  2.5 mm
• Widest Pars plana and Ora  Temporo
p
p
inferior  Safest area
725
Retina : VEGF Session
• VEGF is
– Survival factor
– Neuro protector
– Fenestration

• New vessels  Endothelial tubes

Eurotimes, 2009

726
Angiogenesis factors
•
•
•
•
•

VEGF
bFGF
Angiopoietin
A i
i ti
PGE2
Erythropoietin

Cousins SW 2009
SW,
727
The VEGF
• A sub-family of growth factors
sub family
• More specifically of platelet-derived growth
factor family of cystine-knot growth factors.
cystine knot
• They are important signaling proteins
involved in both of
– Vasculogenesis (the de novo formation of the
embryonic circulatory system)
– Angiogenesis (the growth of blood vessels
from pre-existing vasculature)
728
The VEGF : Production
• VEGFxxx production can be induced in cells that
p
are not receiving enough oxygen.
• When a cell is deficient in oxygen  it produces
Hypoxia Inducible Factor (HIF)  a transcription
factor.
• HIF stimulates the release of VEGFxxx 
among other functions (including modulation of
th f
ti
(i l di
d l ti
f
erythropoeisis).
• Circulating VEGFxxx t e b ds to VEGF
C cu at g
G
then binds
G
Receptors on endothelial cells  triggering a
Tyrosine Kinase Pathway  leading to
angiogenesis
729
The VEGF
Type

Function

VEGF-A

• Angiogenesis
• Migration of endothelial cells
• Mitosis of endothelial cells
• Methane mono oxygenase activity
• αvβ3 activity
• Creation of blood vessel lumen
• Creates lumen
• Creates fenestrations
• Chemo tactic for macrophages and granulocytes
• Vasodilatation (indirectly by NO release)

VEGF-B

Embryonic angiogenesis

VEGF-C

Lymph angiogenesis

VEGF-D

Needed for the development of lymphatic vasculature
surrounding lung bronchioles

PlGF

Important for Vasculo genesis, Also needed for
angiogenesis during ischemia, inflammation, wound
healing, and cancer.
730
VEGF A
•
•
•
•
•

Located on Chromosome 6
Consist of 8 exons and 7 introns
Diffusible
Tightly bound to intracellular matrix
Isoforms
–
–
–
–

A121
A165
A185
A206
Eurotimes, 2009

731
VEGF 165
• Moderate difusible
• Potent inducer of angiogenesis 
–N
Neovascularization
l i ti
– Inflammation
– Increase permeability

Eurotimes, 2009

732
AMD : Intravitreal injections
Drug

Structrure Dosage

Bevacizumab
(Avastin))

Complete
p
immunoglobulin

2.5 mg/0.1 ml
g

Ranibizumab
(Lucentis

Antibody
fragment

0.3–0.5 mg/0.1 ml

Pegaptanib
(Macugen)

Aptamer
(oligonucleotide)

0.3–1.0 mg/0.1 ml

Williamson TH, 2008
733
Potential Methods

1. Adult 
1. Phakic

: 4 mm

2. Aphakic

: 3.5 mm

3.
3 Pseudophakic

: 3.5 mm
35

2. Infant  1 – 1.5 mm
Krieglstein GK, Weinreb RN, 2005

734
Retinal Artery Occlusion: Approach
• Vasodilators: Increase blood oxygen
content
– Sublingual isosorbide mononitrate
– Systemic pentoxifyline
– Carbogen inhalation
– Hyperbaric oxygen

Retinal Physician 2013

735
Retinal Artery Occlusion: Approach
• Reduction retinal edema
– IV methylprednisolone (suspected areteritic
CRAO)

• IOP reducers
– Acetazolamide
– Mannitol
– T i l anti glaucoma
Topical ti l
– Paracentesis
Retinal Physician 2013

736
Retinal Artery Occlusion: Approach
• Dislodge the emboli
– Ocular massage
– Nd:YAG laser embolectomy

Retinal Physician 2013

737
738
Neuro-ophthalmology

739
The optic nerve
•

Intra ocular
– 1.0 mm length
– 1 5 X 1 75 mm diameter
1.5 1.75
– Supplied by retinal arterioles and branches of posterior ciliary arteries

•

Intra orbital
– 25 mm length
– 3-4 mm diameter
– Supplied by intraneural branches of central retinal artery

•

Intra canalicular
– 4-10 mm length
– various diameter
– Supplied by Ophthalmic artery

•

Intra cranial
– 10 mm length
– 4-7 mm diameter
– S
Supplied b b
li d by branches of i t
h
f internal carotic and ophthalmic artery
l
ti
d hth l i
t

American Academy of Ophthalmology

740
Optic nerve : Intra ocular
• Surface
• Prelaminar
• Laminar
– Scaffold for optic nerve axons
– Point of fixation for central retinal artery and vein
– Reinforcement of posterior segment of the g
p
g
globe

• Retrolaminar
American Academy of Ophthalmology

741
Optic disc
A. Surface
B. Pre Laminar
C. Laminar
D. Retro Laminar

742
Vascularization
Surface : branches of central retinal artery
Prelaminar and laminar : posterior cilliary artery
Retrolaminar : central retinal artery and
y
posterior cilliary artery anastomosis

743
Euro ophthalmic
Euro-ophthalmic examination
•
•
•
•
•
•
•
•

History
Visual acuity
Color vision
Pupil reactions
Ocular
O l motility
tilit
Discs
Visual fields
Advanced intracranial examination
Cullen JF, 2007

744
Neurologic and imaging : Indication
•
•
•
•
•
•
•
•

Progressive visual loss more than 4 weeks
No recovery of vision and fields after 10 weeks
Head or periocular pain for more than 4 weeks
Patient older than 50 year
Quadrantic or Hemianopic fields defect
Development of field defect in fellow eye
Atypical features
History of paranasal sinus disease
Kumar SM 2007

745
Neuro imaging
Neuro-imaging : Which?
•
•
•
•
•

Brain
Anterior visual pathway
p
y
Pituitary area
Orbit + Coronal view ?
Base of skull

Cullen JF,
C ll JF 2007
746
Visual pathway
Temporal
Retina

R

L

R

Temporal
Retina

Nasal
Retina

Optic
Nerve

L

Optic
Chiasm
Optic
Tract

LGN

Optic
Radiations

Primary
Visual Cortex

747
Visual cortex
• The term visual cortex refers to
– The primary visual cortex  Striate cortex or V1
– Extrastriate visual cortex  V2, V3, V4, and V5.

• The primary visual cortex is anatomically
equivalent to Brodmann Area 17 or BA17

748
Visual pathway and VF defects

Miller-Keane 2003

749
Intracranial hypertension and VF
defects
d f
(a) Enlarged blind spot.
(b)Nasal step.
(c) Biarcuate scotoma.
(d)Severe visual field
constriction

Kedar, Gathe and Corbett
2011

750
The pupillary light reflex pathway
p p
y g
p
y

751
Afferent pupillary pathway
• Light stimulates p
g
photoreceptors
p
• Signal conveyed to a special set of ganglion cells 
send nerve impulses through the axons in similar
topographic distribution
• Carrying signal to optic nerve
• Decussation occurs at the optic chiasm
• Afferent fibers NOT enter lateral geniculate bodies
• BUT instead exit and pass the brachium of of the
superior colliculus  its synapse on the protectal olivary
nuclei (pontine olivari and sublentiform nuclei)
• This nuclei project bilaterally to Edinger-Westphal nuclei
Kourouyan and Horton, 1997

752
Efferent pupillary pathway
• Efferent parasympathetic response
p
y p
p
– The Edinger-Westphal nuclei send fiber to join the
cranial nerve III
– Follow that course on dorsomedialsurface of the
nerve
– After coursing through the cavernous sinus, fibers
emerge to enter orbit with the inferior oblique branch
of cranial nerve III
– Fibers synapse at ciliary g g
y p
y ganglion
– Enter the eye through short posterior ciliary nerves to
distribute fiber to choroid, ciliary body and iris
Kourouyan and Horton, 1997

753
Efferent pupillary p
p p
y pathway
y
• Efferent sympathetic response
– This believed to start in the hypothalamus and project in an
uncrossed fashion with synapses in mesencephalon and pons
– These neurons project to and synapse upon intermediolateral
cell column from C8-T2 in spinal cord
– These exit the spinal cord and p
p
pass through stellate g g
g
ganglion to
synapse in the superior cervical ganglion
– Fibers go with internal carotic artery
– Enter the cavernous sinus
– G with cranial nerve VI
Go ith
i l
– Enter superior orbital fissure with cranial nerve V
– Go with the nasociliary branch of cranial nerve V
– Pass through the ciliary ganglion without synapsing
– Pass through the long ciliary nerves
– Terminate the dilator muscle
– Some fibers diverge in the superior orbital fissure to innervate
Muller’s muscle
Kourouyan and Horton, 1997

754
Swinging flashlight test

755
RAPD: Grading Scale
g
•

Grade 1+:
– A weak initial pupillary constriction f ll
k i iti l
ill
t i ti followed b greater redilation
d by
t
dil ti
– Minimally detectable

•

Grade 2+:
– An initial pupillary stall followed by greater redilation
– Pupil fails to constrict or dilate slightly when the light swings to weaker
eye

•

Grade 3+:
– An immediate pupillary dilation
– Pupils dilate or “escape” readily

•

Grade 4+:
– No reaction to light – Amaurotic pupil
– Non reactive mydriatic pupil
Kumar SM 2007; Uhwi 2011

756
RAPD
•
•
•
•
•

Dark
D k room
Bright light  torch
2 eyes
Patient fixation is at distance
2-3 seconds per eye  longer may create an
p
y
g
y
iatrogenic RAPD
• Check by your self  do not rely on others

Burton B, Golnik K, 2010
757
Cause of light-near dissociation
• Unilateral
–
–
–
–

Afferent conduction defect
Adie pupil
HZO
Aberrant degeneration of the cranial nerve III

• Bilateral
–
–
–
–
–
–
–

Neurosyphilis
Type I diabetes
T
di b t
Myotonic distrophy
Parinaud dorsal midbrain syndrome
Familial amyloidosis
Encephalitis
Chronic alchoholism
Kanski JJ, 2007

758
Anisocoria
•

Good light reaction
–
–

Physiologic
Horner s
Horner’s Syndrome
•
•
•
•

•

Sympathetic chain disruption
Miosis, Ptosis, Anhydrosis
Anisocoria worse in the dark
Dilatation Lag

Poor light reaction
–

Adie’s tonic
•
•
•
•
•
•

–
–
–

Post ganglionic parasympathetic  usually idiopathic
No ptosis, No ophthalmoplegia
Mydriatic pupil
Segmental iris contraction
Slow (tonic) redilation
Light – Near dissociation

3rd nerve palsy
Pharmacologic
Sphincter damage
•
•
•

Trauma
Surgery
Herpes Zoster

Burton B, Golnik K, 2010

759
Papilledema : Walsh & Hoyt’s
•

Early
E l manifestations
if t ti
–
–

–
–

•

Late
L t manifestations
if t ti
–
–
–

•

As the papilledema continues to worsen, the nerve fiber layer swelling eventually obscures
the normal disc margins and the disc becomes grossly elevated.
Venous congestion develops, and peripapillary hemorrhages become more obvious, along
with exudates and cotton-wool spots.
The
Th peripapillary sensory retina may d
i
ill
ti
develop concentric or, occasionally, radial f ld k
l
ti
i
ll
di l folds known
as Paton lines. Choroidal folds also may be seen.

Chronic manifestations
–
–

•

Disc hyperemia
Subtle edema of the nerve fiber layer can be identified with careful slit lamp biomicroscopy
and direct ophthalmoscopy. This most often begins in the area of the nasal disc. A key
finding occurs as the nerve fiber layer edema begins to obscure the fine peripapillary
vessels.
vessels
Small hemorrhages of the nerve fiber layer are detected most easily with the red-free (green)
light.
Spontaneous venous pulsations that are normally present in 80% of the individuals may be
obliterated when the intracranial pressure rises above 200 mm water.

If the papilledema persists for months, the disc hyperemia slowly subsides, giving way to a
gray or pale disc that loses its central cup.
With time, the disc may develop small glistening crystalline deposits (disc pseudodrusen).

Atrophic manifestations
–
–

Blurred-border and pale disc
Atrophic vessels

Giovannini J, 2005

760
761
Papilledema : Lars Frisen’s Scale
•

Stage 0
– Normal disc with blurring of nasal and temporal disc; no
obscuration of the vessel and the cup is maintained.
p

•

Stage 1
– C shaped blurring of the nasal, superior and inferior borders.
Usually the temporal margin is normal

•

Stage 2
– Elevation of the temporal margin

•

Stage 3
– Elevation of the entire disc with obscuration of the retinal
vessels at the disc margin

•

Stage 4
– Complete obliteration of the cup and obscuration of the vessels
on the surface of the disc.

•

Stage 5
– Dome shaped appearance with all vessels being obscured

Lars Frisen, 2004

762
Stage 0

Lars Frisen, 2004

763
Stage 1

Lars Frisen, 2004

764
Stage 2

Lars Frisen, 2004

765
Stage 3

Lars Frisen, 2004

766
Stage 4

Lars Frisen, 2004

767
Stage 5

Lars Frisen, 2004

768
Differentiating Papilledema from Pseudopapilledema
Papilledema

Pseudopapilledema

Physiologic cup usually present

Central cup often absent, disc diameter small

Vessels arise normally

Vessels from central apex of disc

Arterioles bifurcate

Anomalous branching, trifurcation

Hyperemia due to dilation of the disc capillaries

Absence of superficial capillary telangectasia

C shaped blurring of RNFL in peripapillary region

Disc margins irregular with pigmentary derangement

Diffuse elevation of the disc

Irregular elevation, refractile masses which glow

Peripapillary NFL radial hemorrhage

Rare 'blot' subretinal hemorrhage

Dilation of the retinal veins

No venous dilation

Exudates in chronic situations

p
No exudates or cotton-wool spots

Not usually familial

Familial

Absence of SVP

SVP usually present

Lars Frisen, 2004

769
Optic Neuropathies
p
p
•
•

•
•

Trauma ocular, orbit and skull
• Single or multiple nerve defect
Metabolic
• Early diabetic  Insufficient in vascular to nourish the optic
nerve
Toxic
• Methanol, Ethambutol, Isoniazid
Neuritis
• Primary inflame
• Secondary inflame
• Giant Cell Arteritis
• Multiple Sclerosis
• t th and paranasal sinus i fl
teeth d
l i
inflammation or nearby ti
ti
b tissue
inflammation

770
AION : Symptoms
•
•
•
•
•

Giant cell arteritis
Sudden, painless, non progessive visual loss
Initially unilateral may rapidly bilateral
unilateral,
Older than 60 years, Women greater than Men
Antecedent or simultaneous headache jaw
headache,
claudication or chewing pain, scalp or hair
co b g tenderness, proximal muscle a d jo t
combing te de ess, p o
a usc e and joint
ache, anorexia, weight loss and fever may occur
Will’s Eye Manual

771
AION : Signs
g
• Critical
– Aff
Afferent pupillary defect
ill
d f
– Devastating worse visual loss
– Pale swollen disc with flame shape hemorrhages 
Pale,
atrophy
– Erythrocytes Sedimentation Rates, C Reactive
Protein and platelets may be markedly increased

• Other
– Visual field defect  altitudinal, involving central field
– Non pulsatile temporal artery
– CRAO an cranial nerve palsy may occur
Will’s Eye Manual

772
NAION : Symptoms
• Sudden, painless, non progressive visual
loss of moderate degree
• Initially unilateral, may become bilateral
• 45 65 years, commonl younger than
45-65 ears commonly o nger
AION

Will’s Eye Manual

773
NAION : Etiology
• Idiopatic
– Arteriosclerosis
– Diabetes
– Hypertension
– Hyperhomocystinemia
– Anemia
– Sl
Sleep apnea  risk f t
i k factor
– Relative nocturnal hypotension
Will’s Eye Manual

774
NAION : Risk factors
•
•
•
•
•

Hypertension
Hyperlipidemia
H
li id i
Diabetes mellitus
Smoking
Obesity

Deborah Pavan-Langston, 2008

775
NAION : Signs
g
• Critical
– Afferent pupillary defect
– Pale, swollen disc involving only a segment of the disc with
flame shape hemorrhage
– Normal Erythrocytes Sedimentation Rates
– Non-progressive  sudden decrease of VA and VF, which
stabilized
– Progressive  sudden decrease of VA and VF, followed with
another decrease of VA and VF

• Other
– Visual field defect  altitudinal, involving central field
– Reduced color vision proportional to decrease in acuity
Will’s Eye Manual

776
AION

PION

ON

Symptoms

Sudden i
S dd visual l
l loss, often
ft
on awakening

Sudden i
S dd visual l
l loss, often
ft
on awakening

Rapid loss of vision over
R id l
f i i
several days to 1 week

VA

Can be good if central
field maintained

Can be good if central field
maintained

Good to no perception of
light

CV

Normal in unaffected field

Normal in unaffected field

Disproportionate loss of
color vision

Pupils

Relative afferent pupil
defect

Relative afferent pupil
defect

Relative afferent pupil defect

VF

Most commonly
inferonasal loss, or
altitudinal defects, but
other patterns possible

More commonly central
scotoma seen

Central visual field loss
relatively common, nerve
fiber bundle defects also
possible

Disc

-Hyperemic disc swelling
in early phase
-Pallor developing 3-6
weeks after onset
-However arteritic AION
usually causes chalky
white disc infarction from
onset

-Disc appear normal at
onset
-Pallor develops about 6
weeks after onset

-Hyperemic disc swelling in
early phase
-Pallor developing from
about 6 weeks after onset

Cullen JF, 2007

777
Acquired optic atrophy in childhood
•
•
•
•
•
•
•

Craniopharyngioma
Optic nerve / Chiasmal glioma
Retinal degenerative di
R ti l d
ti disease
Hydrocephalus
Optic neuritis
Post papil edema
Hereditary
Cullen JF, 2007

778
Optic Pit
• Often appear as small, hypopigmented, y
pp
yp p g
yellow
or whitish, oval or round excavated defects.
• Most often within the inferior temporal portion of
the optic cup
cup.
• Approximately 20 to 33 percent are found
centrally, with an average size of 500µm (onethird disc diameter).
thi d di di
t )
• Typically, optic pits occur unilaterally (85
pe ce t)
percent).
• The optic disc in these patients appears larger
than normal, and 60 percent of discs with optic
pits also have cilioretinal arteries
arteries.
779
Optic Pit

780
Optic Disc Drusen
p
• The classic appearance involves bilaterally elevated
optic discs with irregular or "scalloped" margins, a small
scalloped
or nonexistent cup, and unusual vascular branching
patterns that arise from a central vessel core.
• Often there are small, refractile hyaline deposits visible
,
y
p
on the surface of the disc and/or in the peripapillary area.
• Most often manifests on the nasal disc margin, but can
yp
be found within any part of the nerve head.
• In younger patients, the disc elevation tends to be more
pronounced and the drusen less calcific, making them
less visible ophthalmoscopically, and hence offering a
more challenging diagnostic dilemma.
• Unlike true disc edema, its very rarely presents with
juxtapapillary nerve fiber edema, exudate, or cotton-wool
spots.
t
781
Optic Drusen : Pathophysiology
• There is no histopathological correlation between drusen
of the optic nerve head and retinal drusen; the former
represent acellular l i t d concretions, often partially
t
ll l laminated
ti
ft
ti ll
calcified, possibly related to accumulation of axoplasmic
derivatives of degenerating retinal nerve fibers.
• Optic disc drusen are globules of mucoproteins and
mucopolysaccharides that progressively calcify in the
optic disc.
• They are thought to be the remnants of the axonal
transport system of degenerated retinal ganglion cells.
• Optic disc drusen have also been referred to as
congenitally elevated or anomalous discs
discs,
pseudopapilledema, pseudoneuritis, buried disc drusen,
optic nerve head drusen and disc hyaline bodies.
• They may be associated with vision loss of varying
degree
782
Optic Disc Drusen

783
VF Defects in Optic neuropathies
•

Central scotoma
–
–
–
–

•

Demyelination
y
Toxic and nutritional
Leber disease
Compression

Enlarged blind spot
– Papil edema
– Congenital anomalies
– AIBSE (Acute Idiopathic Blind Spot Enlargement)  with flashing light
(
p
p
g
)
g g
seen, normal retina, normal imaging
– AZOOR (Acute Zonal Occult Outer Retinopathy)  with flashing light
and other field loss, normal retina, normal imaging

•

Respecting horizontal meridian
p
g
– Anterior Ischemic Optic Neuropathy
– Glaucoma
– Disc drusen
Kanski JJ, 2007; Burton B, 2010

784
Unexplained visual loss
• Miss the real diagnosis
• Munchausens
– Factitious disorder, or mental illness  repeatedly acts as has a
physical or mental disorder when
– People with factitious disorders act this way because of an inner
need t be seen as ill or i j d not t achieve a concrete
d to b
injured, t to hi
t
benefit

• Hypochondriac
– Health phobia or health anxiety
– Excessive preoccupation or worry about having a serious illness

• Hysteria (Conversion disorder)
– Exacerbation of symptoms during psychological stress
– Relief from tension (primary gain)
– Gain of outside support or attention (secondary gains)

• Malingering
Burton B, Golnik K, 2010

785
Nystagmus
• Clinician’s notes
– Amplitude
– Frequency
– Direction of gaze that induces nystagmus

– Null point  Gaze location where nystagmus at least evident
p
y g
• Concerns
– Congenital or acquired
– Specific lesion location
– True nystagmus or nystagmoid movements (saccadic oscillations)

• Characteristics
– I it conjugate  symmetrically affecting both eyes
Is
j
t
t i ll ff ti b th
– Slow or fast, equal speed or different speed
– Movement  horizontal, vertical, torsional or mixed
American Academy of Ophthalmology

786
Nystagmus : Type
•
•
•
•
•
•

Latent nystagmus
Pendular nystagmus
Congenital motor nystagmus
Spasmus nutan
Acquired pendular nystagmus
Acquired jerk nystagmus
– Gaze paretic nystagmus
– Vestibular nystagmus
Deborah Pavan-Langston, 2008

787
Nystagmus : Other nystagmus form
•
•
•
•
•
•
•
•

Endgaze (physiologic) nystagmus
Upbeat nystagmus
Downbeat motor nystagmus
Rotary nystagmus
Dissociated nystagmus
ssoc a ed ys ag us
Seesaw nystagmus
Optokinetic nystagmus
Other nystagmoid-like oscillations
– Ocular myoclonus
– Ocular bobbling
– Ocular flutter  One plane of ‘Back to Back Saccades’ without inter
saccadic interval
– Opsoclonus  Multi directional of ‘Back to Back Saccades’ without inter
saccadic interval

Deborah Pavan-Langston, 2008

788
Nystagmus : Medical treatment
y g
•

Cyclopentolate 1%
– One drop bid  Latent nystagmus  60 % reduce the amplitude,
p
y g
p
velocity and frequency
– With occlusion  improve visual acuity

•

Baclofen
– 5 mg po tid starting dose  acquired periodic alternating nystagmus
– Dosage increased every 3 days  80 mg maximum per day

•

Botulinum A
– Dampened acquired nystagmus and oscillopsia
– 66%  improve visual acuity

•

Other drugs
–
–
–
–

Gabapentin/Memantine  dampen nystagmus/oscillopsia
Clonazepam  downbeat nystagmus
Carbamazepin  SO myokymia
Propanolol  Opsoclonus

Deborah Pavan-Langston, 2008

789
Nystagmus : Optical treatment
•

Glasses or contact lenses
– Decrease nystagmus in bilateral aphakia

•

Stimulating accommodative convergences
– Overcorrecting with minus lenses  dampening nystagmus at distance
fixation
– Improve visual acuity
p
y

•

Galilean arrangement
– Stabilizing retinal images

•

Base-out prisms
– Promote covergence and dampen nystagmus in Congenital motor
nystagmus

•

Fresnel stick-on prisms
– Displace image at null p
p
g
point in Congenital motor nystagmus
g
y g
– Vertically correct head position in Vertical nystagmus and Acquired
downbeat nystagmus
– Combination prisms  help in Oblique head turns

Deborah Pavan-Langston, 2008

790
Nystagmus : Surgical treatment
• Kestenbaum Anderson procedures
– Recession of horizontal muscles
– The versions are blocked

• F d operation
Fade
ti
– Acts like recession  by creation of a more
posterior attachment
t i
tt h
t
– Reducing the area of contact
Kumar SM 2007

791
Optic Ataxia
•
•
•
•
•
•

Is lack of coordination between visual inputs and hand movements,
resulting in inability to reach and grab objects
objects.
Optic ataxia may be caused by lesions to the posterior parietal
cortex.
p
parietal cortex is responsible for combining and
p
g
The posterior p
expressing positional information and relating it to movement.
Outputs of the posterior parietal cortex include the spinal cord, brain
stem motor pathways, pre-motor and pre-frontal cortex, basal
ganglia and the cerebellum
cerebellum.
Some neurons in the posterior parietal cortex are modulated by
intention.
Optic ataxia is usually part of Balint's syndrome, but can be seen in
isolation ith injuries to the
i l ti with i j i t th superior parietal l b l as it represents
i
i t l lobule,
t
a disconnection between visual-association cortex and the frontal
premotor and motor cortex.

792
Visual Agnosia
• Is an inability of the brain to make sense of or make use
y
of some part of otherwise normal visual stimulus
• Typified by the inability to recognize familiar objects,
people or faces.
• This is distinct from blindness, which is a lack of sensory
input to the brain due to damage to the eye, optic nerve,
or primary visual systems in the brain such as the optic
radiations or primary visual cortex.
• Visual agnosia is often due to damage, such as stroke,
in the
i th posterior occipital and/or t
t i
i it l d/ temporal l b ( ) i th
l lobe(s) in the
brain.

793
Horner Syndrome

794
Uvea and Immunology

In
I remembrance:
b
dr. Muhammad Anie, Sp.M

799
Choroid : Layers

• Th choriocapillaris
The h i
ill i
• Small vessels
• Large vessels

800
Uveitis
• How to avoid complication
– Fi t  C l l i agents
First
Cycloplegic
t

• Complication
– Acute  Cell
– Chronic  Synechiae

801
U ets
Uveitis
Non-granulomatous
Onset
O

Granulomatous

Acute
A

Chronic Hidden
Ch i – Hidd

Pain

Marked

+/-

Photophobia

Marked

Mild

Moderate

Obvious

Marked

Mild

Keratic precipitate

White - smooth

Big – grey / Mutton fat

Pupil

Small - irregular

Small – irregular (vary)

Posterior synechiae

+/-

+/-

Iris nodule

+/-

+/-

Anterior uvea

Anterior and posterior uvea

Often

+/-

Blur vision
Circumcorneal injection

Predilection
Recurrent

Vaughan DG, 2000

802
Flare and Cell
• Flare  Resulting of extra protein in the
aqueous
• Cell  White Blood Cell in the aqueous
– Hallmark of Iritis
– Ob
Observed under Hi h M
d d High-Magnification Slit L
ifi ti
Lamp
examination by 1 X 3 mm field of light
– If its clustering on corneal endothelium 
it l t i
l d th li
Keratic Presipitate
803
Grading anterior chamber cells
g
Grade

Cells in field

0

0

0.5+
0 5+ (Trace)

1-5
15

1+

6-15

2+

16-25

3+

26-30
26 30

4+

> 50
Kanski JJ, 2007

804
Grading anterior chamber flare
g
Grade

Description

0

Nil
(Completely Absent)

1+

Faint
(Barely Present)

2+
2

Moderate
(Iris and lens detail clear)

3+

Marked
(Iris and lens detail hazy)

4+

Intense
(Fibrinous exudates)
Kanski JJ, 2007

805
Type of Allergy

806
Type of Allergy

807
HLA Immunogenic test
g
• Specific ocular inflammatory :
–
–
–
–
–
–
–
–
–

Acute anterior uveitis : HLA-B27, HLA-B8
Adamantiades-Behçet disease : HLA B-51
Birdshot retinopathy : HLA A29
HLA-A29
Multiple sclerosis, uveitis and optic neuritis : DR2
Ocular pemphigoid :HLA-B12, DQw7
:HLA B12,
Presumed ocular histoplasmosis : HLA-B7, DR2
Reiter syndrome : HLA-B27
Sympathetic ophthalmia :HLA-A11, DR4, Dw53
VKH disease : DR4, Dw53, DQw3
Deborah Pavan-Langston, 2008

808
Lipid mediators

809
Lipid mediators : Basic activities

810
Vasoactive amine
• Containing amino groups
• Breakdown of amino acids. Many natural
neurotransmitters like epinephrine
epinephrine,
norepinephrine, dopamine, serotonine,
histamine
• Acts on the blood vessels to alter vascular
permeability or t cause vasodilation.
bilit
to
dil ti

811
Cytokines
• Small secreted proteins which mediate and regulate
p
g
immunity, inflammation, and hematopoiesis.
• Produced de novo in response to an immune stimulus.
• Generally (although not always) act over short distances
and short time spans and at very low concentration.
• Act by binding to specific membrane receptors, which
then i
th signal th cell via second messengers, often
l the ll i
d
ft
tyrosine kinases, to alter its behavior (gene expression).
y
g
g
• Responses to cytokines include increasing or decreasing
expression of membrane proteins (including cytokine
receptors), proliferation, and secretion of effector
molecules.
812
Selected Immune Cytokines and Their Activities*
Cytokine

Producing Cell

Target Cell

GM-CSF

Th cells

progenitor cells

Function**
growth and differentiation of
monocytes and DC

Th cells
IL-1

monocytes
macrophages
B cells
DC

co-stimulation

B cells

maturation and proliferation

IL-2

Th1 cells

IL-3

Th cells
NK cells

NK cells

activation

various

IL-1

inflammation, acute phase
response, fever

activated T and B cells
cells,
NK cells

growth, proliferation,
growth proliferation
activation

Th2 cells

growth and differentiation

mast cells

growth and histamine release

activated B cells
IL-4

stem cells

proliferation and differentiation
IgG1 and IgE synthesis

macrophages
h
T cells

MHC Cl
Class II
proliferation
813
IL-5

Th2 cells

IL-6

monocytes
macrophages
Th2 cells
stromal cells

activated B cells

proliferation and differentiation
IgA synthesis

activated B cells

differentiation into plasma cells

plasma cells
stem cells
various

antibody secretion
differentiation
acute phase response

IL-7

marrow stroma
thymus stroma
y

stem cells

differentiation into progenitor B and
T cells

IL-8

macrophages
endothelial cells

neutrophils

chemotaxis

IL-10
IL 10

Th2 cells

macrophages
B cells

cytokine production
activation
differentiation into CTL
(with IL-2)

macrophages
B cells

activated Tc cells
NK cells

activation

IFN-

leukocytes

various

viral replication
MHC I expression

IFN-

fibroblasts

various

viral replication
MHC I expression

IL-12

814
various
macrophages
IFN-

Th1 cells,
Tc cells, NK cells

Viral replication
MHC expression

activated B cells
Th2 cells
macrophages

Ig class switch to IgG2a
proliferation
pathogen elimination

MIP-1

macrophages

monocytes, T cells

chemotaxis

MIP-1

lymphocytes

monocytes, T cells

chemotaxis

monocytes, macrophages

chemotaxis

activated macrophages
activated B cells

TGF-

IL-1 synthesis
IgA synthesis

T cells, monocytes

various
TNF

macrophages, mast cells, NK
cells

macrophages

proliferation
CAM and cytokine expression
cell death

phagocytes
TNF-

tumor cells

phagocytosis, NO production

tumor cells

cell death

Th1 and Tc cells

815
Reactive Oxygen Intermediate
• Including both radicals and non-radicals.
non radicals.
• Constantly formed in the human body and
have been shown to kill bacteria and
inactivate proteins, and have been
p
implicated in a number of diseases.
• Produced by inflammatory phagocytes to
p
cancer development.
• Important signals controlling cell growth
and cell death
816
Reactive Oxygen Intermediate

817
Immune Systems
Systems  exhibit fascinating complexity and
y
g
p
y
interrelationships that allow them to fine-tune immune
reactions to almost any antigen, or molecule that
p
stimulates an immune response
• Humoral immunity
– Deals with infectious agents in the blood and body tissues
– Managed by B-cells (with help from T-cells)

• C ll
Cell-mediated immunity 
di t d i
it
– Deals with body cells that have been infected.
– Managed by T-cells.
818
Immune Systems : Humoral
y
•

The humoral system of immunity is also called the antibody-mediated
system because of its use of specific immune-system structures called
antibodies.

•

Activation phase
– The first stage in the humoral pathway of immunity is the ingestion
(p g y
(phagocytosis) of foreign matter by special blood cells called macrophages.
)
g
y p
p g
– The macrophages digest the infectious agent and then display some of its
components on their surfaces.
– Cells called helper-T cells recognize this presentation, activate their immune
response, and multiply rapidly

•

Effector phase
– Involves a communication between helper-T cells and B-cells.
– Activated helper-T cells use chemical signals to contact B-cells, which then begin
to multiply rapidly as well B cell descendants become either plasma cells or B
well. B-cell
memory cells.
– The plasma cells begin to manufacture huge quantities of antibodies that will
bind to the foreign invader (the antigen) and prime it for destruction.
– B memory cells retain a "memory" of the specific antigen that can be used to
y
y
p
g
mobilize the immune system faster if the body encounters the antigen later in life.
These cells generally persist for years.

819
Immune Systems : Cell-Mediated
•
•
•
•
•
•
•
•

The cell-mediated immune response involves cytotoxic T-cells, or
killer-T cells.
Body cells that have been infected by foreign matter often present
components of that material on their surfaces.
Killer-T cells recognize these displays and respond by ingesting or
otherwise destroying the infected cell.
Killer-T cells are also important in the body's defenses against
parasites, fungi, protozoans, and other larger cells that might have
found their way into the body.
The killer T cells recognize these large invaders by their foreign
killer-T
proteins and then destroy them.
Killer-T cells also produce T memory cells which "remember" a
specific protein or antigen.
The
Th combination of T ll and B ll memory assures the b d of
bi ti
f T-cell d B-cell
th body f
familiarity with any antigens or foreign agents that have been
present in the body within the last few years.
p
g
g
y
y
A response to an agent against which the body has already formed
memory cells is called a secondary response. All other responses
are primary responses.

820
Inflammatory cascade: Steroids vs NSAID

Cervantes-Coste G et al 2009

821
Retinal arteritis
• Causes
– SLE
– Polyarteritis nodosa
– Churg-Strauss
– Microscopic polyangitis
– Frosted branch angitis
– S hili
Syphilis
– Herpetic viruses
Retinal Physician 2011

822
Retinal phlebitis
• Causes
– Sarcoidosis
– Paraviral
– Toxoplasmosis
– Birdshot
– HIV
– E l di
Eales disease

Retinal Physician 2011

823
Mixed retinal vasculitis
• Causes
– Multiple sclerosis
– Behçet’s disease
Behçet s
– Wegener’s granulomatosis

Retinal Physician 2011

824
Non infectious uveitis: Approach
• ANTIMETABOLITES
– Methotrexate (MTX)
– Azathioprine (AZA)
– Mycophentolate Mofetil (MMF)

Retinal Physician 2013

825
Non infectious uveitis: Approach
pp
• BIOLOGIC RESPONSE MODIFIERS
– Adalimunab
– Interferon 2a
– Anakinra

• ALKYLATING AGENTS
– Cyclophosphamide
– Clorambucil
– Mycophentolate Mofetil (MMF)
Retinal Physician 2013

826
dr. Bakri Abdus Syukur, Sp.M

Orbit and Tumor
829
The orbit
• 7 bones make the bony orbit :
– Frontal
– Zygomatic
– Maxillary
– Ethmoidal
– Sphenoid
–L i l
Lacrimal
– Palatine
American Academy of Ophthalmology

830
The orbit : Margin
g
• Superior by frontal bone, interrupted
p
y
,
p
medially by Supraorbital notch
• Medial above by frontal bone
• Medial bellow by
– P t i l i l crest of l i l b
Posterior lacrimal
t f lacrimal bone
– Anterior lacrimal crest of maxillary bone

• Inferior by maxillary and zygomatic bone
• Laterally by zygomatic and frontal bone
American Academy of Ophthalmology

831
The orbit : Roof
• Orbital plate of frontal bone
• L
Lesser wing of sphenoid b
i
f h
id bone

American Academy of Ophthalmology

832
The orbit : Medial wall
•
•
•
•

Frontal process of maxilla
Lacrimal bone
L i lb
Orbital plate of ethmoid
Lesser wing of sphenoid

American Academy of Ophthalmology

833
The orbit : Lateral wall
• Formed by
– Zygomatic
– Greater wing of sphenoid

• Lateral orbital tubercle of Whitnall
– Check ligament of the lateral rectus muscle
– Suspensory ligament of the eyeball
– Lateral palpebral ligament
– Aponeurosis of the levator muscle
American Academy of Ophthalmology

834
The orbit : Floor
• Formed by
– Maxillary
– Palatine
– Orbital plate of zygomatic

• Very fragile to orbital blunt trauma

American Academy of Ophthalmology

835
The Orbit : Superior orbital fissure
• Above the ring
– Lacrimal nerve of V-1
– Frontal nerve of V-1
– Cranial nerve IV

• Within the ring (Heads of 4 rectuses)
–
–
–
–
–

Superior and inferior division of cranial nerve III
Nasociliary b
N
ili
branch of cranial nerve V 1
h f
i l
V-1
Sympathetic root of ciliary ganglion
Cranial nerve VI
Superior ophthalmic vein

• Bellow the ring
– Inferior ophthalmic vein
American Academy of Ophthalmology

836
The orbit : Cavernous sinus
• Posterior to orbital apex
• Lateral to the sphenoidal air sinus and
pituitary fossa
• Structures located within are :
– Internal carotic artery that
that,
– Surrounded by sympathetic carotid plexus
– Cranial nerves III, IV and VI
– Ophthalmic and maxillary divisions of cranial
nerve V
American Academy of Ophthalmology

837
Orbital surgical space
•
•
•
•

Sub periorbital
Extra
E t conal
l
Intra conal
Episcleral

American Academy of Ophthalmology

838
Retinoblastoma
• Most common primary intraocular malignancy of
p
y
g
y
childhood
• 30-40% occurs bilaterally
– If associated with ectopic intracranial retinoblastoma
 Trilateral retinoblastoma  pineal gland and para
sellar region

• Most abnormal finding
– Leukocoria (50-62%)
– Strabismus (20%)
• Esotropia : Exotropia  50:50

– Redness, painful, glaucomatous, decreased vision,
etc
American Academy of Ophthalmology

839
Retinoblastoma : Histopathology

840
Basalioma
•
•
•
•
•
•
•
•

Basal cell carcinoma
Most common eye lid malignancy  90-95%
y
g
Lower eyelid margin  50-60%
Near medial canthus  25-30%
Upper eyelid  15%
Lateral canthus  5%
Most common  Nodular
Less common  Morpheaform of Fibrosing type
 more aggressive
American Academy of Ophthalmology

841
Basalioma : Managements
• Localized to the adnexa
– 3-5mm excision from macroscopic margin  frozen
section

• Invasion to the orbit
– Exenteration
– Radiation therapy
• Only a palliative treatment
• Generally be avoided for periorbital lesions

• Invasion to intracranial or paranasal sinuses
– Palliative
842
Squamous Cell Ca
• 40 times less common than basalioma 
biologically more aggressive
• Metastasize through :
– Lymphatic transmission
– Bl d b
Blood-borne t
transmission
i i
– Direct extension  often, along nerves

American Academy of Ophthalmology

843
Squamous Cell Ca : Eyelid
•

Localized to the adnexa
– 6 7 mm excision f
6-7
i i from macroscopic margin  f
i
i
frozen section
ti

•

Invasion to the orbit
– Without regional lymphatic nodes involvement
• Exenteration
• Radiation therapy

– With regional lymphatic nodes involvement
• Exenteration
• Lymphatic nodes disection  joint surgery
• Radiation therapy

•

Invasion to intracranial or paranasal sinuses or far metastasizing
– Palliative

844
Squamous Cell Ca : Conjunctiva
• 1-2 mm diameter of tumor
12
– 6-7 mm excision from macroscopic margin
– 70 degree subzero cryotherapy

• 2-5 mm diameter of tumor
– If excision not available  Enucleation or
f
Excenteration

• M
More than 5 mm diameter of t
th
di
t
f tumor
– Excenteration
845
Sebaceous Adeno Ca
•
•
•
•

Highly malignant and potentially lethal tumor
Tarsal plate  meibomian glands
Eyelash  Glands of Zeis
Or,
Or sebaceous glands of caruncle eyebrow or
caruncle,
facial skins
• Patient commonly older than 50 years of age

American Academy of Ophthalmology

846
Sebaceous Adeno Ca : Managements
•

Less than 1 mm diameter of tumor
– wide excision f
id
i i from macroscopic margin  f
i
i
frozen section
ti

•

More than 1 mm diameter of tumor
– Without regional lymphatic nodes involvement
• Exenteration

– With regional lymphatic nodes involvement
• Exenteration
• Lymphatic nodes disection  joint surgery
• Radiation therapy

•

Invasion to intracranial or paranasal sinuses or far metastasizing
–
–
–
–

Exenteration and joint surgery if possible
Lymphatic nodes disection  joint surgery
Radiation therapy
py
Palliative
847
Malignant melanoma
• 5% of cutaneous cancers
• 1% of eyelid malignancies
• Develop de novo or from preexisting
melanocytic nevi or lentigo maligna
• Four clinicopathologic forms
– Lentigo maligna
– Nodular
– Superficial spreading
– Acro-lentiginous
Acro lentiginous
American Academy of Ophthalmology

848
Malignant melanoma : Managements
•

Localized
– Incision biopsy
– 6-7mm full thickness excision from macroscopic margin  frozen
section

•

Invasion to the orbit
– Without regional lymphatic nodes involvement
• Exenteration
• Radiation therapy
• Cytostatic agent and immune therapy

– With regional lymphatic nodes involvement
• Exenteration
• Lymphatic nodes disection  joint surgery
• Cytostatic agent and immune therapy

•

Invasion to intracranial or paranasal sinuses or far metastasizing
–
–
–
–

Exenteration and joint surgery if possible
Lymphatic nodes disection  joint surgery
y p
j
g y
Cytostatic agent and immune therapy
Palliative

849
Epithelial tumors of Lacrimal gland
• 50% of epithelial tumor  malignant
p
g
• Types
– Pleomorphic adenoma (Benign mixed tumor)
– Malignant mixed tumor
– Adenoid cystic carcinoma
• Half of the carcinomas
• Grow in tubules, solid nest or cribiform Swiss cheese pattern
Swiss-cheese

• Management
–
–
–
–
–

Percutaneous biopsy
Permanent section
Radical orbitectomy
High dose radiation with surgical debulking
Palliative
Palliati e
American Academy of Ophthalmology

850
Secondary orbital tumor
• Lung  40% in male
• Breast  68 % in female
• Leukemia
–
–
–
–

Ocular involvement  80%
Choroid is more often affected
Also found in retina, optic disc and vitreous
Retinal hemorrhages and pseudo Roth spots are
common

American Academy of Ophthalmology

851
Thyroid orbitopathy : Classification
Class Mnemonic Suggestion
0

N

No physical signs or symptom

1

O

Only signs

2

S

Soft tissue involvement

3

P

Proptosis o 3 mm o more
op os s of
or o e

4

E

Extra ocular muscle involvement

5

C

Corneal i
C
l involvement
l
t

6

S

Sight loss (due to optic nerve)
Werner, 1963

852
Thyroid orbitopathy : Classification
• Soft tissue involvement
– 0 : Absent
– A : Minimal
– B : Moderate
– C : Marked

Werner, 1963

853
Thyroid orbitopathy : Classification
• Proptosis of 3 mm or more
– 0 : Absent
– A : 3 – 4 mm
– B : 5 – 7 mm
– C : 8 mm or more

Werner, 1963

854
Thyroid orbitopathy : Classification
• Extra ocular muscle involvement
– 0 : Absent
– A : Limitation of motion at extremes of gaze
– B : Evident restriction of motion
– C : Fixation of globe
g

Werner, 1963

855
Thyroid orbitopathy : Classification
• Corneal involvement
– 0 : Absent
– A : Punctate lesions
– B : Ulceration
– C : Necrosis or perforation
p

Werner, 1963

856
Thyroid orbitopathy : Classification
• Sight loss (due to optic nerve)
– 0 : Absent
– A : 20/20 – 20/60
– B : 20/70 – 20/200
– C : Worse than 20/200

Werner, 1963

857
Staging of Disease
• Rundle’s Curve – Disease Activity
– Active (Dynamic) Stage  Proptosis and Lid
retraction
– Static (Partial regression) Stage  Stable
disease with littl i
di
ith little improvement
t
– Inactive (Burnt out) Stage  Spontaneous
relative i
l ti improvement
t

Sanjeev Y, 2010

858
Disease Activity (EUGOGO)
Proptosis

Diplopia

Neuropathy

Mild

19-20 mm

Intermittent Subclinical

Moderate

21 23
21-23 mm

Inconstant

6/9 -6/12
6/12

Marked

> 23 mm

Constant
(Primary)
(P i
)

6/12 and
worse

• Severe disease
– 1 Marked
– 2 Moderate
– 1 Moderate + 2 mild
Sanjeev Y, 2010

859
Auto antibodies
Auto-antibodies
• Anti-TSH.R
• A tit id P
Antityroid Peroxidase
id

Sanjeev Y, 2010

860
Blow out fracture : Signs
• Major signs
– Enophthalmos
– Diplopia
– Hypoesthesia

• Also
– Positive forced duction test
– Cloudiness and fluid level in the maxillary
sinus
861
Le Fort fractures
•

Le Fort I
– Low transverse maxillary fracture above the teeth
– No orbital involvement

•

Le Fort II
– Pyramidal configuration
– Nasal, lacrimal and maxillary bones  medial orbital floor

•

Le F t
L Fort III
– Disjunction of craniofacial bones
– Suspended only by soft tissues
– Orbital floor, medial and lateral
orbital walls are i
bit l
ll
involved
l d

American Academy of Ophthalmology

862
Painful ophthalmoplegia
• Think  Life saving first  Infection ??
– Orbital cellulitis

• Tumor
• Tolosa-Hunt-Syndrome
– High dose steroids usually produce rapid and
dramatic resolution

863
Painful blind eye
•
•
•
•

Think  Life saving first  infection ??
Relieving the pain immediately
Cryo-therapy ?
Enucleation  Last choice that strongly to be
avoided

• Remember :
– Incisional intra ocular surgery strictly contra indicated
in blind eye and in eye with severe decreased vision.
864
Community Ophthalmology

865
What is blindness?
• WHO classification of visual impairment
Criteria
Normal

Vision
6/6 to 6/18

Visual impairment (1)

<6/18 to 6/60

Severe visual impairment (2)

<6/60 to 3/60

Blind (3)
Blind (4)
Totally blind (5)

< 3/60
Or Visual Field 5 10
5-10º
1/60
Or Visual Field < 5º
No light perception
866
Legal Blindness
• Best corrected of visual acuity both eyes
20/200 or less (USA)
• Or, Visual fields in both eyes of less than
10 degree centrally (USA)

Deborah Pavan-Langston, 2008

867
Decreased vision percentage
Distance vision
20/20
20/25
20/40
20/50
20/80
20/100
20/160
20/200
20/400

Decrease (%)
0
5
15
25
40
50
70
80
90
Vaughan DG

868
Decreased vision percentage
Near vision
1
2
3
6
7
11
14

Decrease (%)
0
0
10
50
60
85
95
Vaughan DG

869
Trachoma
• Initially  Chronic follicular conjunctivitis
• Marked on upper tarsal plate
• Pannus
– Usually pronounced on upper half of the cornea
– Corneal infiltrates
– Superficial vascularization

• Art line
– Transverse band of scar  Fine linear
– Occurring on superior tarsal conjunctiva

• Herber pits
– Regression of the follicles formation
– Locate at the limbus
– Sharply defined depression at the base of the pannus
American Academy of Ophthalmology

870
Trachoma : WHO
SIGN

DEFINITION

TF

Trachoma Follicullar

5 or more follicles on superior tarsal
conjunctiva

TI

Trachoma Intense

Pronounced inflammatory thickening of the
upper tarsal conjunctiva  obscures more
than ½ the normal deep tarsal vessels

TS

Trachomatous
T h
t
Scarring

The presence of scarring in the tarsal
conjunctiva

TT

Trachomatous
Trichiasis

At least one eyelash rubbing on the
eyeball

CO

Corneal opacity

Easily visible corneal opacity over the pupil

American Academy of Ophthalmology

871
Trachoma : MacCallan
• Trachoma I
– Immature follicles on upper tarsal plate
– Including in central area
– Without scarring

• Trachoma II
– Mature follicles on upper tarsus  necrotic or soft
– Obscuring tarsal vessels
– Still without scarring

• Trachoma III
– Follicle presents on tarsus
– Definite scarring of the conjunctiva

• Trachoma IV
– No follicles on tarsal plate
– Marked scarring of the conjunctiva
872
Vitamin A deficiency
Xerophthalmia (WHO 1996)
•
•
•
•
•

(XN)
(X1A)
(X1B)
(X2)
(X3A)

•

(X3B)

•
•

(XS)
(XF)

: Nyctalopia
: Conjungtival xerosis
: Conjungtival xerosis + Bitot spot
: Corneal xerosis
: Keratomalacia or corneal ulceration
with < 1/3 corneal involvement
: Keratomalacia or corneal ulceration
with > 1/3 corneal involvement
: Corneal scar
: Xerophthalmia fundus
American Academy of Ophthalmology

873
Fortified topical antibiotics
• Fortified Tobramycin (or Gentamycin)
– Inject 2 ml of 40mg/ml Tobramycin
– Directly into a 5 ml – 0 3% Tobramycin
0.3%
ophthalmic solution
– This gives a 7 ml fortified Tobramycin 
approximately 15 mg/ml
– Refrigerate
– Expires after 14 days
Will’s Eye Manual, 2004

874
Fortified topical antibiotics
• Fortified Vancomycin
– Add non preservative sterile water to 500 mg of
Vancomycin dry powder to form 10 ml of solution
– This provides a strength of 50 mg/ml solution
– To achieve a 25 mg/ml solution  take 5 ml of 50
mg/ml solution
– Add 5 ml sterile water
– Refrigerate
– Expires after 4 days

Will’s Eye Manual, 2004

875
Fortified topical antibiotics
• Fortified Cefazolin
– Add non preservative sterile water to 500 mg
of Cefazolin dry powder to form 10 ml of
solution
– This provides a strength of 50 mg/ml solution
– Refrigerate
– Expires after 7 days

Will’s Eye Manual, 2004

876
Fortified topical antibiotics
• Fortified Bacitracin
– Add non preservative sterile water to
50,000
50 000 U of Bacitracin dry powder to form
5 ml of solution
– This provides a strength of 10,000 U/ml
solution
– Refrigerate
g
– Expires after 7 days
Will’s Eye Manual, 2004

877
Intracameral Antibiotics
• Glycopeptide
– Vancomycin  Use Millipore powder filter

• Cephalosporins
– Cefuroxime
– Cefazolin

• Fluoroquinolones
– Gatifloxacin
– Moxifloxacin
EyeWorld 2009

878
Intravitreal antibiotics ( / 0 1 ml )
0.1
•
•
•
•
•
•

Gentamycin
G t
i
Vancomycin
Amikacin
Chlorampenicol
Amphotericin B
Ceftazidime
Cefta idime

0.1
0 1 mg
1.0 mg
0.4 mg
1.0 mg
5.0 µg
2.0-2.25
2 0 2 25 mg
American Academy of Ophthalmology

879
The Laser

883
Laser
•
•
•
•

Light Amplification
By
Stimulating
The Emission of Radiation

884
Laser : Effect
•
•
•
•

Photochemical
Thermal
Photovaporization
Ionizing effects

885
Laser : Type
• GAS ION LASERS
- Argon, Krypton
• SOLID STATE LASERS
- R b C t l Nd YAG
Ruby Crystal, Nd:YAG
• LIQUID LASERS
-D e
Dye
• DIODE LASERS
886
Laser for Eye
• Photocoagulation  Proteindenaturating processes
– Argon Blue Green
– Argon Green
– Krypton Red
– Diode
– Tunable Dye
– Frequency Doubled Nd:YAG
–X
Xenon Arc
A
887
Laser for Eye
• Photodisruption  Cutting by
optical break down  10,000° K
– Q-switched Frequency Doubled
Nd:YAG Laser

888
Laser for Eye
• Photodecomposition  Carving
 C tti th molecular b d
Cutting the
l
l bond
– UV short wavelength
– Excimer (Excited Dimmer) Laser

889
Laser for Eye

• Photoevaporation  Infra Red
– CO2 Laser
–H l i
Holmium:YAG L
YAG Laser Shorter Long
Wavelength
– Erbium:YAG Laser
Laser

890
MODERN LASERS
• Continuous Wave ( CW )
p
accurate selection of power & emission time
• Efficiency
- lower power and energy consumption
- lower space consumption
- lower cost
- long term use
891
The Lasers
•
•
•
•
•

integrepro multicolor laser (ellex)
PUREPOINT Laser (Alcon Inc)
MicroPulse Fovea-Friendly Laser (IRIDEX)
VISULAS 532s VITE (Carl-Zeiss)
(Carl Zeiss)
PASCAL (Pattern Scan Laser) Photocoagulator
(OptiMedica, now: TopCon)
• Novus Varia multicolor photocoagulator
(Lumenis)
• MC-500 Vixi Multi-Colour Laser (NIDEK)
MC 500
Multi Colour
• Vitra Multispot Laser (Quantel Medical)
892
Laser on Retina

My teacher, my mentor, my friend:

dr.
dr Tjuk Suparjadi Sp M
Suparjadi, Sp.M
895
Laser on Retina : Photocoagulation
• L
Lenses
– PRP Lens
– Goldmann 3 mirror Lens
• 59°, 67°, 73°

–F
Focal and G id L
l d Grid Lens
– +78 and +90 D Lens
– PDT Lens

896
897
LASER ON RETINA
• GREEN LASER : 532 nm
Produced by :
- Gas ( Argon )
- Diode Pumped Solid State (DPSS)
F
Frequency doubled Nd YAG
d bl d Nd:YAG

898
LASER ON RETINA : Argon
g
• 514 nm and 532 nm wavelength
• Clear media  safe and proven effective
• Indications :
– DR
– Veins occlusions
– CNV
– Retinal breaks
899
LASER ON RETINA : Dye Yellow

•
•
•
•
•

577 nm wavelength
Better than Argon for microaneurism
Preferred for Coats disease
Not acceptable in hemorrhage
Macula  absorbed by haemoglobin, unabsorbed b
M
l
b b db h
l bi
b b d by
Xanthophil

900
LASER ON RETINA : Krypton Red
•
•
•
•
•
•
•

647 nm wavelength
Less absorption by blood
Hazy media
Deep b
D
burns
Less NFL damage
Not preferable for Coats disease and Retinal angioma
Indications :
–
–
–
–

DR with vitreous hemorrhage
Veins occlusions with vitreous hemorrhage
Vitreoretinal tractions
CNV  General Peripapillary, Near PMB with pre-retinal
General, Peripapillary
PMB,
pre retinal
membrane
901
LASER ON RETINA : Diode
•
•
•
•
•
•

810 nm wavelength
Deep burns
Less NFL damage
Less absorbed by blood
Not preferable for Coats disease and Retinal angioma
Indications :
–
–
–
–

DR with vitreous hemorrhage
Veins occlusions with vitreous hemorrhage
Vitreoretinal tractions
CNV  General, Peripapillary, Near PMB, with pre-retinal
membrane
b
902
HOW to OPERATE
• TECHNICAL SPECIFICATION
p
1. Laser Specification
2. Electrical Requirement
3. Visualization
- Slit Lamp
- Aiming Beam
- Laser Safety Eye Wear
MPE = maximum permissible exposure
903
How to select the mode
• Type of Laser : Wavelength
• Power : 0 3 - 1 7 W ( DPSS )
0.3 1.7
0.5 - 4.0 W ( Gas )
• S t Size: 50 - 2000 um
Spot Si
• Exposure time : 0.01 - 4.0 s ( DPSS )
0.01 - 1.0 s ( Gas )
• Pulse Interval : 0.1 - 1.0 s
904
Nice to know
• Xantophyl, Oxyhaemoglobin and Melanin
• Indirectly mechanism
• Exposure time :
< 0 1 sec : mechanical effect
0.1
h i l ff t
> 0.1 sec : thermal effect
• Energy Density  inversely proportional to
the focal spot size
905
Applications
• Diabetic retinopathy
– Non-perfusion
– Edema
– Neovascularization

•
•
•
•
•
•

Venous occlusion
Retinal breaks
Retinal degeneration
Retinal vasculitis
CSCR
AMD

• G id
Grid
• Focal
• Pan retinal

906
Applications : Grid LPC
• Grid Laser Photocoagulation
• Macular application  500 µm up to 3000 µm from
foveal center
• Excluded  area of PMB
• Grid Lens / +78 and +90 D Lens
• Start at 100mW power  increments of 10-20mW
• 50-100 µm spot size
• 0.100 second or less duration
• S t spaced at least one burns apart
Spots
d tl
t
b
t
• Supplemental treatment considered at least 3-4 month
after initial coagulation  up to 300 µm
907
Applications : Focal LPC
Focal Laser Photocoagulation
•
•
•
•
•

Grid Lens / +78 and +90 D Lens
Start at 100mW power  increments of 10-20mW
50-100 µm spot size
0.100 second or less duration
Attempt to whiten or darken microaneurysms

908
Applications : PRP
Pan-Retinal Photocoagulation
/ Scatter Laser Photocoagulation
•
•
•
•
•
•
•
•
•

NVD or / and NVE
PRP Lens
Start at 180mW power  increase gradually to achieve the end
point
500 µm spot size
0.100 to 0.200 second duration
1800 total applications
1 – 1.5 burns width apart
3 sessions complete  10 days to weeks apart
Usually, inferior half of retina coagulated first
y,
g
909
Applications : Others
•
•
•
•
•
•
•
•

ROP
Retinoblastoma
Coats disease
Vitreolysis
Retinal cavernosus hemangioma
Choroidal hemangioma
Optic Disc Pit – Maculopathy
Idiopathic Juxtafoveal Retinal talengiectasis
910
Chorioretinal burn intensity
• Light
– Barely visible retinal blanching

• Mild
– Faint white retinal burn

• Moderate
– Opaque, dirty white retinal burn

• Heavy
– Dense-white retinal burn
911
Laser on Retina : PDT

•
•
•
•
•

Systemic administration
Use photosensitizing drugs
Followed b li ht application
F ll
d by light
li ti
Particular wavelength to affected tissue
Incite a localized photochemical reaction
912
Laser on Retina : PDT

• CW beam  500 - 590 µm of low thermal energy
laser
• Extend at least 500 µm beyond lesion margin
y
g
• 50 J/cm2 laser energy
• 600 mW/cm2 dose rate
• 15 minutes after start the infusions
913
Laser on Retina : PDT
• Liposome-encapsulated Benzoporphyrin
 Verteporfin dye (Visudyne)
– Maximum absorption  light near 689 nm
wavelength

• Others :
– Tin Ethyl Etiopurpurin (SnET2, Purytin)
– Lutetium (Lu-Tex)
914
Laser on Retina : PDT

• 30 ml Verteporfin via 10 minutes infusion pump
injection, plus
• 5 ml D5W injected simultaneously via Y tube
• Filtered by 1.2 um filter to venflon catether into
Cubiti vein

915
Laser on Retina : TTT
• Transpupillary Thermotherapy
– Alt
Alternative th
ti therapy f S bf
for Subfoveal CNV
l
– Rise intralession temperature of 4-9° C

•
•
•
•
•

Infra Red Diode laser 810 nm
Within 72 hours of recent FFA
Diode-coated
Diode coated Volk QuadrAspheric Lens
0.8 mm, 1.2 mm, 2.0 mm, 3.0 mm spot size
200 – 600 mW power
W
916
Laser for Glaucoma

919
A Tribute to
Prof. dr. Ratna Kentjana, Sp.M(K)
Prof. d MNE G
P f dr. MNE. Gumansalangi, S M(K)
l
i Sp.M(K)

920
ALT
• Argon Laser Trabeculoplasty

921
ALT : Aims

• I
Increase aqueous outflow
tfl
• By burning the trabecular meshwork
• By applying a low energy of laser

922
ALT : Mechanism
• Absorption of laser by Pigmented TM
• Produces thermal energy
• Shrinkage of collagen of trabecular lamellae
– Probably opens un intratrabecular space in untreated
region
– Trabecular tightening  pulling meshwork centrally 
opens Schlemm’s canal

• Attract phagocytes that clean up debris
• Allows aqueous to flow better
923
ALT : Preparations
• CW Argon laser :
– Bichromatic Blue-Green
– Monochromatic Green

• Krypton Red
• Frequency doubled Nd:YAG laser
q
y
• Diode
– Lesser pain
– Lesser PAS
– Lesser disruption of Blood Aqueous Barrier

• Gonio lens
924
ALT : Protocol
1. Pre-Treatment
● Alpha-adrenergic antagonist (Apraclonidine 1%) and topical anesthetic

2. Treatment
● G i i
Gonioprisms
● Focus aiming beam to target the entire height of TM
● 180° or 360° of TM can be photocoagulated in single or two sessions
● Goniolens rotated clockwise and make 25 burns for each 90°

3. Post-Treatment
●
●
●
●

Alpha-adrenergic antagonist
Topical steroid or NSAID for 3 to 5 days (optional)
1 hour IOP check after treatment
Regular follow-up routine
925
ALT : Indications
•
•
•
•

POAG
Exfoliation syndrome
Pigmentary glaucoma
Glaucoma in aphakia and pseudophakia

926
ALT : Contraindications
•
•
•
•
•
•

Closed or Extremely narrow angle
Corneal haze and diminished aqueous clarity
Vitreous in anterior chamber
Neovascular glaucoma
Active uveitis
Poor responsiveness glaucoma  Congenital
glaucoma and Angle recession glaucoma
927
ALT : Complications
•
•
•
•
•
•

Elevated IOP
Progressive visual fi ld l
P
i
i
l field loss
Iritis
PAS
Hemorrhage
Corneal complications
928
SLT
• Selective Laser Trabeculoplasty

929
SLT : Mechanism
• Uses specific wavelength
• Absorption of laser by Pigmented TM 
selective t
l ti targets  no d
t
damage on N
Nonpigmented TM
Non thermal
• Produces Photothermolysis  Non-thermal
• Trabecular tightening
• Allows aqueous to flow better

930
SLT : Preparations
• 532nm Wavelength Q-switched frequency
doubled Nd:YAG laser
(Neodymium: Yytrium-Aluminum-Garnet)
• 63
635nm W
Wavelength Di d l
l
h Diode laser
• Goldmann, Thorpe or Latina lens
(0° magnification)
ifi ti )

931
SLT
• Allerex
• Ellex

932
SLT : Protocol
1. Pre-Treatment
● Alpha-adrenergic antagonist and topical anesthetic

2. Treatment
● G ld
Goldmann, Th
Thorpe or Latina lens (0° magnification)
L ti l
ifi ti )
● Focus aiming beam to target the entire height of TM
● Set laser to 0.8 mJ (average) and then increase in 0.1 mJ steps until
champagne bubbles appear approximately 50%-70% of the time
50% 70%
● Approximately 50 shots are placed onto the TM in the same pattern as ALT

3. Post-Treatment
3 P
T
●
●
●
●

Alpha-adrenergic antagonist
Topical steroid or NSAID for 3 to 5 days (optional)
1 hour IOP check after treatment
Regular follow-up routine
933
SLT is not ALT
Spot size comparison:

ALT

50µm

SLT

400µm

ALT SLT

ALT

SLT

50 micron

SPOT SIZE

400 micron

500 – 1,000 mW
720 – 1,200 mW

ENERGY OUTPUT

0.8 – 1.5 mJ

10 ms

PULSE DURATION

3 ns

60,000 mJ/cm2

FLUENCE

600 mJ/cm2

934
SLT is not ALT
The SLT technique is much less traumatic to the eye than ALT
ALT,
and evokes a gentle response of the auto-immune system to begin
clearing the TM without the coagulative damage of ALT.

TM tissue after ALT

TM tissue after SLT

935
SLT : Processes
SLT is a non-thermal treatment which uses short pulses of relatively low energy 532nm
light to target and irradiate only the melanin-rich cells in the trabecular meshwork (TM);
the laser pulses affect only these melanin-containing cells, and the surrounding structure
of the TM is unaffected.
During the procedure approximately 50 confluent spots are applied along the meshwork
in order to treat a 180° angle.

Animation

936
1. SLT is selective
SLT selectively targets only the melanin-rich cells of the trabecular
meshwork.

2. SLT is non-thermal
The short pulse duration of SLT is below the thermal relaxation time of
the TM tissue, thereby eliminating the incidence of thermal damage.

3. SLT is repeatable
SLT treatment can be repeated without causing harm or further
p
complications.
937
SLT : Indications
Open Angle Glaucoma
•
•
•
•

POAG
OHT
Pigmentary Glaucoma
Pseudo-exfoliative glaucoma

Poorly compliant to drug therapy
Intolerant or unresponsive to drug therapy
I l
i
d
h
Failed ALT (either 180˚ or 360˚)
Inflammatory glaucoma
Patients currently undergoing drug therapy who wish to use SLT in
conjunction with glaucoma medications

938
SLT represents a whole new approach to managing open-angle glaucoma
Compliance issues minimized
Gentle, non-invasive treatment
SLT does not cause thermal damage of the
trabecular meshwork
No systemic side effects
SLT can be used in conjunction with medicine
to enhance the overall IOP lowering effect
IOP-lowering
Non-penetrating glaucoma surgery is not
compromised as with ALT
The latest in ‘Primary Glaucoma Therapy
Primary
Therapy’
939
ALPI

• Argon Laser Peripheral Iridoplasty

940
ALPI : Aims
•
•
•
•
•

Laser energy placed near iris root
Separate Iris from TM
S
t Ii f
For PACG
Reopening of closed angle
Widening of narrow angle

941
ALPI : Preparations
• 532nm Wavelength Q-switched frequency
doubled Nd:YAG laser
(Neodymium: Yytrium-Aluminum-Garnet)
• Ab h
Abraham contact lens +55 to +66 D
l
66

942
ALPI : Indications
• Plateau iris syndrome
• Unbreakable attack of angle close
glaucoma  laser iridotomy not possible
• Phacomorphic glaucoma
• Adjunct to laser trabeculoplasty
• R t ti peripheral i i stuck
Retracting
i h l iris t k
• Rare case of nanophthalmos
943
ALPI : Contraindications
•
•
•
•

Advanced corneal edema / opacity
Flat anterior chamber
Extensive PAS
Creeping angle glaucoma  not effective

ALPI : Complications
•
•
•
•

Iritis
Corneal endothelial burns
Hemorrhage
Transient IOP rise
944
Nd:YAG Laser Iridotomy

• R li
Relieve th pupillary bl k
the
ill
block
• 532nm Wavelength Q-switched frequency
doubled Nd:YAG laser
(Neodymium: Yytrium-Aluminum-Garnet)
• Abraham contact lens +55 to +66 D

945
Nd:YAG Laser Iridotomy
• Indications :
– PACG :
• A t / Sub acute angle closure
Acute S b
t
l l
• Creeping angle closure

– Fellow eye of ACG
– Non-pupillary block angle closure
• Plateau iris
• Forward lens position

– Narrow or closed angle
946
Nd:YAG Laser Iridotomy
y
• Complications :
–
–
–
–
–
–
–
–
–

Corneal epithelial / endothelial burns
Iritis
Pigment dispersion
Hemorrhages
g
Lens opacities
Retinal burns
Raised IOP
Posterior synechiae
Monocular di l i
M
l diplopia
947
Laser for Glaucoma and Others
•
•
•
•
•

Nd:YAG Laser C
Nd YAG L
Capsulotomy
l
Diode Laser Cyclophotocoagulation
Endoscopic Cyclo Photo Coagulation
Nd:YAG Laser Iridolenticular Synechiolysis
Cyclophotocoagulation
–
–
–
–

•

Transpupillary CP
Endo CP
Nd:YAG Trans-scleral CP  Contact and Non-contact
Diode laser CP (DLCP)

Excimer Laser Trabeculotomy (ELT)
– 308 nm X Cl l
XeCl laser, power 35 55 mJ/mms spot size 200 um, d ti 10
35-55 J/
t i
duration
sec, freq 20Hz

•

Excimer Laser Assisted Deep Sclerotomy
– Argon Fluoride XL 193 nm at 180 mJ x sq cm fluence
g
q
948
Laser for Refractive Surgery
•
•
•
•
•
•

PRK
LASIK
Epi LASIK
SBK
LASEK
LaserACE
949
LASIK : Wood carving

• W dC
Wood
Cornea
• Equipment  Laser
• Carver  Ophthalmologist

950
Argon Fluorine (ArF)
•
•
•
•
•
•

193 nm
Above th h ld t b k molecular b d
Ab
threshold to break
l
l bond
Ablative photodecomposition
Neighboring tissue <10º C (Cold laser)
Minimal collateral damage
Maximal accuracy & precision
951
Solid State UV 213
•
•
•
•
•

213 nm
DPSS Nd YAG P l
Nd:YAG Pulzar 21 (C t Vi )
(CustomVisc)
Less absorbed by neighboring tissue
Much better penetrating
Less sensitive to environmental factor

952
Solid State UV 210
•
•
•
•
•

210 nm
DPSS L
LaserSoft (K t
S ft (Katana T h l i )
Technologies)
Less inflammations
Less pain
Faster visual recovery

953
Lasik
• Pre Lasik
– General Examination
– Mapping  Topography and pachymetry, Aberration
measurement and collecting data
– Making algorithm for laser treatment

• Durante
– Flapping  Micokeratome or Femtosecond
– Eye-tracked Laser treatment
– Recovery management

• Post Lasik
954
Corneal Topography, Corneal
Pachymetry and Aberrometry System

955
Femto and Excimer Laser System

956
Pre Lasik
• Topography - Keratometry
• Ab
Aberrometry
t

957
Topography

3 types
– Placido-based systems
Placido– Elevation-based systems
Elevation– Interferometric system
y
Bausch and Lomb

958
Topography

Provide topography of the cornea, like a map
Bausch and Lomb

959
ORBSCAN II z
Combination of :
• Placido based-system
• Scanning slit imaging (elevation
based system)

Bausch and Lomb

960
Reflective and Slit-Scan Technologies

•
•
•

One image, one surface.
Angle-dependent specular
A l d
d t
l
reflection.
Measures slope (as a
function of distance).
f
ti
f di t
)

•
•
•

Multiple images, multiple
surfaces
Omni-directional diffuse
backscatter
Triangulates elevation
Ti
l t
l
ti

The overwhelming advantage Placido reflective systems is
that they can measure curvature
curvature.
Bausch and Lomb

961
How corneal shape relates to shape factor

962
LASIK  Fit the cornea
Data surface
(cornea)

Fit-zone

Reference surface (Best Fit Sphere)
(
p
)
Bausch and Lomb

963
3D Corneal Topography

BFS

BFS : Reference surface (Best Fit Sphere)

Bausch and Lomb

964
Major points
•
•
•
•
•

Anterior Elevation
Posterior Elevation
Pachymetry Thickness
Keratometry - Surface Curvature
Statistics and Data
•
•
•
•
•
•
•
•

Sim K
Steep and Flat Axis
White to White
Pupil diameter
Thinnest point
Anterior Chamber Depth (ACD)
Angle Kappa
g
pp
Kappa Intercept
Bausch and Lomb

965
Anterior Elevation Map

Curvature M
C
Map

Posterior Elevation Map

Statistics d D
S i i and Data

Pachymetry Map
P h
M

Bausch and Lomb

966
Elevation (f
El
ti (from a reference surface)
f
f
)
Max

Red
• High
• Anterior to the
reference surface

(+)
reference
f
(-)

level
l
l

• Low
• Posterior to the
reference surface
Min

Blue
Bausch and Lomb

967
Elevation Map Reading
• Warmer colors are above “sea level”
sea level
• G
Green i “
is “sea l
level” ( t h with a
l” (match ith
sphere that best matches the cornea)
• Cooler colors are below “sea level”
• Both Anterior and Posterior are read in
the same way
y
Bausch and Lomb

968
Eye #1

Highest Point

Lowest Point

Bausch and Lomb

969
Eye #1

Highest Point

Lowest Point

Bausch and Lomb

970
Pachymetry Maps
• Warmer colors are THINNER
• Cooler colors are THICKER

Pre-Op
Pre Op eyes are usually thinnest in the
temporal and inferior quadrant
Bausch and Lomb

971
Thickness
Min

Red

(+)

• Thin

(+ +)

• Thi k
Thick
Max

Blue
Bausch and Lomb

972
Pachymetry Thickness

THINNEST Area

THICKER Area

Bausch and Lomb

973
Pachymetry map
y
y
p

• Thinnest point  obtain from data sheet

Bausch and Lomb

974
Pachymetry map
• Orbscan pachymetry measurements 
5% to 8% more compared to ultrasonic
– Orbscan measures from epithelium to
endothelium
– Ultrasonic pachymetry : Stroma

Bausch and Lomb

975
High and Low is not always
directly related to Steep and Flat
High Tissue is usually flatter, but not always
g
y
,
y
Low Tissue is usually steeper, but not always
Color coded in elevation map >< curvature map (keratometric)

Ablation requires Elevation Data because
tissue that needs to be removed is high
Bausch and Lomb

976
Color-coded scales
Colors :
– Warm (red, orange, yellow) for steeper
portions of cornea

– Green denotes intermediate portions
– Cool (blue, dark blue) depict flatter
portions

Bausch and Lomb

977
Surface Curvature
S rface C r at re
(+ +)

Max

Red
• Sharp
• Fast bend
• Short radius
• Flat
• Slow bend
• Long radius

(+)
Min

Blue
Bausch and Lomb

978
Bausch and Lomb

979
Orbscan topography prior to refractive surgery
•
•
•
•
•
•
•
•
•
•
•

Ultrasound pachimetry > 475 µm
Residual bed thickness (RBT) > 250 - 300 µm
Posterior elevation < 50 µm
Posterior bed fit sphere < 50 D
Anterior/Posterior Radii-Ratio 1.21 – 1.27
Irregularity (3mm) < 1.5 D
Irregularity (5mm) < 2 0 D
2.0
Peripheral-Central Pachimetry < 20 µm
SimK (Max) < 47 D
Astigmatism variance between eyes < 1.0 D
Symetric bowtie
EyeWorld 2009; Joo CK 2009

980
ANY CAUTIONS

981
Keratoconus

Refractive surgery makes early diagnosis of
corneal abnormalities more important
Bausch and Lomb

982
Close-Fitting Reference Surfaces
Topographic maps of terrestrial landscapes are displayed in
the form of constant-elevation contours, measured from the
“mean sea level” of the earth.
mean sea-level
earth
Data surface
(cornea)

Reference surface (sphere)

Corneal topography differs from terrestrial topography in
that the reference surface is not some fixed “mean sealevel”, but is movable.
Bausch and Lomb

983
Close-Fitting Reference Surfaces
For th
F the cornea, a reference surface (typically, a sphere) i
f
f
(t i ll
h ) is
constructed by fitting the reference surface as close as
p
possible to the data surface.
Data surface
(cornea)

Fit-zone
Reference surface (sphere)

A best-fit minimizes the square difference (always a
p
positive number) between the two surfaces, but only within
)
,
y
a specified region known as the fit-zone.
Bausch and Lomb

984
Elevation Topology: Central Hill
Bausch and Lomb

Sharp center
Flat periphery
The normal cornea is prolate meaning that meridional curvature
prolate,
decreases from center to periphery.
Prolateness of the normal cornea causes it to rise centrally above the
reference sphere. The result is a central hill.
f
h
Th
lt i
t l
Immediately surrounding the central hill is an annular sea where the
cornea dips below the reference surface.

In the far periphery, the prolate cornea again rises above
the reference surface, producing peripheral highlands.

985
Elevation Distortion
Bausch and L b
B
h d Lomb

Spherical
reference surface

Post Lasik
profile

Relative
elevation
p
profile
As an example of distortion, consider the corneal surface following
p
g
myopic lasik correction. It is centrally flattened by the surgery.
To see surface features, elevation must be measured with respect to
some reference surface.
This relative elevation peak is NOT the highest point on the cornea.

This apparent central "concavity" does NOT exist.

986
Normal Post LASIK Anterior Elevation

Bausch and Lomb

Lower in the Center - OD

Lower in the Center - OS

987
Elevation (sphere)

Elevation (sphere)

These are pre-op (left) and post-op (right) elevation maps of
a myopic with-the-rule astigmatic eye corrected with LASIK.
y p
g
y
The post-operative central “sea” is not a concavity but a
central flattening.
The ring of relatively highest terrain is not absolutely higher
(more anterior) than the “sea” bottom near the map center.

988
Abnormal Post LASIK Posterior Elevation

Bausch and Lomb
Abnormally High but
High & De centered - Poor Vision
De-centered
Centered - Moderately Good Vision
• Diplopia at night

989
Normal Band Scale
Bausch and Lomb

Accentuates anomalies

990

Filters small irregularities
Normal B d S l
N
l Band Scale
• Elevation Maps (Anterior & Posterior)
– + 0.25 microns of Best Fit Sphere

• Total Cornea Power
– 40 to 48 Diopter

• Pachymetry
– 500 to 600 microns
Bausch and Lomb

991
Posterior Keratoconus

The normal band scale on the left indicates very small changes on the
anterior corneal surface and a relatively small area of corneal
steepening above 48 D.
These findings are indicative of milder disease than the contra-lateral
contra lateral
eye but probably represents an earlier forme fruste of keratoconus.
Bausch and Lomb

992
The CRS-Master
How d you plan your t t
H
do
l
treatments ?
t
Wavefront

Patient Data

Microkeratome

Refraction

Corneal C
C
l Curvature
t

Pachymetry

• Modern refractive excimer surgery is based on a complex
data set
• I must take into account not only wavefront data, b all
It
k i
l
f
d
but ll
relevant parameters of each individual patient.
Bausch and Lomb

993
Aberrometry

• Collecting aberration data
• Make algorithm for laser treatment
• Minimizing aberration post surgery

Bausch and Lomb

994
Aberration : Category
• Two categories of aberrations commonly are used to
describe vision errors, including:
– Lower-order aberrations consist primarily of nearsightedness
and farsightedness (defocus), as well as astigmatism. They
make up about 85 percent of all aberrations in an eye.
– Higher-order aberrations comprise many varieties of
aberrations. Some of them have names such as coma, trefoil
p
,
y
and spherical aberration, but many more of them are identified
only by mathematical expressions (Zernike polynomials). They
make up about 15 percent of the total number of aberrations in
an eye.

• Order refers to the complexity of the shape of the
wavefront emerging through the pupil — the more
complex the shape the higher the order of aberration
shape,
aberration.
Vessel M, 2008

995
Aberration : What Exactly
y
• A higher-order aberration is a distortion acquired by a
wavefront of light when it passes through an eye with
irregularities of it refractive components (t
i
l iti
f its f ti
t (tear fil
film,
cornea, aqueous humor, crystalline lens and vitreous
body
• Abnormal curvature of the cornea and crystalline lens
may contribute to the distortion acquired by a wavefront
of light.
• Serious higher order aberrations also can occur from
higher-order
scarring of the cornea from eye surgery, trauma or
disease.
• Cataract clouding the eye's natural lens also can cause
eye s
higher-order aberrations. Aberrations also may result
when dry eye diminishes your eye's tear film, which
p
g
y
helps bend or refract light rays to achieve focus
Vessel M, 2008

996
Aberration : How to diagnose
•

•

•

•

Higher-order aberrations are identified by the types of distortions
acquired by a wavefront of light as it passes through your eye.
Because light travels in bundles of rays a common way of
rays,
describing an individual wavefront involves picturing a bundle of light
rays. The tip of each light ray in the bundle has its own point. We
create the wavefront or wavefront map by drawing lines
perpendicular to each point
point.
The shape of a wavefront passing through a theoretically perfect eye
with no aberrations is a flat plane known, for reference, as piston
(see next chart). The measure of difference between the actual
wavefront shape and the ideal flat shape represents the amount of
aberration in the wavefront.
Because no eye is absolutely perfect (emmetropic), a wavefront
passing through an eye acquires certain three-dimensional, distorted
shapes. S f more th 60 diff
h
So far,
than
different shapes, or aberrations, h
t h
b
ti
have
been identified.
Significant amounts of aberrations can pose vision problems
y
y
y
because they interfere with the eye's ability to see clear and distinct
images (focus).
Vessel M, 2008

997
Aberration : Visual quality
• The impact of higher-order aberrations on vision quality
depends on various factors, including the underlying cause of
the aberration.
• People with larger pupil sizes generally may have more
problems with vision symptoms caused by higher-order
aberrations, particularly in low lighting conditions when the
pupil opens even wider.
il
id
• But even people with small or moderate pupils can have
significant vision problems when higher-order aberrations are
caused by conditions such as scarring of the eye's surface
eye s
(cornea) or cataracts that cloud the eye's natural lens.
• Also, specific types and orientation of higher-order aberrations
have been found in some studies to affect vision quality of
q
y
eyes with smaller pupils.
• Large amounts of certain higher-order aberrations can have a
severe, even disabling, impact on vision quality.
Vessel M, 2008

998
Aberration : Symptoms
• An eye usually has several different
higher-order aberrations i t
hi h
d
b
ti
interacting
ti
together.
• Th f
Therefore, a correlation between a
l ti b t
particular higher-order aberration and a
specific symptom cannot easily be drawn
drawn.
• Nevertheless, higher-order aberrations are
generally associated with double vision
vision,
blurriness, ghosts, halos, starbursts, loss
of contrast and poor night vision
vision.
Vessel M, 2008

999
TERMS OF WAVEFRONT
SO
O

Aberrometry

Provide information, h
P id i f
i
how b d the
bad h
Aberrations of the rays inside the eye
gy
 Wavefront technology
1000
What is Wavefront?
• Wavefront Technology is the latest generation of laser
vision correction.
• Light travels in a flat uniform beam.
• When there is nothing disturbing it, such as light going
through space, it is perfectly flat without error.
• This pattern of a straight beam of light is called a
wavefront.
• As light g
g goes through objects, the light beam becomes
g
j
,
g
distorted or becomes more like a wave.
• When light enters the eye, the light rays become
distorted because of the many components of the eyes
optical system.
• Some of these components include the cornea, lens and
aqueous fluid, although the greatest amount of distortion
occurs when light enters th
h li ht t
through th cornea.
h the
1001
What is Wavefront?

Perfect beam

Imperfect beam
p

Wavefront E e
Wa efront in Eye
1002
How does Wavefront Work?
• As the light rays touch the retina, the Wavefront
Analyzer measures the amount of distortion that has
occurred prior to the light entering the eye and after
going through the eye.
• As with the diagram the simulation grid would be
diagram,
considered the ideal or perfect optical grid.
• This grid is projected on to the back of the eye and
is measured.
measured
• The measurement is compared to the original grid
producing what is called a wavefront map.
• This wavefront map calculates the specific
aberrations of the cornea precisely measuring each
section of the cornea to provide the most accurate
p
and detailed information about our vision.
1003
How does Wavefront Work?
• Once the information is collected, it is
,
transferred to the laser.
• The laser then does a customized treatment that
is
i specific to the patient and i not b
ifi
h
i
d is
based on
d
general guidelines of treatment.
• No two wavefront maps are identical therefore a
identical,
customized treatment is specific to that patient,
enhancing the opportunity for superior quality of
vision, reduced or eliminated night vision and
improved uncorrected visual acuity.
1004
Why wavefront technology ?
To reshape corneal surface to
compensate for optical
t f
ti l
aberrations

Real eye:
rays do not intersect

retina

Ideal eye:
all rays intersect in image plane

Determine actual shape
p
of wavefront
Bausch and Lomb

retina

1005
Wavefront methods
• Hartman-Shack
• Tscherning
• Optical Path Difference (OPD) Scan

Deborah Pavan-Langston, 2008
1006
Measurements & Terminology
•
•
•
•
•
•

Zernike polynomials
Point S
P i t Spread F
d Function (PSF)
ti
Root Mean Square (RMS)
Strehl Ratio
Diffraction
Convolution
Bausch and Lomb

1007
Zernike polynomials
• Prof. Frits Zernike
Groningen, Holland
Awarded Nobel prize in Physics 1953

•

The complex shape of wavefront
is approximated by a sum of
function to give a special
geometrical mode
ti l
d

Bausch and Lomb

1008
1009
Zernike polynomials

Bausch and Lomb

1010
LowerLower-order aberrations

2nd

Bausch and Lomb

1011
3 common higher order aberrations
g
most patients suffer from
3rd

3rd

4th
Bausch and Lomb

1012
Aberrations of the eye

Bausch and Lomb

1013
Aberrations of the eye

Bausch and Lomb
1014
Understanding Aberrations
Second Order
Myopia

Cylinder

Bowl Shape

Saddle Shape

Third Order

Fourth Order

Coma

Trifoil

Sph Aber

Bump & Dip

Napoleon’s Hat

Sombrero
Plant Stand
1015
Bausch and Lomb

Quadrafoil
Understanding Aberrations
g
Coma (3rd order)
(
)

Spherical Aberration
(4th order)

Bausch and Lomb

1016
Point Spread Function (PSF)
Normal eye

Monocular Diplopia

Bausch and Lomb

1017
Point Spread Function (PSF)

Bausch and Lomb

1018
Root Mean Square (RMS)
• Single value
• Measure the magnitude of a set of number
• Example :
– Set of no : -2 +5 -6 +4 -1
– Average = 0  not informative
– We want to know the variation, disregard the
signs  average = 3.6
g
g

Bausch and Lomb

1019
Root Mean Square (RMS)
Another way to know the variation :
1. Square all values
2.
2 Take average of the squares
3. Square root of average

Smaller RMS = Less aberrations
General agreement : RMS < 0.38 plano LASIK

Bausch and Lomb

1020
Strehl Ratio
• A metric calculated from :
Actual
A t l peak PSF
k
Diffraction-limited peak PSF

Results closer to 1  less aberration
Bausch and Lomb

1021
Strehl ration
H eye
Strehl ratio 
H dl

Diffraction limited PSF
Aberration free

H dl

Actual PSF with aberrations
Bausch and Lomb
H eye
1022
Diffraction
• Diffraction causes light to bend perpendicular to
the direction of the diffracting edge
• Spreading of light waves as they p
p
g
g
y pass through a
g
small opening. (Christiaan Huygens, 1678)
• Cause the light imaged not as a single sharp
g
g
g
p
point  AIRY DISK
• Smaller apertures generates more diffraction
Bausch and Lomb

1023
Convolution
• Method to portray blur, using PSF in every p
p
y
,
g
y point of
object to stimulate retinal image

Bausch and Lomb

1024
Wavefront Analyzers
•
•
•
•
•

Zywave (Bausch & Lomb Incorporated)
(
)
CRS Master (Carl Zeiss Meditec AG)
WaveScan (Abbott Medical Optics)
g
p y
(WaveLight, Alcon)
g
)
Allegro Topolyzer Vario (
MAXWELL (Ziemer)

1025
Glare
• Glare can be described as “extreme brightness”
from the presence of excessive visible light.
• Glare can be distracting and even dangerous
and can occur day or night in a number of ways.
• Gl
Glare can cause you to squint, resulting i eye
t
i t
lti in
strain and eye fatigue. In extreme cases, glare
can even result in temporary blindness
blindness.

1026
• Distracting glare
– Distracting glare can be caused by car headlights or streetlights
at night.
– It can also be as simple as light being reflected off the front of
your lenses making it difficult for others to see your eyes.
ff
f
– Similarly, it may be from light reflected off the back – or inside –
of your lenses so that you see the distracting reflection of your
own eyes of objects behind you in your forward field of vision.
– As a result, this kind of glare may cause eye fatigue, annoyance
and distraction.
1027
• Discomforting glare
– Glare can be caused by everyday, normal sunlight conditions.
– D
Depending upon one’s li ht sensitivity, thi glare can
di
’ light
iti it this l
be discomforting regardless of weather or time of day.
– It can be present in any level or intensity of light, or when moving
from one lighting condition to another.
– Discomforting glare often causes squinting and eye fatigue

1028
• Disabling glare
– Straylight
– This type of glare comes from excessive, intense light that can
occur when you face directly into the sun.
– Disabling glare can block vision because the intense light can
g
y
g
cause significantly reduced contrast of the retinal image.
– The latent effects can last well beyond the time of exposure.
– It can occur by light scattering from IOL edge, glistenings or
calcifications.
calcifications
1029
• Blinding or reflected glare
– This comes from light reflected off smooth, shiny
g
,
y
surfaces such as water, sand or snow.
– It can be strong enough to block vision.
– Reflected light is polarized and requires polarized
lenses to reduce it optimally.

1030
All being measured to make an
an…

Eye of the Thief

Eye of the Eagle

1031
Another Pre-LASIK examination
Pre LASIK
• Understand the Cornea  Measuring the biomechanical
g
properties of the cornea
• Is to quantify various corneal conditions by means of a
measurable and repeatable metric.
• Low Corneal Hysteresis (CH) demonstrates that the
cornea is less capable of absorbing (damping) the
energy of the air pulse.
pulse
• The differences in CH between normal and
compromised corneas are highly evident, and lead some
experts to theorize that normal eyes exhibiting
t t th i th t
l
hibiti
significantly lower than average CH may be at risk of
developing corneal disorders in the future.
1032
How does it work?
• The Ocular Response Analyzer utilizes a rapid
air impulse, and an advanced electro-optical
system to record two applanation pressure
d
l
i
measurements; one while the cornea is moving
inward,
inward and the other as the cornea returns
returns.
• Due to its biomechanical properties, the cornea
resists the dynamic air puff causing delays in the
inward and outward applanation events,
resulting in two different pressure values
1033
How does it work?
• The average of these two p
g
pressure values
provides a repeatable, Goldmann-correlated IOP
measurement (IOPG).
• Th difference b
The diff
between these two pressure
h
values is Corneal Hysteresis (CH); a new
measurement of corneal tissue properties that is
a result of viscous damping in the corneal tissue.
• The ability to measure this effect is the key to
understanding the biomechanical properties of
the cornea.
1034
How does it work?

Ocular Response
Analyzer (Reichert)

1035
How does it work?
• The CH measurement also provides a basis for
two additional new parameters: CornealCompensated Intraocular Pressure (IOPCC) and
Corneal Resistance Factor (CRF). IOPCC is an
Intraocular Pressure measurement that is less
affected by corneal properties than other
ff t d b
l
ti th
th
methods of tonometry, such as Goldmann
(GAT).
(GAT) CRF appears to be an indicator of the
overall “resistance” of the cornea
1036
Standard vs Customized LASIK
STANDARD

CUSTOMIZED

• No data necessary
y
• Correct defocus only
(Sphere & Astigmatism)
y ()
• Contrast sensitivity (-)

• Use aberration data
• Correct both defocus
and High order
aberration
• Contrast sensitivity
(++)
1037
Aberrometer Zywave
Complete Wavefront Analysis

Zylink 
Generation of optimized Laser
Treatment

OrbScan IIz
Corneal architecture

Laser System

1038
Eye registration
The integrated procedure
•

Ease of Use: Fully automated imaging with online data quality check

WASCA

WASCA

MEL 80

Wavefront
Acquisition

Reference
Image

Surgical
Image

1039
Microkeratomes
•
•
•
•
•
•

Hansatome (Bausch & Lomb)
Moria Evolution 3E (Moria)
Gebauer SL (Gebauer Medizin)
G b
(G b
M di i )
Zyopic XP (Bausch & Lomb)
ML7 (Med Logics Inc)
(Med-Logics,
Amadeus II (AMO, Inc 
Ziemer)

• Make ‘Hinged Flap’
• Take 110 – 180 um
corneal thickness

1040
Microkeratome

Animation

1041
Some kind of older microkeratomes : A Hansatome (Ba sch & Lomb);
A.
(Bausch Lomb)
B. LSK-one (Moria); C. Amadeus (Abbott Medical Optics); D. MK-2000
(Nidek)

1042
Hinged flap

Animation

1043
Femtosecond Laser
• A femtosecond is one millionth of a
nanosecond or 10-15 of a second and is
a measurement used in laser technology
• Procedure of laser corneal flap making
– Increased accuracy and predictability for
corneal flap thickness
– Faster
– Better visual outcomes
1044
Femtosecond Laser
•

Range of uses
– Flap creation 
•
•
•
•
•

IntraLase FS (Abbott Medical Optics)
CUSTOMFLAP TECHNOLAS (Perfect Vision)
FEMTO LDV CrystalLine(Ziemer)
VisuMax (Carl Zeiss Meditec AG)
WaveLight FS200 (Alcon Inc)
g
(
)

– Presbyopia surgery  INTRACOR TECHNOLAS (Perfect Vision)
– CUSTOMSHAPE TECHNOLAS (Perfect Vision)
•
•
•
•
•
•

Astigmatic Keratotomy (AK)
Limbal Relaxing Incisions (LRIs)
Penetrating and Lamellar Keratoplasty (PK/LK)
Endothelial Keratoplasty (FL-EK)
Intrastromal segment insertion  ring implantation (ICRS)
Cross-linking

– Even for glaucoma patient and Cataract surgery
1045
Femtosecond Laser
• Pulse of energy
– Low  Less than 1 µJ
– High  1 µJ and above

• Pulse of frequency
– Low  Bellow 80 kHz
– High  Above 100 kHz
1046
Femtosecond Laser
• High pulse energy and Low pulse
frequency
– IntraLase FS (Abbott Medical Optics)
– TECHNOLAS (Perfect Vision)

• Low pulse energy and High pulse
q
y
frequency
– FEMTO LDV CrystalLine(Ziemer)
– VisuMax (Carl Zeiss Meditec AG)
su a (Ca e ss ed tec G)
1047
Femtosecond : The IntraLase FS
The IntraLase laser
produces tiny bubbles
to be able to lift up the
surface of the cornea
The ability to precisely place
the bubbles up to the edge of
cornea enables an exact
preparation of the flap
The corneal flap is
opened up in order to
treat the deeper layers
of cornea
f
EuroEyes, 2008

1048
Another “Flaps”
Flaps
• Hinged Flap 
– Lasik
– Epi-Lasik  Epi-K (Moria)
– SBK  One Use-Plus SBK (Moria)
• Smaller flap diameter  8 5 mm
8.5
• 100-115 microns flap thickness
• 50% fewer fibers being cut than a 150 microns flap

• Epithelial Scrubber  PRK
– Amoils Epithelial Scrubber
1049
Eyetracker

1050
Decentered ablations : Causes
•
•
•
•
•
•
•

Saccadic eye movements
Improper head alignment
Cyclotorsion
Pupil shift
p
Centroid shift
Eye rolling
Technical misalignment of the laser beam
1051
Cyclotorsion

Diagnostic

Treatment

1052
Cyclotorsion
•
•
•
•

Eye rotates 3.7° + 2.3°
y
Some until 9.1°
60% counter clockwise
counter-clockwise
40% clockwise

1053
Cyclotorsion
•
•
•
•

Iris Recognition
Iris Registration
Eye-Tracker
Dynamic Rotational Eye-Tracker (DRET)

1054
JUST FOR YOU AND SAFETY

Iris structure
i

finger print
fi
i

•Safe
S f
•Compensate pupil center shift & cyclotorsion

1055
SAFETY
• Adapted for medical use from military technology
utilized for high l
tili d f hi h level security control
l
it
t l

1 out of 3,493..E24 or
1 out of 3 493 000 000 000 000 000 000 000
t f 3.493.000.000.000.000.000.000.000
There are not more than 10.000.000.000 people or
20.000.000.000
20 000 000 000 eyes on earth
th
1056
Eyetracker : Ability
y
y
• Not all eyetrackers are created equally.
• The new generation e etracker has a sampling rate
ne
eyetracker
faster than 200 Hertz.
• The reason why this is so important is because your eye
can twitch at a rate of 60 Hz
Hz.
• If the eye twitches faster or at the same speed as the
eyetracker then the eyetracker may not be able to get
the appropriate readings of the movement of the eye
eye.
• In turn, the laser may not be able to place the right pulse
of the laser in the appropriate section of the cornea
because of the lack of information.
information
• What is also extremely important is the ability of the laser
to react to the information being sent to it from the
eyetracker.
eyetracker
1057
Eyetracker : Ability
y
y
• What is also extremely important is the ability of the laser
to react to the information being sent to it from the
eyetracker.
t k
• The response time of the laser must be very fast to
ensure that each laser pulse is placed exactly on the
appropriate part of the cornea
cornea.
• Even if the laser can sample the movement of the eye
1000 times but the laser reacts slowly to this information,
the result is that the laser may be placing pulses on
areas of the cornea based on old information.
• The best example of the relationship between the
eyetracker and the laser is to try and imagine throwing a
ball at a moving object that is going 200 miles an hour.
• Although we can see the moving object, our reflexes are
too slow to adjust to the constant changes of the moving
object.
1058
Eyetracker : Ability
• As a result, every time you throw the ball you are
,
y
y
y
missing the moving object. Slow or older lasers
work on the same principle.
• Al h
Although the eyetracker can see the eye
h h
k
h
moving, it is too slow to react and may miss the
targeted area of the cornea
cornea.
• Eyetracker with the ability to react between 4 to
8 ms  optimizes the ability of each pulse being
placed on the appropriate spot on the cornea
reducing erroneous misplaced pulses of the
laser more common on older laser technology
1059
Laser ablation

1060
Laser ablation
•
•
•
•

Extremely p ec se ab a o s
e e y precise ablations
Disrupting molecular bonds
Vaporising material
Without generating heat

1061
ArF Laser (Photoablation)
• Laser energy ArF = 6.0 eV
• Tissue inter-molecular bond = 3.5 eV
• Ablation  Cut the bond

Laser 6.0 eV

3.5 eV
1062
0.25 um

1063
Energy distributions
Heterogen

Homogen

1064
Beam Size and Profile
• A small diameter laser beam or also known as spot
p
size is very important for both accuracy and
smoothness.
• An ideal beam size is approximately 1mm or less.
less
• If the size of the laser beam is larger the result is that
the beam is too large to make fine adjustments
throughout the cornea.
• Imagine filling a fishbowl with marbles compared to
filling is with sand.
• The marbles allow gaps while the sand contours and
fills the fishbowl exactly.
1065
Beam Size and Profile

1 mm vs 2 mm
1066
Laser Beam Profile
• Gaussian Beam
• Flat Top
• T
Truncated Gaussian Beam
t dG
i B

1067
Gaussian Beam
• Energy not well homogene distributed
• Hi h energy on central
Higher
t l
• Lower energy on peripheral
Energy

Ablation Threshold

Heat sensation
1068
Gaussian Beam
• Advantage : Smoother ablation profile
• Disadvantage : Heat sensation
Energy

Ablation threshold

Absorbed as heat
1069
1070
Flat Top Beam
p
• Homogen energy distribution
• No heat
• Less smooth ablation profile
Energy

Ablation threshold

1071
Truncated Gaussian Beam
• Bausch & Lomb Combine all benefits of Gaussian
Beam + Flat Top Beam
• Smooth ablation surface
• No heat no residual energy
heat,
Energy

Ablation threshold

1072
Gaussian Beam

Flat Top Beam

Truncated Gaussian Beam
u c ed G uss
e

1073
Laser treatment
• WaveLight EX500 (Alcon Inc)
• VISX Star S4 IR Advanced CostumVue (Abbott
Medical Optics)
• MEL 80 and MEL 90 (Carl Zeiss Meditec)
(Carl-Zeiss
• TECHNOLAS Perfect Vision
– SUPRACOR is a new corneal approach to treating
pp
g
presbyopia with TECHNOLAS Excimer Workstation
217P

•
•
•
•

Z LASIK (Ziemer)
(
)
Pulzar ZI (CustomVisc)
LaserSoft (Katana Technologies)
Schwind Amaris (Schwind Eye-Tech)
1074
Laser treatment

Animation
1075
Rinse and Fl closing
Ri
d Flap l i

Animation
1076
Special Laser Vision Correction
• Reduce aberrations
• Improve contras sensitivity
– Scotopic
– Intermediate Mesopic
– Photopic

• Improve reading speed
• Improve the ability to special task force 
p
y
p
Astronauts and Fighter-Pilots
– NASA, US Navy Aviation and US Air Force
– Using :
• iDesign Advanced WaveScan (Abbott Medical Optics)
• 5th Generation Femtosecond IntraLase FS 
iFS Advanced Femtosecond Laser (Abbott Medical Optics)  10
seconds only
• VISX Advanced CustomVue Technology (Abbott Medical Optics)
1077
Once more : Lasik

1078
Flap & Stromal Thickness Analysis

1079
Presby LASIK
y
• Monovision LASIK
• Pseudo-accommodative cornea 
PAC Nidek EC 5000 Excimer Laser (Nidek Co Ltd)

• Aspheric-multifocal cornea 
VISX CustomVue STAR S4 IR Aspheric (Abbott
Medical Optics)

• Lens Femtosecond laser treatment  100
microns thi k
i
thickness th t corresponds t 2 3
that
d to 2-3
Diopters 
INTRACOR (TECHNOLAS Perfect Vision)
1080
Non LASIK Presby Laser
Illuminating LaserACE
• Bladeless microsurgical procedures
• Ablate scleral tissue  Restoring Eye’s natural
Eye s
accommodative ability
• VisioLite Er:YAG Ophthalmic laser system 
LaserACE (ACE Vision Group, USA)
• Laser ablations made in 3 Scleral critical zones

EyeWorld, June 2008

1081
Laser : Miscellaneous Application
• Femtosecond laser assisted Descemet stripping
Endothelial keratoplasty (FS-DSEK)
• Laser suturolysis
• Bleb remodeling
Go opu ctu e
• Goniopuncture
• Laser in DCR
Lids,
• Lids Trichiasis and Punctal occlussion

1082
Laser : Miscellaneous Application
• Deep sclerotomy
• Anterior hyaloidotomy
• Persistent pupilary membrane
removal
• Lysis of vitreous strand

1083
Laser Phacoemulsification
• 2940 nm Erbium:YAG Laser
– Erbium:YAG Phacolase (Carl Zeiss Meditec AG)

• Neodymium:YAG Laser
– Neodymium:YAG Photon Laser PhacoLysis System (Paradigm
Medical)
– Dodick Q-Switched Neodymium:YAG laser (ARC GmbH)

• Femtosecond Laser
– Vi t (TECHNOLAS P f t Vi i )
Victus
Perfect Vision)
– Alcon LenSx (Alcon Inc)  Rhexis, Incision, Nuclear
fragmentation, Limbal Relaxing Incision (LRI)
– L
LensAR
AR
– Catalys (OptiMedica)
– Femto LDV Z Models (Ziemer-S)*
Kohnen T, Koch DD, 2005; Auffarth G, 2010; EyeWorld 2010; Salz JJ, 2010

1084
Laser Phacoemulsification

1085
Acknowledgement
• All My Teachers in Department of Ophthalmology,
Airlangga University, Medical School, 1913
• All My Friends in Laser and Advanced Eye Care Team of
Sumatera Eye Center
• All My Teachers from IOA/Perdami, InaSCRS, ESCRS,
Euretina, APAO, APACRS, ASCRS, EuCornea, AAO,
IIRSI, ICO, AIOS, Cicendo Eye Hospital Bandung,
Jakarta Eye Center, SN Feodorov MSC Moscow, Yale
Eye Center and Yale School of Medicine, Beijing
Tongren Hospital, Mitsui Hospital Tokyo, and Singapore
National Eye Center
1086
And also special thanks to
•
•
•
•
•
•
•
•
•

Alcon, Inc
Bausch & Lomb Incorporated and TECHNOLAS
Abbott Medical Optics
Carl Zeiss Meditec AG
Heidelberg E i
H id lb
Engineering
i
OCULUS Optikgeräte GmbH
Haag Streit
Ziemer
Allergan
g

© May 20, 2008 – 2014
See also: gedepardianto blogspot com
gedepardianto.blogspot.com
Any suggestions : gedepardianto@yahoo.com
1087
Main references
• American Academy of Ophthalmology, Basic and Clinical
Science Course
• Kanski JJ Clinical Ophthalmology
JJ,
• Deborah Pavan-Langston, Manual of Ocular Diagnosis and
Therapy
• Will’s Eye Manual
y
• Vaughan DG, General Ophthalmology
• Kohnen T, Koch DD, Cataract and Refractive Surgery
• Journal of Cataract and Refractive Surgery, Ophthalmology,
g y, p
gy,
American Journal of Ophthalmology, British Journal of
Ophthalmology, Clinical Ophthalmology
• ESCRS, EUROTIMES
• ASCRS EyeWorld USA
ASCRS, E W ld
• APACRS, EyeWorld Asia-Pacific
• Retina Today
• Retina Physician
1088
Support Team
• Sight for a Lifetime.TM
• Bi h
Bring hope t th li ht TM
to the light.
• ACT-G.TM

1089
Sail across Pacific Ocean of the 150 years of Gold Rush in
California ,USA, 1999
USA
© 2008-2014.

100 tahun Kebangkitan Nasional…

KRI Dewaruci : Duta antar bangsa dan lambang kejayaan bangsa bahari

Gede Pardianto - MataPedia2014 for Ophthalmologist

  • 1.
    2014’s 2014’ MataPedia M t Pdi TM for Ophthalmologist (Slides Compilation) Gede Pardianto Sumatera Eye Center Medan Indonesia M d -I d i
  • 2.
    The information providedwithin this book is for educational and scientific purposes only and it should not be construed as commercial advice. Author thanks all of our teachers, fellow ophthalmologists, publishers, sponsors, and all manufacturers for their works those all being cited in this handout book. FREE COPY NOT FOR SALE 2
  • 3.
    • Being anophthalmologist doesn’t mean you can be the rich person or you can do everything. As a little light, the sincerity you can perform in your meaningful life is giving a humble tribute to humanity by serving the people against blindness. Gede Pardianto May 20, 2008 3
  • 4.
    Gede Pardianto • Graduate from – – – • Office – – – • Doctorof Medicine  Airlangga University Ophthalmologist  Airlangga University Doctor of Philosophy  Sumatera Utara University p y y Dr. Komang Makes Hospital Sumatera Eye Center Sumatera Utara University, Medical School y Member of – – – – – – – – IOA InaSCRS APACRS ESCRS ASCRS EuCornea AAO ICO 4
  • 5.
    Here are awardedto the souls of the valiant who gave their lives in the service of their country and who sleep in unknown graves… All Indonesian heroes… Some there be which have no sepulchre. Airlangga University - Medical School 1913 But their name liveth for evermore. Dedicated to 100 Years of the Spirit of Nationality 1908 – 2008 y y and 1 Century of Medical Education in Surabaya 1913 – 2013 5
  • 6.
    Basic and Latest Spiritof Bali Only one on earth
  • 7.
    Visual functions including: • • • • • • Visual acuity Visual fi ld Vi l field Color vision Dark adaptation Contrast sensitivity Binocular single vision 7
  • 8.
  • 9.
    Examination : Finger • • • • Fingercounting Confrontation t t C f t ti test Digital tonometry Open the eye lid 9
  • 10.
    Confrontation Visual Fieldtesting • Technique – Examiner sated about 1 meter opposite patient – Patient directed to cover one eye and fixate on y examiner’s opposite or nose – Patient asked whether examiner’s entire face is visible or specific portions are missing – Patient asked to identify a target of 1,2 or 5 presented at the midpoint of each of four q p quadrants in a p plane halfway between the patient and examiner American Academy of Ophthalmology 10
  • 11.
    Confrontation Visual Fieldtesting – Patient is asked to add total number of fingers g presented in opposing quadrants (double simultaneous stimulation) – A h i uncooperative, sedated i t b t d or very Aphasic, ti d t d intubated young patient can use finger mimicry, pointing, visual tracking or reflex blink to respond and allow gross appraisal of VF integrity. If a patient saccades to a visual stimulus in a given quadrant, the visual field area can be considered to be relatively intact – Check patient’s ability to distinguish color of red object when looking directly at it American Academy of Ophthalmology 11
  • 12.
    Examination : Atleast • • • • • • • • • • • • • • Optotypes charts Phoropter and/or Trial lens and frame Torch Slit lamp Jaegger’s reading chart Lensometer L t Color test  Ischihara’s pseudoisochromatic plates Tonometer Fluorescein for Defect and Siedel’s test Siedel s Ophthalmoscope Amsler grid and Red dots Ruler Placido disc keratoscope Whatman No. 41 paper by 5x30mm for Schirmer test 12
  • 13.
    Examination : Phoropter •A device containing different lenses used for refraction of the eye during sight testing • The instrument used to measure refractive status of the eyes. • It contains many lenses which are then changed in front of the eyes while the p patient is looking at an eye chart. g y • This is when the doctor usually asks, "Which is better, one or two?" 13
  • 14.
    Examination : Optotypes •High contrast visual acuity – Snellen chart – Bailey Lovie chart Bailey-Lovie • Low contrast visual acuity – Reagan chart 14
  • 15.
    Examination : Torch •Light perception • Projection of Illumination / Light projection • Macula Photostress Recovery Test – – – – – Measure visual acuity first Place torch 2 cm from eye 10 seconds illumination Measure visual acuity again Record th ti R d the time needed f recovery b k t previous visual d d for back to i i l acuity – 55 seconds  normal – Larger (90 180)  macular dysfunction (90-180) • Pupil examination • Crude anatomical screening Deborah Pavan-Langston 15
  • 16.
    Examination : Slitlamp • How to adjust – Up and down – Horizontal move – Pupil distance – Light – Angle – Slit maneuver and rotation d t ti – Color option 16
  • 17.
  • 18.
    Examination : Ophthalmoscope •How to use : – Power switch – Size of illumination – Diopter – Color  Red free – Placido disc  Crude 18
  • 19.
    Dilating drops • Mydriatic –Phenylephrine 2.5%, 10%  20 min  3 hours • Cycloplegics – – – – – Tropicamide 0.5%, 1%  20-30 min  3-6 hours Cyclopentolate 0.5%, 1%, 2%  20-45 min  24 hours Homatropine 2%, 5%  20-90 min  2-3 days Scopolamine 0.25%  20-45 min  4-7 days Atropine 0.5%, 1%, 2%  30-40 min  1-2 week(s) Will’s Eye Manual, 2004 19
  • 20.
    Examination : Amslergrid • Boldly cross-hatched paper • Will b mandatory i : be d t in – Metamorphopsia – Central scotoma – Discomfort “perfect” vision – Color vision disturbance 20
  • 21.
  • 22.
    To use thegrid g • Sit in an area with good lighting, and hold the chart at eye level and at a comfortable distance • You may find it convenient to attach the grid to a wall at eye level and stand 12 inches to 14 inches away (comfortable reading distance) • If you wear glasses, keep them on. If you wear bifocals, use the bottom or reading portion of the lens • Cover one eye completely • Stare with your other eye at the central dot on the grid. While doing this, observe the pattern of vertical and horizontal lines • Repeat the test with the other eye 22
  • 23.
    Schirmer test I • • • • • • • • WhatmanNo. 41 paper p p Filter strip 5x30mm, folded 5mm Dimly light room Place l Pl lower palpebral conjunctiva at it l t l 1/3 l b l j ti t its lateral Eye kept open and look upward Blinking is permissible Remove after 5 minutes 10-30 mm wet  normal or basal secretion may be low but compensated for by reflect secretion • Less than 5 mm wet  repeated  hyposecretion of basic tearing Deborah Pavan-Langston, 2008 23
  • 24.
    Examination : Add1 • • • • • • • • • • • 76 or 90 D lens Goldmann’s 3 mirrors lens Hruby lens Indirect hth l I di t ophthalomoscopy Manual or automatic keratometry Standard A-Scan biometry A Scan Retinometer WFDT Prisms Streak retinoscopy Hertel s Hertel’s exophthalmometer 24
  • 25.
    Examination : Goldmanns 3 Mirrors Goldmann’s • • • • Central Oval O l Trapezium Square : Posterior pole :G i Gonioscopy : Equator : Periphery 25
  • 26.
    Examination : Add2 • Visual field test  – – – – Bjerrum’s tangent screen Goldmann’s perimetry SAP, SWAP, FDT, HPRP For AMD  Preferential Hyperacuity Perimeter (PHP)  Foresee PHP (Notal Vision) – For Retina  Micro Perimeter MP-1 (Nidek) • Advanced biometry – Partial Co e e ce Laser Interferometer a t a Coherence ase te e o ete – Non-contact Optical Coherence Biometry – Laser Interferometry Technique • Advanced High Definition AB-Scan USG g – Aviso (Quantel Medical) – VuMax II (Sonomed) • Standard digital fundus camera with FFA g – VisuCam (Carl Zeiss Meditec AG), AFC-330 (NIDEK) 26
  • 27.
    Visual Field Analyzers FDTPerimetry Octopus 101 Perimetry Goldmann Perimetry Humphrey Perimetry 27
  • 28.
    Examination : Add2 • Advanced anterior examination – Pachy-Autorefrakto-Keratometer • PARK 1 (OCULUS Optikgeräte GmbH) • Galilei G4 (Ziemer)  Placido and Dual Scheimpflug – Anterior Optical Coherence Tomography • Visante OCT (Carl Zeiss Meditec AG) • SL OCT (Heidelberg Engineering) • TOMEY SS-1000 (TOMEY GmbH) – Scheimpflug Camera Pentacam  Keratometry Corneal Keratometry, topography, Pachimetry, Corneal wavefront, AC and angle analyzer, Lens analyzer, Phakic IOL and Post refractive surgery biometry y • Pentacam HR (OCULUS Optikgeräte GmbH) 28
  • 29.
    Examination : Add2 • Advanced anterior examination – Keratograph  Oculus Keratograph (OCULUS Optikgeräte GmbH) – E d th li Endothelium S Specular Mi l Microscope – Advanced High Definition Ultrasound Biomicroscopy ( (UBM) ) • P60 UltrasoudBioMicroscope (Paradigm) • Aviso (Quantel Medical) • VuMax (Sonomed) – Very high frequency (VHF) ultrasound eye scanner  Artemis (ArcScan, Inc) – HRT3 with Cornea Module (Heidelberg Engineering) 29
  • 30.
    Advanced anterior examination Artemis(ArcScan, Inc) P60 UltrasoudBioMicroscope (Paradigm) Visante OCT (Carl Zeiss Meditec AG) Pentacam HR (OCULUS Optikgeräte GmbH) 30
  • 31.
    Examination : Add2 • Advanced posterior examination – Posterior Optical Coherence Tomography • St t OCT (C l Z i M dit AG) Stratus (Carl Zeiss Meditec • 3D OCT 2000 FA Plus Swept-Source SS OCT and DRI (TopCon) ( p ) • 3D OCT-1 Maestro OCT (TopCon) • RS3000 Advance (Nidek) • RTV FD OCT (O t RTVue (Optovue) ) • High Definition Cirrus + SmartCube HD OCT (Carl ) Zeiss Meditec AG) • SOCT Copernicus (Reichert) • HRA OCT Spectralis (Heidelberg Engineering) • E i P di t i SDOCT (bi ti Envisu Pediatric (bioptigen) ) 31
  • 32.
    Examination : Add2 • Advanced posterior examination – Scanning Laser Ophthalmoscopy • OCT-SLO (Opko Instrumentation) • O t Ultra Widefield I Optos Ult Wid fi ld Imaging S t i System (O t ) (Optos) – Scanning Laser Polarimetry • GDxVVC  Glaucoma Diagnosis - Variable g Corneal Compensation (Carl Zeiss Meditec AG) – Confocal Scanning Laser Tomography 3 e de be g et a o og ap y • HRT3  Heidelberg Retinal Tomography (Heidelberg Engineering) 32
  • 33.
    Stratus OCT (CarlZeiss Meditec AG) RTVue FD OCT (Optovue) HRA-OCT Spectralis (Heidelberg Engineering) HRT3 (Heidelberg Engineering) GDxVCC (Carl Zeiss Meditec AG) Cirrus HD OCT (Carl Zeiss Meditec AG) 33
  • 34.
    Examination : Add2 • Pediatric visual examination – Pictures cards  Allen card – Letter  HOTV – Matching games  Lea symbols • Binocular vision test – Titmus, TNO, Lang, Madox’s Rod, – Bargolini striated test – Hering-Bielschowsky afterimage test • Al f t t Also for teatment  t – Synophtophore – Holme’s stereoscope • H Hess S Screen • ERG and EOG • Visual Evoked Potential (VEP) 34
  • 35.
    Contrast sensitivity tester •Aberrometry • Glare – Letter  Pelli-Robson Chart Pelli Robson – Grating  • • • • • Functional Acuity Contrast Test (FACT) Chart Contrast Sensitivity Tester 1800 Landolt-C based Miller Nadler Glare Tester Frankfurt-Freiburg Contrast and Acuity Test System (FF-CATS) Grating-based Charts CSV-1000 (Vector Vision) – Scotopic testing  lower than 0.032 cd/m 0 032 cd/m² • Rodenstock Nytometer (Rodenstock) • Mesoptometer (Oculus Optikgeräte GmbH) • Scatter – Van den Berg Stray Lightmeter • Haloes – Tomey G a e a d Halo So t a e ( o ey) o ey Glare and a o Software (Tomey) Kohnen T, Koch DD, 2005 35
  • 36.
    Examination equipment • • • • • • • • Well accepted pp Wellapproved Well proven Easy to learn its manual Easy to use Easy and comfortable for patient Easy to make accurate and reliable interpretation Reproducible 36
  • 37.
  • 38.
    American Academy ofOphthalmology Neuroectoderm -Neuresonsory retina -Retinal p g e t ep t e u et a pigment epithelium -Pigmented ciliary epithelium -Nonpidmented ciliary epithelium -Pigmented iris epithelium -Sphincter and dilator muscles of iris -Optic nerve, axons, and glia -Vitreous DERIVATIVES OF EMBRYONIC TISSUES : ECTODERM Cranial Neural Crest cells -Corneal stroma and endothelium -Trabecular meshwork -Sheaths and tendons of extraocular muscles Sheaths -Connective tissues of iris -Ciliary muscles -Choroidal stroma -Melanocytes (uveal and ephitelial) g p -Meningeal sheaths of the optic nerve -Schwann cells of ciliary nervers -Ciliary ganglion -All midline and enferior orbital bones, as well as part of orbital roof and lateral rim -Cartilage -Connective tissues of orbit -Muscular l M l layer and connective ti d ti tissues sheaths of all ocular and orbital vessels h th f ll l d bit l l Surface Ectoderm -Ephitelium, glands, cilia of skin of eyelids and caruncle -Conjuntivital ephiyelium -Lens -Lacrimal glan -Lacrimal drainage system -Vitreous 38
  • 39.
    DERIVATIVES OF EMBRYONIC TISSUES : MESODERM • Fibersof extra ocular muscles • Endothelial lining of all orbital and ocular blood vessels l • Temporal portion of sclera • Vitreous American Academy of Ophthalmology 39
  • 40.
    American Academy ofOphthalmology 22 days Optic primordium appears in neural folds (1 5-3 0 mm) (1.5-3.0 mm). 25 days Optic vesicle evaginates. Neural crest cells migrate to surround vesicle 28 days Vesicle induces lens placode. Second Invagination of optic and lens vesicles. month Hyaloid artery fills embryonic fissure. Closure of embryonic fissure begins. Pigment granules appear in retinal pigment epithelium epithelium. Primordial of lateral rectus and superior oblique muscles grow anteriorly Eyelid folds appear. Retinal differentiation begins with nuclear and marginal zones. Migration f ti l ll begins. Mi ti of retinal cells b i Neural crest of corneal endothelium migrate centrally. Corneal stroma follows. y Cavity of lens vesicle is obliterated. Secondary vitreous surrounds hyaloid system. Choroidal vasculature develops. Axons from ganglion cells migrate to optic nerve. Glial lamina cribrosa forms forms. Bruch’s membrane appears. 40 .
  • 41.
    Third Precursors of rodsand cones differentiate. month Anterior rim of optic vesicle grows forward Ciliary body starts to develop. Sclera condenses. Vortex veins pierce sclera. Eyelid folds meet and fuse. Fourth Retinal vessels grow into nerve fiber layer near optic disc. month Choroidal vessels form layers. Iris t I i stroma is vascularized. i l i d Eyelids begin to separate. Sixth Ganglion cells thicken in macula. g month recurrent arterial branches join the choroidal vessels. Dilator muscle of iris forms. Seventh Outer segments of photoreceptors differentiate differentiate. month Central fovea starts to thin. Fibrous lamina cribrosa forms. Chorodial melanocytes produce pigment. Circular muscle forms in ciliary body American Academy of Ophthalmology 41
  • 43.
  • 44.
    Eye lid layer y y •Anterior lamellar – Skin and subcutaneus tissue – Muscles of protraction  Ocular orbicular muscle • Medial lamellar – O bit l septum Orbital t – Orbital fat – Muscles of retraction • Palpebral levator muscle • Muller’s muscle • Posterior lamellar – Tarsus – Conjunctiva American Academy of Ophthalmology 44
  • 45.
    OP : Ptosis 1.PSEUDOPTOSIS 2. CONGENITAL 3. ACUIRED – MYOGENIC • BLEPHAROPHIMOSIS SYNDROME • MYASTHENIA GRAVIS • PROGRESSIVE EXTERNAL • OPHTHALMOPLEGIA – NEUROGENIC PTOSIS • HORNER’S SYNDROME • MARCUS GUNN JAW WINKING • THIRD NERVE PALSY • BOTULISM • CEREBRAL PTOSIS – APONEUROTIC PTOSIS • INVOLUTIONAL PTOSIS • POST CATARACT SURGERY • POST EYELID TRAUMA • POST EYELID OEDEMA • POST CONTACT LENS WEAR – MECHANICAL PTOSIS • EYELID TUMOURS • ORBITAL LESIONS • CICATRIZING CONJUNCTIVAL DISORDERS • ANOPHTHALMOS 45
  • 46.
    Diagnostic keys g y • • • • • • Levator Function Marginreflex distance (MRD) Margin limbal distance ( g (MLD) ) Inter palpebral fissure Lid lag Bell’s phenomenon  Eye lid closing failure without moving eye ball upward or outward at the SAME time • Ocular motility 46
  • 47.
    Levator function • Themost practical measure of the strength of the levator muscle • Excursion of the upper lid from extreme down-gaze to extreme up-gaze • Normally 15 mm 47
  • 48.
    MRD • A simpleway to measure the height of the upper lid. • N Normally 4 5 mm ll 4-5 • MRD 1 = distance of the upper lid f from th corneal the l light • MRD 2 = distance of the lower eye lid from the corneal light reflex 48
  • 49.
    Skin Ski crease heightand strength h i ht d t th • The distance from the lid margin to crease – Men  6-8 mm, Asia  5-6 mm – Women  8-10 mm, Asia  7-8 mm • A weak levator muscle  creates less pull on the skin the crease is weak • MLD  Normal 9-10 mm 49
  • 50.
    System for Ptosissurgery Levator function > 10 mm < 10 mm Degree of ptosis Levator function < 2 mm > 2 mm > 2 mm < 4 mm Fasanella servat Aponeurosis surgery Levator resection Brow suspension Collin JRO, 1989 50
  • 51.
    System for myogenicptosis Collin JRO, 1989 51
  • 52.
  • 53.
  • 54.
  • 55.
    Fascia lata :How to get • • • • • • Mark outside of thigh 1/3 distally Skin incision 4-5 Ski i i i 4 5 mm  d ll undermine dull d i Find the white fascia Take 3 X 1.5 cm of fascia Suture the edge of fascia Suture sub cutan and skin 55
  • 56.
    OP : Entropion CLASSIFICATION: –C Congenital it l • Entropion • Epiblepharon – Acquired : • Involutional • Spastic y • Cycatrical 56
  • 57.
    Entropion : Involutional •Overriding of lower lid protractor muscle • Horizontal eye lid laxity  lateral and medial canthus ligament • Disinsertion or weakness of lower lid retractor muscle t t l • Fat atrophy enophthalmos • Anteriorly prolapse of orbital fat 57
  • 58.
    Involutional Entropion :Examination • Horizontal laxity – Pi h / Distraction t t Pinch Di t ti test – Snap back test • Medial canthal laxity • Lateral canthal laxity y • Vertical laxity  Retractor dehisence 58
  • 59.
    Pinch / Distractiontest • Distant between globe and lower lid g pull margin after full lower lid p out • None  5 mm • Mild  5 7 mm 5-7 • Moderate  10-12 mm • Severe  more than 12 mm 59
  • 60.
    Snap back test •Dynamic test  Pull downward lower lid margin then rapidly released • Normal  Lid margin back on its position spontaneous without blinking t ith t bli ki • Laxity  Not spontaneous back on position 60
  • 61.
    Medial canthal laxity •Lateral distraction test  Position shift of inferior lacrimal punctum • Normal  The punctum must be stable on semilunar plica while pulled to lateral – 1 2 mm shift i youth 1-2 hift in th – 3-4 mm shift in elderly • If any greater position shift  Laxity 61
  • 62.
    Medial canthal laxity 0 1 2 3 4 5 6 Gradeof Lancrimal punctum position shift 62
  • 63.
    Cycatrical Entropion Pathophysiology p y gy •Cycatric at posterior lamellar  Posterior lamellar shortening  lid margin inversion to the globe  Entropion  Trichiasis 63
  • 64.
    System for upperlid entropion Lid closure possible? Yes No Keratinisation of marginal tarso-conjunctiva? Corneal graft considered? Yes Lashes abrading cornea? Rotation of terminal tarsus No Posterior lamellar graft Yes No Tarsal excision No Yes Anterior lamellar reposition Tarsus thickened? Yes No Tarsal wedge resection Lamellar division +/- MM graft Collin JRO, 1989 64
  • 65.
  • 66.
    Congenital Entropion :Surgery • Congenital epiblepharon – Could be disappear by age – If there any punctate keratopathy Tarsal fixation 66
  • 67.
    Involutional Entropion :Surgery • Without lid laxity – Everting suture g – Wies procedures • With lid laxity – Wies procedures with tarsal strip 67
  • 68.
    Cycatrical Entropion :Surgery • Mild to Moderate – Anterior lamellar reposition (ALR) – Tarsotomy • S Severe – Posterior lamellar graft – Terminal tarsus rotation 68
  • 69.
    OP : Ectropion CLASSIFICATION: – Congenital – Acquired : • Involutional • Paralytic • Mechanical • Cycatrical 69
  • 70.
    Ectropion : Principalsurgery • Laxity – Tarsal strip – Pentagonal excision  Medial Canthal Medial, Canthal, Lateral – Medial canthus ligament shortening • Cycatrix – Ski graft Skin ft 70
  • 71.
    System of acquired ectropion p Shortageof skin? No Yes Normal eyelid closure? Cicatricial ectropion Yes Localized defect? No Paralytic t i P l ti ectropion Yes No Z - plasty Skin replacement Medial canthal tendom laxity? Yes Y No N Lump in lid Medial ectropion only? Yes No Involutional ectropion Mechanical ectropion t i Medical canthal resection No Yes Medical canthoplasty + lat canth. sling lat. canth Medical canthoplasty Ectropion mainly medial? Collin JRO, 1989 Yes No Horizontal lid laxity? Exess skin? No Horizontal lid shortening h t i Yes Horiz .lid short. + blepharoplasty bl h l t No Yes Excision of diamond of tarso-conjunctiva t j ti Med.canth. tendom lax? No Lazy - T Yes Med.canth. tendom placation or resection 71
  • 72.
  • 73.
    OP : Trichiasis •Cilia emerge from their normal anterior lamellar location • Associated with cicatrizing processes of the conjunctiva 73
  • 74.
    OP : Blepharospasme •Eye lid squeezing disorders • L Long standing  association with : t di i ti ith – Eye lid and brow ptosis – Dermatochalasis – Entropion – Canthal tendon abnormalities 74
  • 75.
    OP : Blepharophimosis -G Generalized narrowing of the palpebral li d i f th l b l fissure - A CONGENITAL ANOMALY - EPICANTHUS INVERSUS - MICROBLEPHARIA PTOSIS AND - VERTICAL STRETCHING OF THE BONY ORBIT 75
  • 76.
    COLOBOMA PALPEBRA or BLEPHAROSCHIZIS •FULL THICKNESS DEFECTS OF THE EYELIDS • RARE. UNILATERAL OR BILATERAL • THE CONFIGURATION  TRIANGULAR OR QUADRILATERAL • THE CORNEA EXPOSE  CORNEAL OPACITY • THE RISKS ARE GREAT INVOLVES THE CENTER OF THE LID 76
  • 77.
    OP : Blepharochalasis p •Thin and wrinkled eyelid skin • Familial variant of angioneurotic edema • Idiopathic episodes of inflammatory edema of the eyelid • Most frequently in young females • Younger patient than dermatochalasis • Different with Dermatochalasis  • Redundancy of eyelid skin • Often associated with orbital fat protrusion or prolapse • Upper eye lid  indistinct or lower than normal eyelid crease American Academy of Ophthalmology 77
  • 78.
    Contracted sockets • Causesof – Radiation – Extrusion of an enucleation implant – Severe initial injury – Poor surgical technique – Multiple socket operations –P l Prolonged periods of conformer or prothesis d i d f f th i removal American Academy of Ophthalmology 78
  • 79.
  • 80.
  • 85.
    Prof. dr. MardionoMarsetio, Sp.M(K) and Prof. dr. Wisnujono Soewono, Sp.M(K) Ocular surface 85
  • 86.
    Tear film :Functions • Maintains optical clear for cornea • Moistening, lubricating and protecting surface of conjunctiva and cornea • Inhibits microorganism growth by mechanism processes and anti-microbial h i d ti i bi l actions • Feeding the cornea Vaughn GD, 2000 86
  • 87.
    Tear film :Layers y • Monomolecular lipid layer – – – – • Superficial Origin from Meibomian glands Inhibits evaporation Closed palpebra  Water-tight barrier Aqueous layer – Origin from major and minor lacrimal glands – Water soluble salts and proteins • Mucin layer – Secreted principally by conjunctival goblet cells – Glycoprotein  coating conjunctiva and cornea – Absorbed by hydrophobic corneal epthelial cells membrane  on microvilio – Normally on 15-45 seconds of Break-up time test – Abnormally on less than 10 seconds of Break-up time test Vaughn GD, 2000 87
  • 88.
    Tear film :Formations • • • • • • Thickness  7-10 µm 7 10 Volume  7 + 2 µL each eye pH  7 35  vary from 5 20 8 35 7.35 5.20-8.35 Isotonic  295-309 m osmol/L Albumin Alb i  60% t t l protein total t i Defence mechanism by  Lisozym, Ig A, Ig I G and Ig E dI Vaughn GD, 2000 88
  • 89.
    Tear dynamics • Tearvolume is 10 µ L or less • The maximum volume of fluid that can be contained in the “cul-de sac” without overflow is 30 µL. • Th eye d The drop volume i approximately 40 µL l is i l L • The excess fluid instilled is rapidly removed by spillage j from the conjunctiva sac  until the tear fluid returns to its original volume • The reflex tearing after the instillation of an irritating drug may produce up to 400 µL excess tears tears. • Dilution of 5–50 fold usually occurs in the first 2 minutes, depending on the irritating power of the substance Cornea, 2002 89
  • 90.
    Ocular surface :Hyperemia • Conjunctival j • Corneal • Scleral 90
  • 91.
    Ocular surface :Red eye • • • • Conjunctivitis Uveitis Keratitis K titi Glaucoma 91
  • 92.
    Acute Conjunctivitis Acute Iritis Acute Glaucoma Acute Keratitis Incidence ++ + +/- + Secret ++ - - + VA - +/- ++ + Pain - + ++ +/++ Injection Diffuse, to fornices Circumcornea Circum cornea Circum cornea Cornea C Clear Cl Usually clear U ll l Cloudy Cl d Clearance Cl change Pupil Normal Small Oval dilated Normal or Small Light response Normal Decrease None Normal IOP Normal Normal Increase Normal Organism + No organism No organism Only in ulcers Swap 92
  • 93.
    Sign Injection Hemorrhage Chemosis Secret Pseudo membrane Bacterial Viral Allergic Toxic Trachoma Marked Moderate Mild/ Moderate Mild/ Moderate Moderate + + - - - ++ +/- ++ +/- +/- Purulent Scant/ Watery String/White - Scant +/- +/- - - - Streptococcus/ Corynebacterium Papillae +/- - + - - Follicles - + - + + (Medication) Peri auricular node + ++ - - +/- Pannus - - - - + (Except Vernal) 93
  • 94.
    Staining : Gram g •Older technique – – – – – 3 seconds of Carbol Gentian Violet on fixated object glass ¾ seconds Lugol solution 1 second 90% Alcohol Wash by water y 3 seconds Watery Fuhcin • New technique q – – – – – – – ½ - 1 second(s) Ammonium oxalate crystal violet Wash by water 1-2 seconds Lugol solution Wash by water 1 second Acetate alcohol Wash by water 1 second S ff d Sofframin i 94
  • 95.
    Staining : Giemsaand KOH • Giemsa – Giemsa solution : Aquadest  1 : 10 – 2 seconds Methanol on Fixated object glass – Waste and add 10-15 seconds Giemsa stain – Wash by water and make it dry y y • KOH – 1-2 drops 10% KOH on object g p % j glass – Place specimens on object glass – Covered with coverglass g 95
  • 96.
    Ocular surface :Conjunctiva j • Follicle – Focal lymphoid nodule y p – With accessory vascularization • Papilla – Dilated, talengiectatic conjunctival blood vessels , g j – Anchoring septa – Dot like changes to enlarged tufts, surrounded by edema and inflammatory cells • G Granuloma l – Nodule of chronic inflammatory cells – With fibrovascular proliferation • Phl t Phlyctenule l – Nodule of chronic inflammatory cells – Often at or near the limbus American Academy of Ophthalmology 96
  • 97.
    Follicle and Papilla p Areato be examined Follicles Papillae 97
  • 98.
  • 99.
    Phlycten and Phlyctenule y y Phlycten Phlyctenule Staphylococcus Delayedhypersesitivity Good Poor + - Limbus Without progression Limbus To central All ages g Children Cycatrix - + Recurrence - + Triangular Base at limbus Triangular Apex at limbus Topical antibiotic Steroid based on Underlying disease Etiology General condition Conjunctivitis Location Age Shape Therapy py 99
  • 100.
    Ocular surface: Cornea •Epithelium – 5-6 layer structure – 50 100 µm thickness 50-100 – Great sensitivity – Composed • Basal cells layer • Wing cells layer • Surface cells layer Deborah Pavan-Langston, 2008 100
  • 101.
    Ocular surface :Cornea • Bowman’s layer Bowman s – Homogenous condensation of anterior stromal lamellae • Stroma – 90% of corneal thickness – Bundles of collagen fibrils of uniform thickness enmeshed in mucopolysaccharide subtance bt – Maintain corneal clarity Deborah Pavan-Langston, 2008 101
  • 102.
    Ocular surface :Cornea • Dua’s Layer Dua s – Discovered by examining the separation that often occurs along the last row of keratocytes during the big bubble (BB) technique – Attached to the deep stroma – is not "residual stroma." – Distinct layer that is 10 15 ± 3 6 microns thick 10.15 3.6 between stroma and descemet membrane EuroTimes, 2013 102
  • 103.
    Ocular surface :Cornea • Descemet membrane – Basement membrane of the endothelial cells – Can be easily stripped – Homogenous glasslike structure – Anterior  Composed of stratified layers of very finecollagenousfilaments – Posterior  Amorphous layers that increases with age Deborah Pavan-Langston, 2008 103
  • 104.
    Ocular surface :Cornea • Endothelium – Single layer – 5 18 µm size of approximately 500 000 5-18 500,000 polygonal cells – Maintain corneal deturgescence – Contributes the formation of Descemet membrane Deborah Pavan-Langston, 2008 104
  • 105.
    Ocular surface :Cornea • Blood supply – Predominantly from • Conjunctival vessel • Episcleral vessel • Scleral vessel – Arborize about the corneoscleral limbus • Innervation – Sensory  mostly  ophthalmic division of the trigeminal nerve g – Is via long ciliary nerves that branch in the outer choroid near ora serrata region Deborah Pavan-Langston, 2008 105
  • 106.
    Ocular surface :Keratititis Location Marginal keratitis k titi Peripheral Bacterial keratitis k titi Central Size < 1 mm > 1 mm Epithelial defect Small or absent Present Uveitis Absent Present Kanski JJ, 2007 106
  • 107.
    Chemical trauma :Hudge Grade I II III IV Good Good Intermediate Poor Epithelial Epithelial Epithelial loss Hazy Iris/Pupil detail Visible Visible Blurred Very blurred Ischemia None <1/3 limbus 1/3 -1/2 limbus > 1/2 limbus Prognosis Broken cornea 107
  • 108.
    Corneal endothelial layer •Normal  2 000 – 3 000 cells / mm² 2,000 3,000 mm • Stressed  800 -1,500 cells / mm² • D Decompensate  < 500 cells / mm² t ll ² 108
  • 109.
    Keratoplasty • Penetrating Keratoplasty(PK) • Barron’s Keratoplasty • Sterile Cornea Allograft  VisionGraft (TBI/Tissue Bank International) • Deep Anterior Lamellar Keratoplasty (DALK) • Femtosecond laser-assisted Anterior Lamellar Keratoplasty (FALK) • Femtosecond laser-assisted Descemet Stripping Endothelial Keratoplasty ( dot e a e atop asty (F-DSEK) S ) 109
  • 110.
    Keratoprostheses: Boston KPro EuroTimes 2006 110
  • 111.
  • 112.
  • 113.
  • 114.
  • 115.
    Refraction Prof. Dr. dr.Admadi Soeroso, Sp.M, MARS 115
  • 116.
    Visual acuity • Vi Visualthreshold l th h ld – Light discrimination • • • • Brightness sensitivity (minimum visible) Brightness di i i ti ( i i B i ht discrimination (minimum perceptible) tibl ) Brightness contrast Color discrimination – Spatial discrimination • Minimum separable • Vernier acuity (hyperacuity)  – Separated by little as 3 5 seco ds o a c Sepa a ed e 3-5 seconds of arc – Considerable less than the diameter of single foveal cone – The basis of Amsler’s grid • Minimum legible acuities • Di t Distance di i i ti discrimination • Movement discrimination – Temporal discrimination • Flickering light American Academy of Ophthalmology 116
  • 117.
    Some basic acuity Type Description Pointacuity ( arc minute) y (1 ) The ability to resolve two distinct point targets. y p g Grating acuity (1-2 arc minutes) The ability to distinguish a pattern of bright and dark bars from a uniform grey patch. Letter acuity (5 arc minutes) The ability to resolve a letter. The Snellen eye chart is a standard way of measuring this ability. 20/20 vision means that a 5-minute letter target can be seen 90% of the time Stereo acuity (10 arc seconds) The ability to resolve objects in depth. The acuity is measured as the difference between two angles for a just-detectable depth difference. just detectable Vernier acuity (10 arc seconds). The ability to see if two line segments are collinear Healey CG, 2005 117
  • 118.
    Visual acuity indifferent notation FEET METERS MINIMUM ANGLE OF RESOLUTION LOGMAR DECIMAL NOTATION 20/10 6/3 0.50 -0.3 2.0 20/15 6/4.5 6/4 5 0.75 0 75 -0 1 0.1 1.5 15 20/20 6/6 1.00 0.0 1.0 20/25 6/7.5 1.25 0.1 0.8 20/30 6/9 1.50 1 50 0.2 02 0.7 07 20/40 6/12 2.00 0.3 0.5 20/50 6/15 2.50 0.4 0.4 20/60 6/18 3.00 3 00 0.5 05 0.3 03 20/80 6/24 4.00 0.6 20/100 6/30 5.00 0.7 20/120 6/36 6.00 6 00 0.8 08 20/150 6/45 8.00 0.9 20/200 6/60 10.00 1.0 0.1 20/400 6/120 20.00 20 00 1.3 13 0.005 0 005 American Academy of Ophthalmology 0.2 118
  • 119.
    Visual acuity :Development y p Age Visual acuity 2 months 20/400 (6/120) 6 months 20/200 (6/60) 1 year 20/100 (6/30) 2 years 20/60 (6/18) 3 years 20/30 (6/9) y 4-5 years 20/20 (6/6) ( ) Duke Elder 119
  • 120.
    Visual acuity :Various test in children AGE (Years) 0-2 0-2 0-2 02 2-5 2-5 25 2-5 5+ 5 VISION TEST VEP Preferential looking Fixation behavior Allen pictures HOTV E-Game Snellen h t S ll chart NORMAL 20/30 20/30 CSM CSM* 20/40-20/20 20/40-20/20 20/40 20/20 20/40-20/20 20/30-20/20 20/30 20/20 * CSM Method : Refers to Corneal light reflex, Steadiness of fixation and Maintain alignment American Academy of Ophthalmology 120
  • 121.
    Light : Basic •Wavelength of visible light  380-760nm 380 760nm • Velocity of light waves  – 300 000 k / 300.000 km/second or d – 86.000 mils /second • Character of light – Hue – Saturation – Brightness or Luminance 121
  • 122.
    Illumination • Radiometry – Measuresterm of power – Irradiance = watts per square meter, lamberts • Sunny day = 10,000 – 30,000 foot lamberts • Photometry – – – – – Measures units based on the response of the eye 1 candela = 12.6 lumens Illuminance = lumens per square meter Luminance of surface is amount of light that reflected or emmited Apostlib  surface perfectly emitting or reflecting 1 lumen per square meter – Ideally 100 watt lamp bulb provides about minimum • 600 foot candles 3 feet away • 150 foot candles 6 feet away American Academy of Ophthalmology 122
  • 123.
    Photobiology gy • Scotopic visionis the monochromatic vision of the eye in low light. Since cone cells are nonfunctional in low light, scotopic vision is produced exclusively through rod cells so therefore there is no color perception. Scotopic vision occurs at luminance levels of 10-2 to 10-6 cd/m². cd/m . • Mesopic vision occurs in intermediate lighting conditions (luminance level 10-2 to 1 cd/m²) and is effectively a combination of scotopic and photopic vision vision. This however gives inaccurate visual acuity and color discrimination. • Ph t i vision  I normal light (l i Photopic i i In l li ht (luminance l level 1 t l to 106 cd/m²), the vision of cone cells dominates  good visual acuity (VA) and color discrimination Lars Olof Björn, 2002 123
  • 124.
    The cone cells •Sharp photoreceptor • A human eye can see wavelengths in the range of 380 to 760nm. This range is called the visible region y yp , • Trichromatic Theory  3 types of cones, each with a different iodopsin (a photosensitive pigment) • Each type of iodopsin can absorb and respond to a range of wavelengths • Photosensitive pigments  – Erythrolabe  maximum absorption at 565nm (red) – Chl l b  maximum absorption at 535 Chlorolabe i b ti t 535nm ( (green) ) – Cyanolabe  maximum absorption at 440nm (blue) 124
  • 125.
  • 126.
    Chromatic aberration • Thetype of error in an optical system in which the formation of a series of colored images occurs, even though only white light enters the system. system • Chromatic aberrations are caused by the fact that the refraction law determining the path of light through an optical system contains the refractive index which is a index, function of wavelength. • Thus the image position and the magnification of an optical system are not necessarily the same for all wavelengths, nor are the aberrations the same for all wavelengths 126
  • 127.
    Chromatic aberration • Shortwavelength light focused more anterior than long wavelength li ht l th light • Violet focused more anterior than Red 127
  • 128.
    Spherical aberration • Ablurred image that occurs when light from the margin of a lens or g g mirror with a spherical surface comes to a shorter focus than light from the central portion. • Also called dioptric aberration 128
  • 129.
    Spherical aberration • • • • A perfectlens (top) focuses all incoming rays to a point on the optic axis A real lens with spherical surfaces (bottom) suffers from spherical aberration It focuses rays more tightly if they enter it far from the optic axis than if they enter closer to the axis It therefore does not produce a perfect focal point 129
  • 130.
    Spherical aberration • Mirrorspherical aberration • Reflective Caustic generated f d from a circle and parallel rays 130
  • 131.
    Accommodation table Age (years) Rateof Accommodation (Diopters) 8 13.8 25 5 99 9.9 35 7.3 40 5.8 58 45 3.6 50 1.9 55 1.3 Vaughan DG 131
  • 132.
    Refractive index (HeliumD Line) • • • • • • Air Water Cornea Aqueous and vitreous Spectacle crown glass PMMA 1.000 1.333 1.376 1.336 1 336 1.523 1.492 1 492 American Academy of Ophthalmology 132
  • 133.
    Refracting power (D) •Corneal system 43.05 – Anterior surface – Posterior surface 48.83 - 5.88 • Lens system – Relaxed – Maximum accommodation 19.11 33.06 33 06 • Complete optical system – Relaxed – Maximum accommodation 58.64 70.57 American Academy of Ophthalmology 133
  • 134.
    DIOPTER CONVERTION -MILIMETER K K Reading (D) Radius (mm) Reading (D) Radius (mm) 47.57 47.50 47 50 47.25 47.00 47 00 46.75 46.50 7.07 7.11 7 11 7.14 7.18 7 18 7.22 7.26 46.25 46.00 46 00 45.75 45.50 45 50 45.25 45.00 7.30 7.34 7 34 7.38 7.42 7 42 7.46 7.50 134
  • 135.
    Pinhole visual acuitymeasurement • If visual acuity improves  refractive error usually present • Disease of macula  – Unable to adapt to amount of light through the pinhole – Visual acuity can decrease markedly • M t useful  1 2 mm Most f l 1.2 – Refractive error – 5.00 to + 5.00 D American Academy of Ophthalmology 135
  • 136.
    Refraction Common Disorder Moderate Severe -1.00 t –4 00 1 00 to 4.00 Diopters -4.00 t – 6 00 4 00 to 6.00 Diopters -6.00 and above 6 00 d b Diopters Hyperopia +1.00 to +2.00 Diopters +2.00 to +4.00 Diopters +4..00 and above Diopters Astigmatism -1.00 to –2.00 Diopters -2.00 to -4.00 Diopters -4.00 and above Diopters Myopia Mild 136
  • 137.
    Refraction • Myopia (Nearsightedness) –Pathophysiology • Axial Curvature Increased index of refraction Axial, Curvature, – Severity • Mild Moderate High Mild, Moderate, – Clinical • Simplex/Stationary, Progressive, Malignant Deborah Pavan-Langston, 2008 137
  • 138.
    Myopia y p • • Children bornmyopic  small percentage  not become emmetropic by age 6-8 years Previously emmetropic children or h P i l t i hild hyperopic may b i become myopic i – Hyperopes greater than +1.50 D rarely become myopic and may become more hyperopic • • Prevalence of myopia begins to increase at about age of 6 y y p g g years Juvenile-onset myopia – 7-16 years of age – Primarily due to growth in globe axial length – L Largest i t increase i girls at age 9 10 years and i b in i l t 9-10 d in boys at age 11 12 t 11-12 years – Usually stops in middle teen years, 15 for girls and 16 for boys • • Myopia starting after 16 is less severe and less common y p g Adult-onset myopia – Begins at about 20 years of age – Risk factor  extensive near work American Academy of Ophthalmology 138
  • 139.
    Significant myopia inchildhood g y p • • • • Cycloplegic refraction are mandatory Full refractive error, including cylinder, should be corrected Young children tolerate cylinder well On theory  prolonged accommodation increase development of myopia – Some  undercorrection myopia – S Some use bif bifocal, with or without At i l ith ith t Atropine • Parents should be educated about – Progression of myopia – Need for frequent refraction – Possible prescription changes • • • Contact lenses  older children  avoid problem of image magnification by high minus lenses Intentional undercorrection f myopic esotrope  d I t ti l d ti for i t decrease th the angle of deviation  well tolerated Intentional overcorrection for myopic error  controlling ( ) exodeviation (some value) American Academy of Ophthalmology 139
  • 140.
    Refraction • Hypermetropia (Farsightedness) –Structural • Axial, Curvature, Index of refraction – Accommodative • Latent, manifest, total – Severity Uncorrected can causes • Strabismus  Esotropia • Ambliopia Deborah Pavan-Langston, 2008 140
  • 141.
    Correcting hyperopia inchildhood • No esodeviation and reduced vision  NOT necessary correcting low hyperopia • Significant astigmatic error must be fully corrected d • Hyperopia coexists esotropia  full correction of the cycloplegic refractive error • In a school age child  full correction may cause b u ed vision blurred s o – Because inability to relax accommodation fully – A short course of cycloplegia may help American Academy of Ophthalmology 141
  • 142.
    Clinical refraction • Refractionapproach  ARK • Subjective  Trial and error by trial optical lenses • Objective  Streak retinoscopy – Characteristic of reflex • Speed • Brilliance • Width – Four characteristic of STREAK reflex • • • • Break Width Intensity Skew American Academy of Ophthalmology 142
  • 143.
  • 144.
    Finding Neutrality • • • • • • • In againstmovement, the far point is between the examiner and the perfect therefore, to bring the far point to the examiner’s pupil, minus, lenses should be placed in front of the patient’s eye. patient s Similarly, in the case of with movement plus lenses should be placed in front of the patient’s eye. Similarly, in the case of with movement, plus lenses should be placed in front of the patient s eye patient’s eye. This leads to the simple clinical rule: if you see with motion, add plus lenses (or subtract minus); if you see against motion, add minus lenses (or subtract plus). Lens power should be added (or subtracted) until neutrality is reached y Since it is considered easier to work with the brighter, sharper with image, it is preferable to overminus the eye and obtain a with reflex and then reduce the minus (add plus) until neutrality is reached. , Be aware that the slow, dull reflex and then reduce the minus refractive errors may be confused with the pupil-filling neutrality reflex or with dull reflexes (as seen in patients with hazy media). Place high-power plus and minus lens over the eye and look again. American Academy of Ophthalmology 144
  • 145.
  • 146.
    Finding the cylinderaxis g y • Before retinoscope is used to measure the powers in each of the principal meridians, the axes of the p p meridians must be determined. • Characteristics of the streak reflex can aid in determining axis. – Break. A break is seen when the streak is not parallel to one of the meridians. The are projecting the line is discontinuous, or broken. The break disappears (ie, the line appears continuous) g when the streak is rotated on to the correct axis. The correcting cylinder should be placed at this axis. – Width. The width of the streak varies as it rotated around the correct axis. It appears narrowest when the streak aligns with the axis – Intensity. The intensity of the line is brighter when the streak is on the correct axis. (This is a subtle finding, useful only in small cylinders) American Academy of Ophthalmology 146
  • 147.
    Finding the cylinderaxis g y American Academy of Ophthalmology 147
  • 148.
  • 149.
    Finding the cylinderaxis g y American Academy of Ophthalmology 149
  • 150.
    Finding the cylinderaxis g y American Academy of Ophthalmology 150
  • 151.
    Finding the cylinderaxis g y American Academy of Ophthalmology 151
  • 152.
    Finding the cylinderpower • • Once the two principal meridians are identified, the axis separately in turn. With two spheres spheres. – Neutralize one spherical lens. If the 90º axis is neutralize with a +1.50 sphere and the 180º axis is neutralized with a +2.25 sphere, the gross retinoscopy would be +1.50 + 0.75 x 180. The examiner’s working distance should be subtracted from the sphere to obtain the refractive correction. • With a sphere and cylinder. – Neutralize one axis with spherical lens. To continue working using with reflexes, reflexes neutralize the lens plus axis first Then with this spherical lens first. Then, in place, neutralize the axis 90º away by adding a plus cylindrical lens directly from the trial lens application. The spherocylindrical gross retinoscope can be read directly from the trial lens application. • It is also possible to use two cylinders at right angles to each other for this gross retinoscopy ; however, this variant does not seem to provide any advantages over the other methods. American Academy of Ophthalmology 152
  • 153.
    Aberrations of theRetinoscopic Reflex • • • • • With irregular astigmatism, almost any type of aberration may appear in the reflex. Spherical aberration tend to increase the brightness at the center or periphery of the pupil, depending on whether the aberrations are positive or negative. As the point of neutrality is approached one part of the reflex may approached, be myopic while the other is hyperopic relative to the position of the retinoscope. This will produce the scissors reflex. Sometimes a marked irregular astigmatism or optical opacity produces confusing, distorted shadows that can markedly reduce confusing the precision of the retinoscopic result. In such as subjective refraction should be used. All of these aberrant reflexes become more noticeable with larger papillary di ill diameters. I these cases, considering the central portion In h id i h l i of the light reflex yields the best approximation. American Academy of Ophthalmology 153
  • 154.
    Summary of retinoscopy 1. 2. 3. 4. 5. Thesteps below summarize how to performing streak retinoscopy using a plus cylinder phoropter. Set the phoropter to 0 D sphere and 0 D cylinder. cylinder Use cycloplegia if necessary Otherwise fog the eyes or use a necessary. Otherwise, non accommodative target. Hold the sleeve of the retinoscope in the position that produces a divergent beam of light. (If the examiner can focus the linear filament of the retinoscope on a wall, the sleeve is in the wrong position) wall position). Sweep the streak of light (the intercept) across the pupil perpendicular to the long axis of the intercept and watch the papillary light reflex. Sweep in several different meridians. Use the right eye to examine the patient’s right eye, and use the left eye to examine the patient’s left eye. patient s Add minus sphere (dial up on a phoropter) until the retinoscopic reflex shows with motion in all meridians. Add a little extra minus sphere if uncertain. If the reflex are dim or indistinct, consider high refractive errors and make large changes in sphere ( D, -6 D, -9 D, etc). g g (-3 ) Add plus sphere (dial down on a phoropter) until the retinoscopic reflex neutralizes or shows a small amount of residual with motion in one meridian. If all meridians neutralizes simultaneously, the patient’s refractive error is spherical. Proceed to step 9. American Academy of Ophthalmology 154
  • 155.
    Summary of retinoscopy y py 6. 7. 8. 9. 10. Rotatethe streak 90º and set the axis of the correcting plus cylinder parallel to the streak. Sweep this meridian to reveal additional with motion. Add plus cylinder power until the remaining with motion is neutralized. neutralized Now the retinoscopic reflex should be neutralized in all meridiens simultaneously. Refine the correcting cylinder axis by sweeping 45º to either side of it. Move in slightly closer to the patient to pick up with motion. Rotate the axis of the correcting plus cylinder a couple of degrees toward the “guide” guide line, the brighter and narrower reflex. Repeat until both reflexes are equal. Refine the cylinder power by moving in closer to the patient to pick up with motion in all directions. Back away slowly, observing how the reflexes neutralize. Change sphere or cylinder power as appropriate to make all meridians neutralize simultaneously. Subtract the working distance. If working at 67 cm, subtract 1.5 D. if the examiner’s arms are short or the examiner prefers working closer, the p g , appropriate dioptric power for the distance chosen should be subtracted. Record the streak retinoscopy findings and, if possible, check the patient’s visual acuity after he or she has had time to wear the prescription and readjust to ambient room light. American Academy of Ophthalmology 155
  • 156.
    Retinoscopy: Final correction • • Ifwe use working lenses  Another correcting lenses  Final correction If for example in 50 cm working distance, we use S +2.00 working lenses, and we 2.00 get: Horizontal S -6.00 and Vertical S 3 00, t e 3.00, the Final correction: a co ect o – S -6.00 C +3.00 A 90 or, – S -3 00 C +3 00 A 180 3.00 +3.00 156
  • 157.
    Lenses • Meniscus Lensor Curve Lens  Lens with one spherical convex surface and the other spherical concave. Meniscus lenses often have a base of 6 D for the surface of lesser curvature. • Polarizing Lens A lens that transmits light waves vibrating in one direction only. In the other direction perpendicular to it, the light waves are absorbed In this way reflected glare absorbed. is reduced. 157
  • 158.
    The Basic Lenses (A),biconvex; (B), biconcave; (C), planoconvex; (D), plano concave; (E),concavoconvex, periscopic convex, converging meniscus; (F), convexoconcave, periscopic concave, diverging meniscus; (G, H), cylindrical lenses, concave and convex. MedDict 2007 158
  • 159.
  • 160.
    Sphere Lens Biconvex Lenses CaF2Lenses Plano Concave Lenses Biconcave Lenses Meniscus Sphere Lenses Changch Jixiang 2006 hun g, Plano Convex Lenses 160
  • 161.
    Spheric correction • Leastminus for myopia – More minus forces contraction of cilliary muscles for unnecessary accommodation  Fatigue • Most plus for hyperopes – Less plus retains accommodation 161
  • 162.
    Spherical aberrations • Moreperipheral rays focused anteriorly • Exacerbates myopia in low light (night myopia) about – 0.50 D • Increase as fourth power of pupil diameter – Small pupil can cause better vision • Can also occurs following refractive surgery – Aspheric cornea becomes more spherical American Academy of Ophthalmology 162
  • 163.
    Achromatic lenses • • • • • Achromatic Lensesconsist of two or more elements, usually of crown and flint glass that have been corrected for chromatic aberration with respect to two selected wavelengths. Most company provides achromatic lenses consisting of two elements. These lenses have considerably reduced not only chromatic aberration bust also spherical aberration and coma aberration. These are designed with respect to three wavelength 480nm, 546.1nm 546 1nm and 643 8nm 643.8nm. They are best used in replacing singlet where improved performance is required. – Positive Achromatic Lenses – Negative Achromatic Lens Changchun Jixiang, 2006 163
  • 164.
    Achromatic lenses Positive AchromaticLenses Negative Achromatic Lenses Changchun Jixiang, 2006 164
  • 165.
    Astigmatism g • Classified as –Sh Shape • Regular astigmatism – With the rule » Common in children » Vertical meridians is steepest » A i near 90º Axis – Against the rule  opposite » Older adult • Irregular astigmatism – Rigid contact lenses may be useful American Academy of Ophthalmology 165
  • 166.
    Circle of leastconfusion Conoid of Sturm 166
  • 167.
  • 168.
    Cylinder lenses Plano ConvexCylindrical Lenses Plano Concave Cylindrical Lenses Biconvex Cylindrical Lenses Biconcave Cylindrical Lenses Changchun Jixiang, 2006 Meniscus Cylindrical Lenses 168
  • 169.
    Cylinder axis American Academyof Ophthalmology 169
  • 170.
    Astigmatic dial technique •Obtain best visual acuity using SPHERES only y g y • FOG the eye to about 20/50 by adding PLUS sphere • Note the BLACKEST and SHARPEST line of the astigmatic dial • Add MINUS CYLINDER with axis PERPENDICULAR to the blackest and sharpest line (Rotate minus cylinder if necessary) until all lines APPEAR EQUAL es QU • REDUCE plus sphere or ADD minus until best acuity is obtained with the visual acuity chart American Academy of Ophthalmology 170
  • 171.
    Astigmatic correction g • Forchildren  full correction with correct axis • For adult  adaptable full correction • Reduce distortion – – – – Use minus cylinder y Minimize vertex distance Rotate axis toward 180º or 90º Reduce cylinder power and use spherical equivalent • Spatial distortion is binocular phenomenon  occlude one eye to verify • If fail to reduce distortion  use contact lenses or iseikonic corrections American Academy of Ophthalmology 171
  • 172.
    Toric lenses American Academyof Ophthalmology 172
  • 173.
    Toric lenses • Shapedlike a section through a rugby ball • P Prescribed t correct astigmatism  ib d to t ti ti contact lenses and IOLs • Toric lenses can be plus, minus, one principle meridian plus with the other minus p y • Referred as Spherocylinder lenses 173
  • 174.
  • 175.
    Prisms aberration • Inaddition to chromatic aberration • Producing colored fringes at the edges of objects viewed through the prism • Other aberration – Asymmetrical magnification of field – Asymmetrical curvature of field • Usually insignificant but  produce symptoms even with low-power p prisms. ophthalmic p American Academy of Ophthalmology 175
  • 176.
    Prismatic effect ofdecentred lens • Convex lens  two prisms cemented together at their BASEs BASE • Concave lens  two prisms cemented together at their APEXs • Decentred lens  Prism effect  Base in or Base out Decrease convergence Increase convergence
  • 177.
    Bifocals • A lenshaving one section that corrects for distant vision and another section that corrects for near vision. vision 177
  • 178.
    Bifocals The dot indicatesthe optical centre of the near portion A, executive-type segment; B, flat-top segment; C, round segment; D, D curved segment d MedDict 2007 178
  • 179.
    Trifocals • Three prescription powers:a distance power, a mid-range power, and a near power. • The distance power helps to see things at a distance, the mid-range power helps to see things at intermediate distances and the near power distances, corrects vision close up. • Tri-focal lenses are available in a variety of options, including thin and light lenses, impact resistant lenses and transition lenses (lenses that change from light to dark). MedDict 2007 179
  • 180.
    Progressive Lens • Characterized bya gradient of increasing lens power added to power, the wearer's correction for the other refractive errors. • The gradient starts at a minimum, or no addition power, at the top of the lens and reaches a maximum addition power, magnification, at the bottom of the lens. • The length of the progressive power gradient on the lens surface is usually between 15 and 20 mm with a final addition power between 1 00 to 3 00 1.00 3.00 dioptres. MedDict 2007 180
  • 181.
  • 182.
    S - 6.00C + 3.00 A 90º 0.00 - 6.00 - 6.00 - 6.00 +3.00 +3.00 0.00 - 6.00 - 6.00 Make the transposition of it - 3.00 - 3.00 - 6.00 182
  • 183.
    Transposition • New sphereis the ALGEBRAIC SUM of old sphere and cylinder • New cylinder is same value with old cylinder but with cylinder, OPOSITE sign • Change axis of cylinder by 90º S - 6 00 C + 3 00 A 90º 6.00 3.00 90 S - 3.00 C - 3.00 A 180º IS IT SAME OR EQUAL ??? 183
  • 184.
    S - 3.00C -3.00 A 180º - 3.00 - 3.00 0.00 0.00 - 3.00 - 3.00 - 3.00 - 3.00 - 6.00 EQUAL - 3.00 - 3.00 - 6.00 184
  • 185.
    Is your correctioncorrect? y • Duke Elder  add + 0.25 or – 0.25 D – I it bl Is i blurred or still clear ? d ill l – Smaller, darker, farther away or any such change • Duochrome test  RAM-GAP – Red add minus, green add plus Binocular balance • Fogging • Prism dissociation • Cycloplegics American Academy of Ophthalmology 185
  • 186.
    Refraction : Correction • • • Spectacle/ glass Contact lenses Keratorefractive surgery – – – – – – – – RK  Radial keratotomy PRK  Photo Refractive Keratotomy / Keratectomy Laser Thermal Keratoplasty LASIK (Laser-assisted in-situ Keratomileusis), EpiLASIK SBK  Sub-Bowman Keratomileusis LASEK  Laser-assisted Sub-Epithelial Keratomielusis LaserACE  Restoring accommodative ability CK  Conductive Keratoplasty  Radio-frequency-based Collagen shrinking procedures – Arcuate keratotomy – Intrastromal corneal ring • IOL – AC Lens, Claw lens (25-6)  Artisan (Ophtec), Verisyse ( , ( ) ( p ), y (Abbott Medical Optics), STAAR Visian ICL and Toric ICL – Posterior lens by CLE / RLE (>13) 186
  • 187.
    Corneal Collagen Cross-Linking g g •Corneal thermal remodeling  (also) can be induced by Microwave Keratoplasty Micro a e Keratoplast  treat Keratocon s and Keratoconus Refractive Errors • UV radiation  accelerates corneal stiffening by riboflavin • Cross-linking occurs between collagen helix, aminoglycans and other substances in corneal substrate • D li i “Controlled I Delivering “C t ll d Insult” t St lt” to Stromal C ll l Collagen Fib Fibers bellow epithellium and Bowman’s layer  change shape without cutting. • Fatten the cornea  after Lasik or incisional surgery • Achieve corneal rigidity equivalent to 600 years of natural ageing Marshall J, 2010 187
  • 188.
    Corneal Collagen Cross-Linking g g • • Olderprocedure  30 minutes riboflavin soaks and 30 minutes UV p exposure  potential endothelial damage, complication to lens and retina Newer procedure  2 minutes riboflavin soaks and 3 minutes UV exposure with mask-covered protection at peripheral and central of the cornea  protecting endothel, corneal stem cells, lens and retina  Keraflex KCL (Avedro) (A d ) Marshall J, 2010 188
  • 189.
  • 190.
    Contact lenses :Materials 1. 1 HEMA (Hydroxyethyl methacrylate) 2. Non HEMA  Hydrogel lenses  Hydrophyllic 3. HEMA + PVP (Polyvinylpyrrolidone) ( y y py ) - To increase water holding ability , - PVP  Yellowing by age / heat disinfection 4. 4 HEMA + MMA (Methylmethacrylate) (M th l th l t ) - To increase stiffness. - Lens more durable durable. - The pores are smaller than any known bacterium or virus 190
  • 191.
    Contact Lenses Fitting • Basecurve – – – – – • Radius of curvature to be cut on the posterior surface of the lens Minimal apical clearance Guided by the K measurements along two principal meridians Selected to ensure a comfortable and healthy fit for patients Range from 8.40 mm (40.25 D) to 7.00 (48.25 D) Diameter – Optical zone range between 6.0 – 8.0 mm – Central thickness  less than 0.10 mm • Peripheral curve – Curve radii range between 8 40 – 13 00 mm 8.40 13.00 – Curve width  0.10 – 0.45 mm • • Power Lens surface design – – – – Spherical lens Back surface toric lens Front surface toric lens Bitoric Bit i American Academy of Ophthalmology 191
  • 192.
    The Contact Lenses Peripheralcurve width Optic zone Base curve Peripheral curve radii Peripheral curve width Center thickness 192
  • 193.
    VERTEX DISTANCE CORRECTION VertexDistance (mm) Spectacle Power (D) 10 11 12 13 10 12 13 Contact Lens Power Minus Lenses 4.00 4.50 5.00 5.50 6.00 6.50 7.00 7.50 8.00 11 3.87 4.25 4.75 5.25 5.62 6.12 6.50 7.00 7.37 3.87 4.25 4.75 5.12 5.62 6.00 6.50 6.87 7.37 3.87 4.25 4.75 5.12 5.62 6.00 6.50 6.87 7.25 Plus Lenses 3.75 4.25 4.75 5.12 5.50 6.00 6.37 7.25 7.62 4.12 4.75 5.25 5.75 6.37 7.00 7.50 8.12 8.75 4.12 4.75 5.25 5.87 6.37 7.00 7.62 8.12 8.75 4.25 4.75 5.25 5.87 6.50 7.00 7.62 8.25 8.87 4.25 4.75 5.37 5.87 6.50 7.12 7.75 8.25 8.87 193
  • 194.
    FITTING STEPS Good fit 1.Sufficient movement 2. Proper centration 3. Stable vision 4. 4 Sharp retinoscopic reflex 5. Clear keratometry mires 194
  • 195.
    FITTING STEPS Tight fit 1. 1Vision fluctuates (clears briefly after blink) 2. Bubbles trapped under the lens 3. Declining comfort over a span of hours as the lens is worn 4. A burning sensation following by redness or an indication appearing around the corneal circumference 5. Restricted or no movement of the lens 6. Keratometry mires that are distored, but clear on blinking 7. A fuzzy retinoscope reflex that clears on blinking 195
  • 196.
    FITTING STEPS Loose fit 1.Variable vision (briefly clears after blinking) 2. 2 Bothersome lens awareness 3. Lack of centration 4. Too much movement 5. Lens edge stand off l 5 L d t d ff lens d decenter onto th sclera t t the l 7. Bubbles forming under the lens edge 8. Keratometry mires that are clear, but blurs on blinking, and than clear 9. A clear retinoscopic reflex, that blurs after blinking 196
  • 197.
  • 198.
    Toric contact lenses •An astigmatic eye is not perfectly round (like a soccer ball) but more shaped like a rugby ball. • O i f One-in-four people with l l i h low amounts of f astigmatism can get away with wearing normal (spherical) contact lenses lenses. • A person with higher amounts of astigmatism needs to wear special contact lenses called toric lenses 198
  • 199.
    What makes ato c co tact lens d e e t at a es toric contact e s different? • If you think of the eye as a rugby ball, that ‘rugby ball’ is y y g y , g y positioned at a certain angle in the eye socket. • In order for the contact lens to correct astigmatism, it needs to lie at that same angle in front of the eye eye. • Usually contact lenses rotate on the eye with each blink. A toric contact lens is designed in such a way, that it won t won’t rotate on the eye eye. • Most toric lenses are made slightly thicker at the bottom of the lens. • The thicker part will weigh the lens down at the bottom, preventing it from turning on the eye. 199
  • 200.
  • 201.
  • 202.
    Laser assisted Laser-assisted insitu Keratomileusis 202
  • 203.
  • 204.
  • 205.
  • 206.
    Aniseikonia • Translated fromGreek aniseikonia means "unequal images". • It is a binocular condition so the image in condition, one eye is perceived as different in size compared to the image in the other eye eye. • Two different types of aniseikonia can be differentiated: static and dynamic diff ti t d t ti dd i aniseikonia 206
  • 207.
    Aniseikonia • Static aniseikoniaor aniseikonia in short means that in a static situation where the eyes are gazing in a certain direction • The perceived (peripheral) images are different in size 207
  • 208.
  • 209.
    Aniseikonia • Dynamic aniseikoniaor (optically induced) anisophoria means that the th eyes h have t rotate a different to t t diff t amount to gaze (i.e. look with the sharpest vision) at the same point in space p • This is especially difficult for eye rotations in the vertical direction 209
  • 210.
  • 211.
    Aniseikonia Schematic presentation ofthe different steps to get to a perceived image size and the visualization of a field angle α 211
  • 212.
    Aniseikonia Features : a)Example of a single aniseikonia test image, b) same aniseikonia test image as on the left, but now with an (exaggerated) vertical fixation g , ( gg ) disparity compensation (click on image to enlarge). 212
  • 213.
    Anisophoria • Is acondition in which the balance of the vertical muscles of one eye differs from that of the other eye  the visual lines do not lie in the same horizontal plane • Eye muscle imbalance  the horizontal visual plane of one eye is different from that of the other 213
  • 214.
    Amblyopia y p Type : •St bi i amblyopia Strabismic bl i – Frequently  in esotropia patients • A i Anisometropic (R f ti ) amblyopia t i (Refractive) bl i – Difference in refraction greater than 2.50 D • Isoametropic amblyopia – Bilateral refractive error grater than + 5.00 or – 10.00 D • Deprivation amblyopia – Caused by such as media opacities Deborah Pavan-Langston, 2008 214
  • 215.
  • 216.
  • 217.
  • 218.
    Position of gaze g •Primary position – Straight ahead • Secondary position – Straight up, straight down – Right gaze, left gaze • Tertiary position  Four oblique position – Up and right, up and left – Down and right, down and left • Cardinal position American Academy of Ophthalmology 218
  • 219.
    Cardinal position andYoke muscles RSR LIO Right Gaze LSR RIO RLR LMR LLR RMR RIR LSO LIR RSO Left Gaze American Academy of Ophthalmology 219
  • 220.
    Eye movement • Agonist –Primary muscle moving the eye in a GIVEN direction • Synergist – – – – – Muscle in the same eye As the agonist That can act with agonist Produce a GIVEN movement E.g Superior rectus with I f i oblique  elevate the eye E :S i t ith Inferior bli l t th • Antagonist – – – – Muscle in the same eye As the A th agonist i t That can act with in the direction opposite E.g : Medial rectus and lateral rectus American Academy of Ophthalmology 220
  • 221.
    Basic • Sherrington’s lawfor reciprocal innervation – Increased innervation and contraction of GIVEN EOM  – Accompanied by reciprocal decrease of innervation and contraction of its antagonist EOM f O • Yoke muscle – Two muscle (one in each eye) – Are Prime mover of their respective eyes – In GIVEN position gaze – E.g : right gaze  RLR and LMR simultaneously innervated and contracted  to be “yoked” together yoked American Academy of Ophthalmology 221
  • 222.
    Basic • Hering’s lawof motor correspondence Hering s – The state  equal and simultaneous innervation flow to Yoke muscle – Concerned with the desired direction of the gaze American Academy of Ophthalmology 222
  • 223.
    EOM : Functions Muscle Primary Secondary Lateralrectus Abduction None Medial rectus Adduction None Superior rectus Elevation Adduction Intorsion Inferior rectus Depression Adduction Extorsion Superior oblique Intorsion Depression Abduction Inferior oblique Extorsion Elevation Abduction Vaughan DG 223
  • 224.
    EOM : Origin g Muscle Origin Functional origin ii Lateral rectus Annulus of Zinn Annulus of Zinn Medial M di l rectus t Annulus of Zi A l f Zinn Annulus of Zi A l f Zinn Superior rectus Annulus of Zinn Annulus of Zinn Inferior rectus Annulus of Zinn Annulus of Zinn Superior oblique Orbit apex above Annulus of Zinn Trochlea Inferior oblique Behind lacrimal fossa Behind lacrimal fossa American Academy of Ophthalmology 224
  • 225.
    EOM : Insertionfrom limbus • • • • Medial rectus Lateral rectus Superior rectus Inferior rectus 5.5 5 5 mm 6.9 mm 7.7 mm 6.5 mm American Academy of Ophthalmology 225
  • 226.
    EOM : Wideand Length • • • • • Superior Rectus  5.0 mm and 41.8 mm Inferior Rectus  4.2 mm and 40 mm Lateral Rectus  6 5 mm and 40.6 mm 6.5 40 6 Medial Rectus  4.0 mm and 40.8 mm Superior Oblique  1 2 mm and  1-2 – Muscle part 40 mm – Tendineus part 20 mm • Inferior Oblique  1-2 mm and 37 mm Kumar SM 2007 226
  • 227.
    EOM : Gazes Upand right RSR - LIO Up and left LSR – RIO Right RLR – LMR Left LLR - RMR Down and right RIR - LSO Down and left LIR - RSO Vaughan DG 227
  • 228.
    Eye movement • Versions –Eyes move in the same direction • Vergences  Disconjugate binocular eye movement – – – – – Convergence  15-20 ∆ distance and 25 ∆ for near Divergence  6-10 ∆ distance and 12-14 ∆ for near Incyclovergence  2-3º Excyclovergence y g Vertical vergence  2-3 ∆ American Academy of Ophthalmology 228
  • 229.
    Eye movement :Supranuclear control system • Saccadic system – G Generates all fast eye movements or refixation t ll f t t fi ti – Up to 400-500º/sec • Smooth pursuit – Generates all following, or pursuit eye movements following pursuit, – Pursuit latency is shorter than for saccades – Maximum velocity 30-60º/sec • The vergence system – Controls disconjugate eye movements • The position maintenance – Maintains a specific gaze position – Allowing an object to interest to remain on the fovea • The non optic reflex – Integrated eye movement with the body movement – Most important system is Labyrinthine system American Academy of Ophthalmology 229
  • 230.
    Variation of deviation Withgaze position or fixating eye • Comitant (Concomitant) – Deviation doesn’t vary in size with direction of gaze or fixating eye • Incomitant (Noncomitant) – Deviation varies in size with direction of gaze or fixating eye – Most  paralytic or restrictive – In acquired condition  may indicate neurologic or orbital problems or diseases American Academy of Ophthalmology 230
  • 231.
    Grades of binocularvision • 1st Grade – Simultaneous perception • 2nd Grade – Fusion • 3rd Grade – Stereopsis Kanski JJ, 2007 231
  • 232.
    Fusion • • Cortical unification ofvisual object into a single percept Made by simultaneous stimulation of corresponding retinal areas Sensory fusion – Relationship between retina and visual cortex – Corresponding retinal points project to same cortical locus – Corresponding adjacent retina points have adjacent cortical representations Motor fusion – – – – Vergence movement Causes similar retinal i C i il i l image Fall and be maintained on corresponding retinal areas Disparities can be induced by, E.g : phoria, etc American Academy of Ophthalmology 232
  • 233.
    Stereopsis and Depthperception • Stereopsis p – Binocular sensation – Relative or subjective ordering of visual objects in depth or 3 dimensions • Depth perception –M Monocular clues i l d l l include • • • • • Object overlap Relative object size Highlight and shadow Motion parallax Perspective American Academy of Ophthalmology 233
  • 234.
    AC/A Ratio • Accommodative Convergence/ Accommodation Ratio – Normal is between 3:1 to 5:1 – AC/A = PD + ∆n – ∆o D Gradient method – PD = pupil distance (millimeter) – ∆n = near deviations (prism diopter) – ∆o = distance deviations (prism diopter) sign convention : – Esodeviation + – Exodeviation - – D = diopter of accommodation – Distance 6 m – Near 0.33 m American Academy of Ophthalmology 234
  • 235.
    ESODEVIATION • Esodeviation – Esophoria •Controlled by fusion under condition of normal y binocular vision – Intermittent esotropia • C t ll d b f i under condition of normal Controlled by fusion d diti f l binocular vision • Spontaneous becomes manifest • Particularly with fatigue or illness – Esotropia American Academy of Ophthalmology 235
  • 236.
    Esotropia • • Pseudoesotropia Congenital esotropia – Classicessential – Nystagmus and esotropia y g p • Accommodative esotropia – Refractive (Normal AC/A ratio) – Non refractive (High AC/A ratio) – Partially accommodative • Non-accommodative acquired esotropia – – – – – – • Basic Acute Cyclic Sensory depriviation Divergence insufficiency and divergence paralysis Spasm of near synkinetic reflex Incomitant esotropia – Sixth nerve paresis – Medial rectus restriction  Thyroid and trauma y – Duane’s syndrome and Möbius syndrome American Academy of Ophthalmology 236
  • 237.
    Pseudoesotropia • Infant oftenhave a wide, flat nasal bridge with prominent medial ep ca a folds a d po e ed a epicanthal o ds and a small interpupillary distance. • May appear esotropic • I fact their eyes are straight. In f t th i t i ht • No real deviation exists • Both corneal light reflex and cover testing results are normal. 237
  • 238.
    Congenital Esotropia • • • • Large constantesotropia (usually > 40 PD) Onset birth to 6 months of age Amblyopia common (50%-60%) Associated motor phenomenon ( p (usually y present after 1 year of age) : – Inferior Oblique Over Action (IOOA) – Dissociated Vertical Deviation (DVD) – Latent nystagmus 238
  • 239.
    Non-surgical treatment Congenital esotropia • • • • • • • Abductionshould be full or only slightly limited. Mild (-1) limitation of abduction is common and does not necessarily indicate a lateral rectus paresis. Try the dolls head maneuver or spinning the child (vestibular stimulation) to elicit full abduction in infants Check for inferior oblique overaction and V-pattern Check fixation preference: strong fixation preference for one eye indicates amblyopia in the fellow eye. Cross-fixate  fixing with right eye for objects in the left visual field and with left eye for objects in the right visual field Cross-fixate  indicate no significant amblyopia. Measure deviation : – Prisms Alternate Cover Test (PACT) is the BEST. – KRIMSKY test  if PACT i unobtainable t t is bt i bl • Cycloplegic refraction – Use cyclopentolate 0.5% in infant < 24 year of age and 1% for older children – If cycloplegic refraction shows > 3 D  prescribe full hyperopic correction. – If ET > 10 to 15 PD persist after prescribe full hyperopic correction  SURGERY is required 239
  • 240.
    Accommodative esotropia • CLINICALFEATURES – Usually acquired around 2 to 4 years of age – Moderate to large esotropia (20 to 50 PD) – Variable angle that is often intermittent – Associated with hyperopia usually +2 to +6 D – Classify as • R f ti (Normal AC/A ratio) Refractive (N l ti ) • Non refractive (High AC/A ratio) • Partially accommodative 240
  • 241.
    Non surgical treatment • Refractiveaccommodative esotropia – Corrective lenses • Full amount of hyperopia as determined under cycloplegia • Full time spectacle wear  instill Atropine 1% at bed time to make initial compliance • Esotropia fully corrected distance and near – – – – Full hypermetropic correction ET < 8 to 10 PD Single vision spectacle (without bifocal) Surgery is not needed. needed • Distance corrected, but there is residual esotropia at near (high AC/A ratio) – – – – – Full hypermetropic correction Distance deviation resulting fusion (i.e, < 10 PD ET) Residual ET at near that can not be fused (i e > 10 PD ET) (i.e Prescribe a flat-top bifocal add. (start : + 2.50 to + 3.00 D) Prescribe the least amount of near add to obtain fusion while leaving a small near esophoria (E < 5 PD) • Residual esotropia distance and near ( p (Partially Accommodative esotropia) y p ) – With full hypermetropic correction – Distance esotropia persist can not be fused (usually > 10 PD).  SURGERY is INDICATED – Miotic agent  subtitutes for glasses American Academy of Ophthalmology 241
  • 242.
    Non surgical treatment •Non-refractive accommodative esotropia – Bifocals • • • • • Flat-top design preferred +2.50 to +3.00 D Top of the segment should CROSS the pupil Vertical height not exceed distance portion of the lens Progressive lens must be fitted higher of 4 mm than adult fitting with maximum bifocal power of +3.50 D • Give detail to opticians • Acceptance value  – Fusion at distance – L Less th 10 ∆ residual esotropia at near than id l t i t – Long-lasting cholinesterase inhibitors  0.125% echothiophate iodide both eye one time daily for 6 weeks American Academy of Ophthalmology 242
  • 243.
  • 244.
    Order for surgery •Surgery between 6 months and 2 years of age (most reference recommend) • Surgery between 6 months and 1 year of age (standard approach). • Early surgery between 3 and 5 months of age (controversial, but may improve sensory outcome) outcome). 244
  • 245.
    Surgical Approach • Theprocedure of choice  bilateral medial rectus muscle recession g g • Near deviation as the target angle. • In older patients with irreversible amblyopia  recession medial rectus and resection lateral l t l rectus t amblyopic eye t to bl i • The surgical goal  not to operate the patients out of glasses but to achieve glasses, alignment and fusion with full hypermetropic correction 245
  • 246.
    Non accommodative Non-accommodative esotropia •CLINICAL FEATURES : – – – – – Usually emmetropic, may be myopic Onset after 2 years, even in late adulthood Full duction Late onset ET of unknown etiology Surgery is the treatment of choice • Bilateral lateral rectus recession • Often undercorrection increase the amount of recession • Try using prism adaptation to determine the full target angle angle, especially if there is a disparity between the distance and near deviation. • Operate for the full prism adapted angle 246
  • 247.
    Sensory Esotropia • Associatedwith a monocular blindness or dense amblyopia amblyopia. • Treatment : recession lateral rectus and resection medial rectus muscle is performed on the eye with poor vision • To obtain Cosmetic appearance of straight eyes. 247
  • 248.
    EXODEVIATION • Exodeviation – Pseudoexotropia •An appearance of exodeviation when in fact the pp eyes are properly aligned • Positive angle kappa • Wide interpupillary distance – Exophoria • Controlled by fusion u de co d o o normal Co o ed us o under condition of o a binocular vision – Intermittent exotropia American Academy of Ophthalmology 248
  • 249.
    Intermittent exotropia • Classified by –Difference distance and near between alternating prism and cover test measurement – Change in near measurement by unilateral occlusion or +3.00 D lenses • Clinical features – – – – – – Most common form of exotropia Usually present after 1 year of age Large exophoria that spontaneusly becomes to a tropia g p p y p High grade stereopsis when fusing; suppression when tropic Squint one eye to bright sun light The exotropia is typically manifest when the patient is fatigued, daydreaming or ill – Symptoms  blurred vision, asthenopia, visual fatigue and rarely diplopia in older children and adults American Academy of Ophthalmology 249
  • 250.
    Intermittent exotropia • Basictype – Same at near and distance • Divergence excess – Greater at distance – True divergence excess • Greater at distance even after a periods of monocular occlusion • High gradient AC/A ratio at near by +3.00 D lenses – Simulated divergence excess • Greater than distance • Same after one eye is 1 hour occluded  to remove the effect of tenacious proximal fusion • Convergence insufficiency – Greater at near than distance – Excludes isolated convergence insufficiency American Academy of Ophthalmology 250
  • 251.
    Non surgical treatment • Correctivelenses – Improve retinal image clarity • Additional minus lens power – Usually 2-4 D beyond refractive error correction – Temporarily stimulate accommodative convergence • Part time patching – Passive orthoptic treatment – 4-6 hours per day or alternate daily patching – Treatment for small to moderate-sized deviation • Active orthoptic treatment – – – – • Anti suppression therapy / diplopia awareness Fusional convergence training Alone or in combination with patching, minus lenses and surgery Good for deviations of 20∆ or less Base in prism – Promote fusion – Not recommended for long term treatment  cause a reduction in fusional vergence amplitudes f i l lit d American Academy of Ophthalmology 251
  • 252.
    Surgical treatment • • • • • Deviation of15 ∆ or more Nearly constant exotropia Still i t intermittent itt t Before 7 years of age Before 5 years of strabismus duration American Academy of Ophthalmology 252
  • 253.
    NOTE • Children under4 years of age are at risk f d i k for developing postoperative l i t ti amblyopia and losing binocular vision. • It is probably best to postpone surgery until 4 years of age unless the patient demonstrates progressive loss of fusion control. 253
  • 254.
    Another exodeviation • Constantexodeviation – Congenital exotropia – Sensory exotropia – Consecutive exotropia – Exotropia Duane’s retraction syndrome – Neuromuscular abnormalities – Di Dissociated h i i t d horizontal d i ti t l deviation American Academy of Ophthalmology 254
  • 255.
    A-V Patterns inhorizontal strabismus A V P tt i h i t l t bi • A Pattern – Eyes closer together in up gaze – 10 PD difference compares to down gaze • V P tt Pattern – Eyes closer together in down gaze – 15 PD difference compares to up gaze Deborah Pavan-Langston, 2008 255
  • 256.
    A Pattern • Etiology –Most f frequent  overaction of SO f – With or without underaction of IO – As SO acts abduction in downward gaze • Esotropia decreases • Exotropia increases – If no overaction of SO  suspect underaction of LR • Treatment – Deviation more than 10 PD – Bilateral weakening  Tenotomy with silicone expander – Horizontal surgery g y • With upward displacement of MR • With downward displacement of LR – Bilateral SO surgery  avoided in patient with foveal bifixator Deborah Pavan-Langston, 2008 256
  • 257.
    V Pattern • Etiology – Mostfrequent  overaction of IO – Primary underaction of SO – As IO acts abduction in upgaze • Esodeviation decreases • Exodeviation increases – Overaction of LR  V exotropia • Head position – V esodeviation  chin held down close work – V exodeviation  chin held up • Treatment V esotropia – Recession or disincertion of overacting IO – Recession or downward the MR if obliques are normal • Treatment V esotropia – Recession or disincertion of LR if IO overacts Deborah Pavan-Langston, 2008 257
  • 258.
    Strabismus : Positiontest Measurement of deviation • Hiscberg test • C Cover t t test • Cover uncover test • Krimsky test • Prisms Cover test • Prisms Alternate Cover Test (PACT) American Academy of Ophthalmology 258
  • 259.
  • 260.
  • 261.
  • 262.
  • 263.
  • 264.
    Strabismus : Sighttest • WFDT • Maddox’s rod 264
  • 265.
  • 266.
  • 267.
  • 268.
  • 269.
    Approach to Recessionsurgery Minimal (mm) Average maximum (mm) Maximum ever (mm) LR 4 8 - 10 MR 2.5 7 adult 6 children 5 - 5.5 6-7 14 for nystagmus SR 2.5 5 IR 2.5 10 5 Eugene M. Helvestone 269
  • 270.
    Approach to Resectionsurgery Minimal (mm) Average maximum (mm) Maximum ever (mm) LR 5 8 infant 10 children and adult - MR 5 8 infant 10 children and adult - SR 2.5 - 3 5 - IR 2.5 - 3 5 - Eugene M. Helvestone 270
  • 271.
    Prisms Muscle Prisms-Muscle lengthconversion • 5 ∆ Di t f 1 mm MR recession Diopter for i • 2.5 ∆ Diopter for 1 mm LR recession • 2.5 ∆ Diopter for 1 mm MR and LR resection 271
  • 272.
    Both eye surgeryfor Esodeviation : Angle of esotropia (∆) Recess MR OU (mm) OR Resect LR OU (mm) 10 3.0 4.0 20 3.5 35 5.0 50 25 4.0 6.0 30 4.5 7.0 35 5.0 8.0 40 5.5 9.0 50 6.0 9.0 American Academy of Ophthalmology 272
  • 273.
    Monocular surgery forEsodeviation Angle of esotropia (∆) Recess MR OU (mm) AND Resect LR OU (mm) 10 3.0 4.0 20 3.5 35 5.0 50 25 4.0 6.0 30 4.5 7.0 35 5.0 8.0 40 5.5 9.0 50 6.0 9.0 American Academy of Ophthalmology 273
  • 274.
    Both eye surgeryfor Exodeviation : Angle of exotropia (∆) Recess LR OU (mm) OR Resect MR OU (mm) 15 4.0 3.0 20 5.0 50 4.0 40 25 6.0 5.0 30 7.0 6.0 40 8.0 6.0 American Academy of Ophthalmology 274
  • 275.
    Monocular surgery forExodeviation : Angle of exotropia ( ) g p (∆) Recess LR OU (mm) AND Resect MR OU (mm) ( ) ( ) 15 4.0 3.0 20 5.0 4.0 25 6.0 5.0 30 7.0 6.0 40 8.0 6.0 50 9.0 7.0 60 10.0 10 0 8.0 80 70 10.0 9.0 80 10.0 10.0 American Academy of Ophthalmology 275
  • 276.
  • 277.
  • 278.
    Glaucoma : Basic •Definition – Optic neuropathy – Visual field defect – Rise of IOP as major risk 278
  • 279.
  • 280.
    Glaucoma : Basic • • • • • • • • IOPmeasure Angle examination Optic nerve head examination Vascular change RNFL examination i ti Visual field examination Central corneal thickness and rigidity General eye examination* 280
  • 281.
    IOP : Basic • • • • • • • NormalIOP  10-20 mmHg 10 20 Average  15 mmHg Fluctuation Fl t ti  2 56 mmHg 2.56 H Diurnal Variation  3-6 mmHg Peak period  Morning Decrease during the night Hypotony < 5-6 mmHg Gumansalangi MNE, 2003 281
  • 282.
    IOP : Determiningfactors F = C (P – P ) (Po Pe) • F • C = rate of aqueous outflow (normal 2 µl/min) = facility of aqueous outflow (normal 0.2 µl/min/mmHg • Po = IOP in mmHg • Pe = episcleral venous pressure (normal 10 mmHg) Kanski JJ, 2007 282
  • 283.
    How to measurethe IOP • First line – Applanation tonometer  Nowadays Gold standard  AT 900D (Haag-Streit International) – Dynamic contour tonometer  E g : PASCAL (Ziemer) E.g • Second line – Air-puff non-contact tonometer – Corvis ST Air-puff non-contact tonometer with Scheimpflug Camera Cornea Monitoring (OCULUS) – Tono-Pen, The Pachmate DGH 55, Diaton, Schiotz tonometer – iCare ONE tonometer, SOLX IOP sensor*  IOP monitoring 283
  • 284.
    IOP : Flow • • • • • Cilliarybody Posterior chamber Pupil P il Anterior chamber Delivery – Trabecular pathway (85-95%) (85 95%) – Uveo-scleral pathway (5-15%) – Iris (Kanski) 284
  • 285.
    IOP : Flow •Aqueous come in to eye by : – Diff i Diffusion – Ultrafiltration –C Carbonic Anhydrase II activity – Active secretion American Academy of Ophthalmology 285
  • 286.
    Glaucoma: Vascular dysregulation yg • Endhotelial dysfunction – Impaired endothelium-derived nitric oxide activity – Abnormalities of the endothelin system  altered Endothelin-1 (ET1) vasoreactivity • Defective auto regulation of ocular blood flow • Instable blood supplies to the tissue Henry E, 2006; Araie M, 2010 286
  • 287.
    Glaucoma : Angle • • • • • • • Torch VonHerrick Slit-lamp Gonioscopy Ultrasound Biomicroscopy (UBM) Anterior A t i OCT Scheimpflug Camera Pentacam Very high frequency (VHF) ultrasound eye scanner  Artemis (ArcScan, Inc) 287
  • 288.
  • 289.
  • 290.
    Angle Examination :Van Herick Von Herrick and Shaffer grades Grade Ratio of aqueous gap/cornea Clinical interpretation Shaffer angle degrees 4 >½/1 Closure impossible 45-35 3 ½-¼ /1 Closure impossible 35-20 2 ¼/1 Closure possible 20 1 <¼/1 Closure likely with full dilation 10 or less 0 Nil Closed 0 290
  • 291.
    Angle Examination :Gonioscopy 291
  • 292.
    Identification of Schwalbe’sLine Schwalbe s Thomas R, 2006 292
  • 293.
    Shaffer’s Intepretation Classification Angle Width VisibleStructure Clinical Intepretation Grade 0 Closed Schwalbe’s line is not visible Totally closed angle Grade I 10° Schwalbe’s line visible Considerable risk of closure Grade II 20° Anterior trabeculum is visible Bear watching Grade III 30° Scleral spur is visible No risk of angle closure Grade IV 40° Ciliary body is visible No risk of angle closure 293
  • 294.
  • 295.
  • 296.
  • 297.
  • 298.
    Angle Examination :UBM Normal eye’s angle Angle : Pupillary block 298
  • 299.
    Angle Examination :Anterior OCT Visante OCT (Carl Zeiss Meditec AG) 299
  • 300.
  • 301.
    Artemis ( Ultralink) 50MHz ArcScan 301
  • 302.
  • 303.
    Shaffer s Shaffer’s Intepretation Classification Cl ifiti Angle A l Width Visible St Vi ibl Structure t Clinical I t Cli i l Intepretation t ti Grade 0 Closed Schwalbe’s line is not visible Totally closed angle y g Grade I 10° Schwalbe’s line visible Considerable risk of closure Grade II 20° Anterior trabeculum is visible Bear watching Grade III 30° Scleral spur is visible No risk of angle closure Grade IV 40° Ciliary body is visible No risk of angle closure 303
  • 304.
    Optic disc A. Surface B.Pre Laminar C. Laminar D. Retro Laminar 304
  • 305.
    GON : Evaluation •Indirect ophthalmoscope* • Direct ophthalmoscope • Slit lamp : stereoscopic view • H b or El B Hruby Bayadi l di lens • 60, 78, 90 D • Contact lens Thomas R, 2006 305
  • 306.
    GON : Evaluation • • • • • • • Disc Generally Cup Neuro R ti l Ri (NRR) N Retinal Rim Peripapillary hemorrhage Circum Linear Vessels (CLV) Para Papillary Atrophy (PPA) Retinal Nerve Fiber Layer (RNFL) 306
  • 307.
    GON : Evaluation Generalized Largeoptic cup L ti Asymmetry of the cup Progressive enlargement of the cup Focal Narrowing ( t hi ) of th rim N i (notching) f the i Vertical elongation of the cup Cupping to the rim margin Regional palor Splinter hemorrhage S li t h h Nerve fiber layer loss Less specific Exposed l i cribosa E d lamina ib Nasal displacement of vessels Baring of circumlinear vessels Peripapillary crescent (TJ et al, 2003) al 307
  • 308.
  • 309.
  • 310.
    Definition of Cup: Disc Ratio • Disc Diameter • Cup Diameter • CDR = c / d c d • Horizontal > Vertical Thomas R, 2006 310
  • 311.
  • 312.
    a. Normal C/DRatio 0.2 b. Same Disc 1 year later with C/D Rasio 0 5 R i 0.5 c. Cup enlarge to Infero Temporal and Splinter Hemorrhages d. Cup enlarge to Superior and show Inferior Bayoneting Sign e. Advance Cupping Oval Disc enlarge to superior and inferior f. Pale Papil with deep excavasion 312
  • 313.
  • 314.
  • 315.
    Cup Depth • • • • Not ofmuch importance In normal : depends on disc area In glaucoma : type & level of IOP Deepest with high IOP – Juvenile POAG – Angle recession Thomas R, 2006 315
  • 316.
    Neuro Retinal Rim(NRR): Shape • Sloping rim in small and intermediate discs • Steep or over hanging with oblique insertion • Supero nasal tilt in normal • Nasal tilt in myopes Thomas R, 2006 316
  • 317.
    NRR in Glaucoma •Loss of physiological shape • ISNT rule i b k l is broken • Vertical cup enlarges Thomas R, 2006 317
  • 318.
    Jonas ISNT Rule • Lessmarked in large discs • Rim more evenly distributed • Punched out well defined cup in large discs • p Also compare Inferior & Superior to temporal rim • Inferior to Temporal 2 : 1 • Superior to Temporal 1.5 : 1 Thomas R, 2006 318
  • 319.
    NRR : IS N T • Partially depends on exit of central retinal vessels l • Rim furthest away is more affected • May explain unusual configuration of rim Thomas R, 2006 319
  • 320.
    Temporal Portion ofRim • Papillo macular bundle • Preferential cupping temporally with field loss near fixation • POAG with Myopia and NTG Thomas R, 2006 320
  • 321.
    Glaucoma & Contourof Rim • May cause a backward bowing of the rim tissue • Deep extension of the cup in one meridian • Gentler sloping backward : Saucerization Thomas R, 2006 321
  • 322.
    Rim contour :Normal Thomas R, 2006 322
  • 323.
    Saucerization • Slight backward bowing: like saucer • Periphery or a portion ti • Or whole disc • May be first change Thomas R, 2006 323
  • 324.
    Shelving : NoField Defect ? Thomas R, 2006 324
  • 325.
    Excavation : FieldDefect Thomas R, 2006 325
  • 326.
    Excavation : FieldDefect Thomas R, 2006 326
  • 327.
    Excavation : Superiorand Inferior Thomas R, 2006 327
  • 328.
  • 329.
    Disc Hemorrhage • Rarein normals (1%) • 4 -7 % in glaucoma 7 • > In “NTG” • Lasts 10 weeks (1035) Thomas R, 2006 329
  • 330.
    Disc Hemorrhage • Splinteror flame shaped • Border of disc • Inferior or superior temporal region • RNFL defects, Notching, Focal perimetric loss Thomas R, 2006 330
  • 331.
    Circum Linear Vessels(CLV) • Vessel hugging gg g the NRR • Exits disc for macula • Normally present in 50 % of eyes Thomas R, 2006 331
  • 332.
    Circum Linear Vessels(CLV) Thomas R, 2006 332
  • 333.
    Circum Linear Vessels“Bared” in Glaucoma • N Normal CLV l • As rim is lost : gap between vessel and rim – Implies loss of rim • F i l specific Fairly ifi • Superficial or deep CLV normally present in 50 % of eyes Thomas R, 2006 333
  • 334.
    Para Papillary Atrophy(PPA) • Central beta zone • Peripheral alpha zone • Rare nasally or circumferential • Correlate with myopia and age Thomas R, 2006 334
  • 335.
    Para Papillary AtrophyIn Normals • Beta zone : 20 % • Alpha zone : 95 + % Thomas R, 2006 335
  • 336.
    PPA : AlphaZone • • • • Peripheral to beta or disc margin Irregular Hyper and Hypo pigmentation Thinning of RPE Relative scotoma Thomas R, 2006 336
  • 337.
    PPA : BetaZone • • • • • Central to alpha Peripheral to disc margin Marked atrophy of RPE Visible choroidal vessels & sclera Absolute scotoma Thomas R, 2006 337
  • 338.
    PPA in Glaucoma •Central beta zone more important • Peripheral alpha zone Thomas R, 2006 338
  • 339.
    PPA in POAG •B t larger in hi h Beta l i high myopic POAG • Next in age related POAG • Less in SOAG • ? NTG and POAG Thomas R, 2006 339
  • 340.
    Disc Hemorrhage ad Para Papillary Atrophy sc e o age and a a ap a y t op y • PPA associated with h ith hemorrhages h • PPA  marker for old hemorrhages Thomas R, 2006 340
  • 341.
  • 342.
    Glaucoma : RNFLDefect 342
  • 343.
    Normal RNFL : AxonsBundled by Mueller Cell Processes Bright fine striations • Best seen  Inferior and superior temporal p p (Inferior > Superior) • Bright Dark Bright • Fans off the disc to periphery Thomas R, 2006 343
  • 344.
    RNFL Visibility • • • • Clear media Withoutyellowing of lens Deeply pigmented RPE Decreases with age D ith – Loose 4000 - 5000 per year Thomas R, 2006 344
  • 345.
    RNFL : Normal? • “Obscures” normal vessels • Slit like or groove like defects • Narrower than retinal vessels Thomas R, 2006 345
  • 346.
    Localized RNFL Defects • • • • • Darkwedge Larger than vessel Touching disc Fan out Broad at temporal raphe Thomas R, 2006 346
  • 347.
    Localized RNFL Defects •Not seen in normal • 20% of Glaucoma eyes – Less with early glaucoma – Touch the disc • Other causes of atrophy – Drusen, Toxoplasmosis, Ischemia, Papiledema, Optic Neuritis Thomas R, 2006 347
  • 348.
    Localized RNFL Defectsa d Disc Hemorrhage oca ed e ects and sc e o age • Disc hemorrhage • Localized defect – 6 - 8 weeks • Localized type of disc damage : Notch Thomas R, 2006 348
  • 349.
    Diffuse RNFL Defects •I f i less visible Inferior l i ibl than Superior • Bright Dark, Bright Bright, Dark pattern lost g • Macula as bright as Superior and Inferior • “N k d” vessels “Naked” l Thomas R, 2006 349
  • 350.
    Frequency of RNFLDin Glaucoma • More with focal NTG • Less with – Age related POAG – Highly myopic OAG –J Juvenile OAG il Thomas R, 2006 350
  • 351.
    Importance of LocalizedRNFL p Defects in Early Diagnosis • E Eyes with normal ith l IOP and Visual Fields • Show field loss on follow up • “Pre perimetric” Glaucoma • J t’ R l # 2 Jost’s Rule Until proved otherwise, all glaucoma (suspects) have a RNFL defect Thomas R, 2006 351
  • 352.
    Subtle Retinal NerveFib L S btl R ti l N Fiber Layer D f t Defect Thomas R, 2006 352
  • 353.
  • 354.
    With More Experience: Thomas R, 2006 354
  • 355.
  • 356.
    Many Optic DiscChanges Have Been Described in Glaucoma Loss of ISNT pattern Localized notch in the rim Acquired Pit Disc Hemorrhage Wedge / diffuse loss of retinal nerve fibers  Absent rim inferiorly, superiorly, temporally & or nasally  Increase in cupping over time          • • • • • • Asymmetry in CDR > 2 y y Cup large for disc size Vertically oval cup Baring of CL vessels Over pass phenomenon Large CDR CDR of > 0.7 Deep cup Laminar dot sign g Thinned retinal arterioles Don t Don’t Just Use The Cup : Disc Ratio ! Thomas R, 2006 356
  • 357.
  • 358.
    RNFL Examination • Ophthalmoscope(Red free light) • R dF Red Free Ph t Photographs h • HRT, OCT, GDxVCC Slit lamp (Green light) 358
  • 359.
    SLP, OCT andCSLO/T • • • Pre Perimetric Glaucoma Detection Non Perimetric Glaucoma Progression Analysis RNFL analysis over Optic disc analysis 359
  • 360.
    Scanning laser polarimetry –GD VCC (Carl Zeiss Meditec AG) GDxVCC (C l Z i M dit 360
  • 361.
  • 362.
  • 363.
    OCT : Symmetricoptic discs with C/D ratio of 0.3 Optic Nerve Head Analysis Results Vert. Integrated Rim Area (Vol.) Horiz. Integrated Rim Width (Area) Disk Area Di k A Cup Area Rim Area Cup/Disk Area Ratio Cup/Disk Horiz. Ratio p Cup/Disk Vert. Ratio .321 mm3 1.717 mm2 2.53 2 53 mm2 2 .938 mm2 1.592 mm2 0.371 0.647 0.593 Optic Nerve Head Analysis Results Vert. Integrated Rim Area (Vol.) Horiz. Integrated Rim Width (Area) Disk Area Cup Area Rim Area Cup/Disk Area Ratio Cup/Disk Horiz. Ratio Cup/Disk Vert. Ratio .313 mm3 1.706 mm2 2.217 mm2 .764 mm2 1.453 mm2 0.345 0 345 0.622 0.586 RNFL analysis demonstrates a typical p y yp pattern in the OD and flattening of the RNFL p g pattern in the OS. Thinning of the superior RNFL is consistent with the visual field defect and the diagnosis of glaucoma. This was later confirmed by visual field with infero-nasal defect, OS 363
  • 364.
    OCT : ODappears within normal limits with a C/D ratio of 0.5. OS has large cup with C/D ratio of 0.7. Visual fields within normal limits Optic Nerve Head Analysis Results Vert. Integrated Rim Area (Vol.) Horiz. Integrated Rim Width (Area) Disk Area Di k A Cup Area Rim Area Cup/Disk Area Ratio Cup/Disk Horiz. Ratio p Cup/Disk Vert. Ratio .327 mm3 1.578 mm2 1.998 1 998 mm2 2 .646 mm2 1.352 mm2 0.323 0.538 0.58 Optic Nerve Head Analysis Results Vert. Integrated Rim Area (Vol.) Horiz. Integrated Rim Width (Area) Disk Area Cup Area Rim Area Cup/Disk Area Ratio Cup/Disk Horiz. Ratio Cup/Disk Vert. Ratio .188 mm3 1.597 mm2 2.973 mm2 1.766 mm2 1.207 mm2 0.594 0 594 0.775 0.791 Anatomic large nerve head with normal RNFL. Only distinguished with Stratus OCT Crossg y g sectional imaging is vital in the analysis of RNFL thickness in vivo, particularly in differentiating healthy RNFL from glaucomatous RNFL 364
  • 365.
    Glaucoma RNFL scanningon Cirrus OCT NEW Optic Disc cube 200 X 200 scan pattern 365
  • 366.
    Optic Disc Cube200 X 200 scan pattern Auto Center™ Center of ONH automatically identified. Measurement of TSNIT graph thickness is automatic. Less operator dependant and crucial for f repeatibility tibilit 366
  • 367.
    Cirrus HD-OCT Normal OURNFL printout i t t Similar to Stratus OCT RNFL thickness reporting format thi k ti f t RNFL thickness map RNFL thickness deviation map ( p (LSO fundus) RNFL thickness values ISNT and Average Multi-ethnicity (Including Asian Eye) NDB 367
  • 368.
    Cirrus HD-OCT RNFL thicknessreport OS RNFL loss at 6 o’clock 368
  • 369.
    Cirrus HD-OCT OU nerveloss RNFL printout p 369
  • 370.
  • 371.
    Confocal scanning lasertopography – HRT3 (Heidelberg Engineering GmbH)  provides objective measurements of the optic nerve head and surrounding RNFL – High quality stereo photographs of the optic disk 371
  • 372.
  • 373.
    The Moorfields RegressionAnalysis HRT measurements have been shown to have high diagnostic accuracy for detecting glaucoma. glaucoma The Moorfields Regression Analysis had a sensitivity and specificity of 84% and 96% respectively. An analysis based on the shape of the optic disc and surrounding RNFL resulted in a sensitivity and specificity of 89% and 89%. A sophisticated type of neural network analysis called a Support Vector Machine 373 resulted in a sensitivity and specificity of 91% and 90%
  • 374.
    VISUAL FIELD (VF) () • Isopter /isop·ter/ (i-sop´ter) a curve /isop ter/ (i sop ter) representing areas of equal visual acuity in the field of vision • A curve of equal retinal sensitivity in the visual field – Designated by a fraction – The numerator being the diameter of the test object – The denominator being the testing distance MedWeb, 2008 374
  • 375.
    Indication of Visualfield test • • • • • • • • • • Raised IOP Suspected GON Asymmetric C/D Ratio  > 0.3 3 mmHg IOP difference on both eyes H diff b h Glaucoma on other eye Previous retinal detachment Unexplained low visual acuity Discomfort “perfect” vision sco o t pe ect s o Unexplained headache and migraine Injured eye Gumansalangi MNE, 2003 375
  • 376.
    Visual field :Normal • The field of vision is defined as the area that is perceived simultaneously by a fixating eye. • The limits of the normal field of vision are 60° into the superior 60 field, 75° into the inferior field, 110° temporally, and 60° nasally. • An island of vision in the sea of darkness • The island represents the perceived field of vision, and the sea of darkness is the surrounding areas that are not seen. • In the light-adapted state, the island of vision has a steep light adapted state central peak that corresponds to the fovea, the area of greatest retinal sensitivity. MedWeb, 2008 376
  • 377.
  • 378.
    THE NORMAL VISUALFIELD • The contour of the island of vision relates to both the anatomy of the visual system and the level of retinal adaptation. • The highest concentration of cones is in the fovea, and most of these cones project to their own ganglion cell. • This one-to-one ratio between foveal cone and ganglion cell results i maximal resolution i the li ll l in i l l i in h fovea. MedWeb, 2008 378
  • 379.
    KINETIC PERIMETRY • Inkinetic perimetry a stimulus is moved from a nonseeing perimetry, area of the visual field to a seeing area along a set meridian. • The procedure is repeated with the use of the same stimulus along other meridians usually spaced every 15°. meridians, 15 • In kinetic perimetry, one attempts to find locations in the visual field of equal retinal sensitivity. • By j y joining these areas of equal sensitivity, an isopter is g q y, p defined. • The luminance and the size of the target is changed to plot other isopters. • In kinetic perimetry, the island of vision is approached horizontally. • Isopters can be considered the outline of horizontal slices of the island of vision. vision MedWeb, 2008 379
  • 380.
    STATIC PERIMETRY • Instatic perimetry the size and location of the test perimetry, target remain constant. • The retinal sensitivity at a specific location is determined by varying the brightness of the test target. • The shape of the island is defined by repeating the threshold measurement at various locations in the field of vision. MedWeb, 2008 380
  • 381.
  • 382.
    MANUAL PERIMETRY: THEGOLDMANN VISUAL FIELD • The Goldmann perimeter is the most widely used instrument for manual perimetry. • It is a calibrated bowl projection instrument with a background intensity of apostilbs (asb), which is i well within th photopic range. ll ithi the h t i • The size and intensity of targets can be varied to plot different isopters kineticall and determine kinetically local static thresholds. MedWeb, 2008 382
  • 383.
    THE GOLDMANN VISUALFIELD • • • • First in 1945 by Hans Goldmann Photopic background ( 10 cd/m² ) Moving and static circular targets The stimuli used to plot an isopter are identified by a Roman numeral, a number, and a letter. p j • The Roman numeral represents the size of the object, from 0.05º Goldmann size 0 (1/16 mm2) to 1.7º Goldmann size V (64 mm2) . • Each size increment equals a twofold increase in diameter and a f f ld i di d fourfold increase i area in • Visual angle + 90º MedWeb, 2008 383
  • 384.
  • 385.
    GOLDMANN VISUAL FIELD •The number and letter represent the intensity of the stimulus. 5 db • A change of one number represents a 5-db (0.5 log unit) change in intensity, and each letter represents a 1-db (0.1 log unit) change i i t h in intensity. it • The dynamic range of the Goldmann perimeter from the smallest/dimmest target (01a) to the largest/brightest target (V4e) is greater than 4 log units, or a 10,000-fold change. h MedWeb, 2008 385
  • 386.
    GOLDMANN VISUAL FIELD •The number and letter represent the intensity of p y the stimulus. A change of one number represents a 5-db (0.5 log unit) change in intensity, intensity and each letter represents a 1 db (0 1 1-db (0.1 log unit) change in intensity. • The dynamic range of the Goldmann perimeter from the smallest/dimmest target (01a) to the largest/brightest target (V4e) is greater than 4 log it l units, or a 10 000 f ld change. 10,000-fold h MedWeb, 2008 386
  • 387.
    GOLDMANN VISUAL FIELD •Isopters in which the sum of the Roman numeral (size) and number (i t b (intensity) are equal can b considered equivalent. it ) l be id d i l t For example, the I4e isopter is roughly equivalent to the II3e isopter. • A change of one number of intensity is roughly equivalent to a change of one Roman numeral of size. • The equivalent isopter combination with the smallest target size usually is p y preferred because detection of isopter edges is p g more accurate with smaller targets. • One usually starts by plotting small targets with dim intensity (I1e) and then increasing the intensity of the target until it is maximal before increasing the size of the target target. • The usual progression then is I1e (ARW1) I2e (ARW1) I3e (ARW1) I4e (ARW1) II4e (ARW1) III4e (ARW1) IV4e (ARW1) V4e e MedWeb, 2008 387
  • 388.
  • 389.
    AUTOMATED PERIMETRY • Theintroduction of computers and automation heralded a new era in perimetric testing. • St ti testing can be performed in an objective Static t ti b f di bj ti and standardized fashion with minimal p perimetrist bias. • A quantitative representation of the visual field can be obtained more rapidly than with manual testing. testing • The computer allows stimuli to be presented in a pseudorandom, unpredictable fashion. MedWeb, 2008 389
  • 390.
    AUTOMATED PERIMETRY • Patientsdo not know where the next stimulus will appear, so fixation is improved, thereby increasing the reliability of the test. • Random presentations also increase the speed with which perimetry can be performed by bypassing th problem of l b i the bl f local retinal adaptation, l ti l d t ti which requires a 2-second interval between stimuli if adjacent locations are tested tested. MedWeb, 2008 390
  • 391.
    Static suprathreshold andthreshold testing • Is processes to determine sensitivity of the retina to light stimulus • In addition to plotting isopters kinetically, static suprathreshold and threshold testing can be performed manually. ll • Once an isopter is plotted, the stimulus used to plot the isopter is used to statically test within the isopter to look for localized defects. • In this way, it acts as a suprathreshold stimulus. • Static thresholds also can be determined along set meridians to obtain profile plots of the visual field, but like any multiple thresholding task, it is time consuming. MedWeb, 2008 391
  • 392.
    Visual Fields :Advanced Concepts • The Threshold Strategy – The threshold strategy defines the threshold as being that level of light intensity that the patient responds to 50% of the time – Th most common example i th H The t l is the Humphrey Vi h Visual A l l Analyzer 24 2 th h ld 24-2 threshold strategy for glaucoma. – In this strategy, a grid of 54 points is tested in the central 24 degrees • Swedish Interactive Thresholding Algorithm (SITA) – Designed to reduce testing time while still providing an adequate test of visual sensitivity. – Reduced test time should increase attentiveness and result in a more reliable test – There are two different SITA programs : • SITA Standard  designed to replace the Full Threshold program (e.g. Full Threshold 30-2  a grid of 76 test points). • SITA Fast  designed to replace Fastpac, which is a simplified Threshold program • The Suprathreshold or Screening Strategy – Screening strategies use knowledge of the normal threshold values to present only suprathreshold stimuli that are just above the normal threshold values. – If the patient misses a significant number of these stimuli then the program is stimuli, considered to have detected a defect that warrants further testing 392
  • 393.
    Visual Field Analyzer y •Standard Achromatic Automated Perimetry (SAP) – – – – – – – – White-on-white perimetry Whit hit i t First established 1972 by Franz Frankhauser et al Mesopic to Photopic background (1.27 cd/m² or 10 cd/m²) Static test targets with 0.43º Goldmann size III for Standard test 1.7º Goldmann size V for low vision testing Standardized-high availability-wide dynamic range Feasible visual range usually ± 30º, theoretically up to ± 90º SAP : • Humphrey Visual Field Analyzer II (Carl Zeiss Meditec AG), program 24 2 software version 3 4 and the SITA testing 24-2, f i 3.4.7, d h i algorithm • Centerfield 2 Compact Perimetry (Oculus Optikgeräte GmbH) Survey of Ophthalmology, 2007 393
  • 394.
    Automated perimetry :Indicator • Fixation errors: the number of times the patient looks away from the central target. This is a key indicator of patient cooperation or fatigue fatigue. • False positives: the number of times the patient pushes the button when, in reality, a light source is not illuminated. • False negatives: the number of times the patient fails to push the button when, in reality, there is a light source illuminated. These spots can be repeat tested by the onboard computer at exactly the same spot to best understand the patient's ability to produce an accurate fi ld d d h i ' bili d field test. • Points tested: indicates the total number of separately illuminated testing points and therefore data points points, presented to the patient for testing. Reliable patients can produce a very useful field with a limited number of test po ts points. MedWeb, 2008 394
  • 395.
    Automated perimetry :Indicator • Reliability index : the overall reliability of the patient's testing for each eye. Poor reliability may indicate patient fatigue, fatigue insufficient understanding of the test or poor test, vision for other reasons such as cataracts. Visual field tests can also be used to ferret out malingerers. • Standard deviation: the difference in peripheral field acuity when compared to a normative data base, or simply put, a large group of similar normal patients. This tells the doctor whether or not a particular p of the p part peripheral field is normal, depressed, or absent. • Visual field map: the final basic report indicating the patient's visual field anywhere from the central 10 degrees all the way out to the farthest reaches of the field at 90 degrees. Altered patterns in the field map from reliable patient testing are often extremely useful in the diagnosis of ocular or neurological disorders disorders. MedWeb, 2008 395
  • 396.
    ASSESSING RELIABILITY False-Positive CatchTrials • A sound cue is given before each stimulus is presented in automated tests. • Periodically, the sound cue is given but no test stimulus is presented. • Af l false-positive result occurs if th patient responds t th sound cue iti lt the ti t d to the d alone. False-Negative Catch Trials • A false-negative catch trial is recorded if a patient does not respond at a location that had a measurable threshold earlier in the examination. g g y patient • A high number of false-negative catch trials may indicate p inattentiveness and an unreliable visual field. • The false-negative response rate is higher in eyes with extensive visual field defects than in those with normal visual fields. MedWeb, 2008 396
  • 397.
    How to Interpret: HFA Single Field Analysis ( g y (SFA) p ) print out : • Test parameter • Patient’s data • Reliability indices • dB graph • Gray scale pattern • Total deviation • Localized pattern deviation • Glaucoma Hemifield Test (GHT) • Global indices 397
  • 398.
    HFA Interpretation :Acceptability • Right test data • Correct patient’s data 398
  • 399.
    HFA Interpretation :Reliability • Fi ation Loss < 20 % Fixation • False positive < 33 % • False negative < 33 % 399
  • 400.
    Normality : dBGraph • The dB test by HFA range between “0” and “50” dB 50 • A typical “normal” reading is around 30 dB • A value at or above 40 dB is very unusual 400
  • 401.
    Normality : Grayscale • The actual threshold value on the dB graph converted to a Gray scale • The value less than or equal to 0 dB represented b solid d by lid black • The value above 40 dB are represented by total white • Commonly  we can not make a diagnosis based on g y the gray scale • The gray scale format quite useful when the patients to be explained about their visual field status 401
  • 402.
    Total deviation :Numerical plot • The numeric plot is the actual decibel deviation at each point as compared to normative data – Zero  Threshold – Positive  More sensitive – Negative  Depressed 402
  • 403.
    Total deviation :Probability plot • The probability plot indicates the statistical significance and predicts the possibility of such an normality in normal population • Gray scale pattern – “ < 5 % “ means l less th 5 of 100 normal than f l people (control) have this result – “ < 0.5 % “ means less than 5 of 1000 normal 05 people (control) have this result 403
  • 404.
    Total deviation • TheTotal deviation plot p highlights any overall depression of visual field – Generalized loss – Localized loss (scotoma) • The generalized field loss is caused by – – – – – Cataract Corneal opacities Media opacities Miosis Refractive errors 404
  • 405.
    Pattern deviation • Showssensitivity y losses after an adjustment to remove any generalized depression • Primarily highlights only significant localized visual l li d i l field loss • The most useful analysis 405
  • 406.
    Deviation : Normality TotalDeviation Pattern Deviation Interpretation No symbol No symbol Normal Some symbols Same pattern Pure localized loss Many symbols No symbols Pure generalized loss Many symbols Fewer symbols Mixed loss No or fewer Many symbols Trigger happy 406
  • 407.
    Glaucoma Hemifield Test(GHT) • It compares points on the upper field to corresponding points on lower one • The GHT based on : – The sensitivity of field should be similar on both hemifield – In Glaucoma the upper and lower hemifield are often significantly different • Sensitivity difference between the upper and lower hemifield are hallmark of glaucomatous field loss 407
  • 408.
  • 409.
    GHT : Result • • • • • Outsidenormal limits Borderline General Reduction of sensitivity Abnormally hi h sensitivity Ab ll high iti it Within normal limits 409
  • 410.
    Global indices • MeanDeviation (MD) • Pattern Standard Deviation (PSD) 410
  • 411.
    Mean Deviation (MD) •Th average measure of how much elevation or The fh h l i depression the patient’s visual field compared to a normal person of the same age • Derived from the Total deviation • Shows how much the whole field departs from normal • Very sensitive to generalized loss • A small defect will not affect MD significantly 411
  • 412.
    Pattern Standard Deviation(PSD) • It is a measure of th d i f the degree t which th to hi h the shape of the patient’s field differs from the normal age-corrected reference fi ld l t d f field • An index of localized non uniformity of the surface of the hill of vision f f th f i i • Strongly sensitive to the localized defect • I not affect by purely generalized d f t Is t ff t b l li d defect • Very helpful in diagnosing early glaucoma 412
  • 413.
    Global indices :Summary MD PSD Interpretation Normal Normal Probably Normal y Abnormal Normal Generalized loss Normal Abnormal Small localized defect Abnormal Abnormal Large defect with significant Localized component 413
  • 414.
    Normality : DefinitivelyAbnormal • GHT  Outside normal limits • PSD  p < 5 % 414
  • 415.
    Visual Field Loss: Indicator • Mean Deviation  < - 5 dB • Mean Deviation  p < 10% 415
  • 416.
  • 417.
    Defect identification :Type •G Generalized li d • Localized • Mixed 417
  • 418.
    Defect identification :Pattern • • • • • • • Paracentral scotoma Nasal step Arcuata Temporal wedge T l d Altitudinal Hemianopsia Etc 418
  • 419.
    Defect identification :Tendency • • • • Glaucoma Retinal disorders Neurological problems Artifact 419
  • 420.
    Anderson s Anderson’s criteria Itmust be Glaucoma • GHT  Outside normal limits • PD  Cluster of 3 or more non-edge points p < 5% with one of p < 1% • PSD  p < 5 % 420
  • 421.
    GLAUCOMATOUS VISUAL FIELDDEFECTS • Any clinically or statistically significant deviation from the normal shape of the hill of vision can be considered a visual field defect. • In glaucoma, these defects are either diffuse depressions of the visual field or localized defects that conform to p nerve fiber bundle patterns. MedWeb, 2008 421
  • 422.
    Glaucomatous VF Defect Mostappearances • Paracentral • Arcuate • Nasal step • Temporal wedge • Altitudinal defect American Academy of Ophthalmology 422
  • 423.
    GON and VFDefect Progression Community Eye Heath 2012 423
  • 424.
    PARACENTRAL DEFECTS • Circumscribedparacentral defects are an early sign of localized g g glaucomatous damage. g • The defects may be absolute when first discovered, or they may have deep nuclei , y y p surrounded by areas of less dense involvement. • The dense nuclei often are numerous along the course of the nerve fiber bundle MedWeb, 2008 424
  • 425.
  • 426.
    ARCUATE SCOTOMAS • Moreadvanced loss of arcuate nerve fibers leads to a scotoma that starts at or near the blind spot, arches around the point of fixation, and terminates abruptly at the nasal horizontal meridian . • An arcuate scotoma may be relative or absolute. • In the temporal portion of the field, it is narrow because all of the nerve fiber bundles converge onto the optic nerve. nerve • The scotoma spreads out on the nasal side and may be very wide along the horizontal meridian. MedWeb, 2008 426
  • 427.
    ARCUATE SCOTOMAS • • • A notchat the inferior pole of the optic disc (A) reflects damage to retinal nerve fibres projecting in an arcuate pattern, (B) resulting in an arcuate field defect. Section through the optic disc (C) illustrates that nerve fibres from peripapillary areas (red arrow) are located centrally in the optic nerve while fibres from peripheral areas (green arrow) are located near the nerve sheath. Damage occurring midway between sclera and cup yields a paracentral d f t (blue arrow). t l defect (bl ) 427
  • 428.
    Differential Diagnosis ofArcuate Scotomas MedWeb, 2008 428
  • 429.
    NASAL STEP DEFECTS •Because of the anatomy of the horizontal raphe, all complete arcuate scotomas end at the nasal horizontal meridian. • A steplike defect along the horizontal meridian results from asymmetric loss of nerve fiber bundles in the superior and inferior hemifields. MedWeb, 2008 429
  • 430.
    NASAL STEP DEFECTS •Nasal step defects may be evident in some isopters but not in others, depending on which nerve fiber bundles are damaged. • The width of the nasal step also varies. Nasal f steps frequently occur in association with arcuate and paracentral scotomas, but a nasal p , step also may occur in isolation. • Approximately 7% of initial visual field defects are peripheral nasal step defects defects. MedWeb, 2008 430
  • 431.
    TEMPORAL WEDGE-SHAPED DEFECTS WEDGESHAPED • Damage to nerve fibers on the nasal side of the optic disc may result in temporal wedge-shaped defects. • These defects are much less common than defects in the arcuate distribution. • Occasionally, they are seen as the sole visual field defect. • Temporal wedge defects do not respect the horizontal meridian. MedWeb, 2008 431
  • 432.
    TEMPORAL WEDGE-SHAPED DEFECTS WEDGESHAPED Community Eye Heath 2012 432
  • 433.
    Altitudinal Scotoma Altit dil S t • A more extensive arcuate defect • Involving 2 quadrants in either the superior or inferior field American Academy of Ophthalmology 433
  • 434.
    Altitudinal Scotoma: Causes • RETINALCAUSES – B Branch R ti l A t h Retinal Artery O l i Occlusion – Branch Retinal Vein Occlusion – Retinal Coloboma • OPTIC NERVE LESION – Ischemic optic neuropathy (both arteritic and non-arteritic types) – Papil edema – Optic disc coloboma • LESION IN CEREBRAL CORTEX – – – – Superior or Inferior calcarine cortex lesion Temporal lobe lesion Parietal lobe lesion Tumors affecting both occipital lobe may produce bilateral superior or inferior ltit di l field defect. i f i altitudinal fi ld d f t 434
  • 435.
    GLOBAL INDICES • Themean deviation (HFA) or mean defect ( ) (Octopus) reflects the overall depression or elevation of the visual field. • The deviation from the age-matched normal value is calculated at each location in the visual field. • Th mean deviation i simply th average The d i ti is i l the (Octopus) or the weighted average (HFA) of the deviation values for all locations tested. • Like the mean sensitivity, the mean deviation is most sensitive to diffuse changes and is less sensitive to small localized scotomas scotomas. MedWeb, 2008 435
  • 436.
    GLOBAL INDICES • Patternstandard deviation (HFA). Such ( ) irregularities can be due to a localized visual field defect or to patient variability. • Th corrected l The d loss variance or corrected pattern i d standard deviation provides a measure of the irregularity of the contour of the hill of vision that is not accounted for by patient variability (shortterm fluctuation). • It is increased when localized defects are present MedWeb, 2008 436
  • 437.
    INTEREYE COMPARISONS • Thedifference in the mean sensitivity between a patient s patient's two eyes is less than 1 dB 95% of the time and less than 1.4 dB 99% of the time. • Intereye differences greater than these values are suspicious if they are unexplained by non g glaucomatous factors, such as unilateral , cataract or miosis. MedWeb, 2008 437
  • 438.
    New opinions inVF analyzing • Nowadays SAP armed by Visual field progression software, E.g : i ft E PROGRESSOR GPA software package for f HFA (C l Z i M dit AG) (Carl Zeiss Meditec 438
  • 439.
    Glaucoma Progression Analysis(GPA) • Advancing the Science of Progression Analysis with improved GPA d i  d t i d design determine th stage of disease i the t f di and the rate of progression, and assess your patient’s risk of future vision loss  all at a glance • N New single-page G id d P i l Guided Progression A l i (GPA) i Analysis report delivers current exam results, trends the entire visual field history and projects future vision loss. • New Visual Field Index (VFI)  an improved measure of a patient’s visual function status and is optimized for glaucoma progression analysis. • New software reporting offers guidance for severely depressed visual fields • New GPA algorithm allows GPA analysis to be run on more patients right away by allowing a mix of Full Threshold and SITA exams. 439
  • 440.
    New opinions inVF analyzing • But still SAP can only detect the visual field defect after about 50% loss of the ganglion cells • How to detect earlier ? 440
  • 441.
    Weinreb’s Structural/ FunctionalRelationship in Glaucoma as the Disease Progresses g VF Early % Loss s As compared to GCC, RNFL is still most widely used and accepted by thought leaders and Drs worldwide orld ide Moderate Severe Time Adapted f Ad t d from Professor Robert N. Weinreb P f R b tN W i b Hamilton Glaucoma Center, University California San Diego 441
  • 442.
  • 443.
    Latest generation : g Ganglioncell VF Analyzer • Short-Wavelength Automated Perimetry (SWAP) – – – – First 1986 by Pam Sample et al Photopic background Static test targets with 1.7º Goldmann size V and 440 nm Blue color In SWAP, a 440-nm, narrow-band, 1.8° target is presented at 200ms duration on a bright 100 cd/m2 yellow background and selectively tests the short-wavelength–sensitive cones and their connections – Selecti e test for Koniocell lar path a  Bl e sensitive cones Selective Koniocellular pathway Blue sensiti e – Feasible visual range + 30º – Detecting glaucoma 5 years earlier than white on white perimetry Survey of Ophthalmology, 2007 443
  • 444.
    Latest generation : Ganglioncell VF Analyzer • F Frequency-Doubling Technology Perimetry D bli T h l P i t (FDT) – First 1966 by Don Kelly et al – FDT was measured with the frequency-doubling visual field instrument (Carl Zeiss Meditec AG) using Welch-Allyn technology (Skaneateles Falls, NY) and the N-30 program, software version 3.00.1 – Magnocellular  Motion detecting sensitivity – The targets consist of a 0.25-cyc/deg sinusoidal g grating that undergoes a 25-Hz counterphase flicker g g p Survey of Ophthalmology, 2007 444
  • 445.
    Latest generation : Ganglioncell VF Analyzer • Frequency Doubling Technology Perimetry Frequency-Doubling (FDT) – The test involves a modified binary search staircase y threshold procedure with stimuli presented for a maximum of 720 ms. FDT measures the contrast needed for detection of the stimulus – Each grating target is a square subtending approximately 10° in diameter. – Targets are presented in one of 18 test areas located within the central 20° radius of the visual field temporally and 30° nasally Survey of Ophthalmology, 2007 445
  • 446.
    Latest generation : Ganglioncell VF Analyzer • High-Pass Resolution Perimetry ( g y (HPRP) ) – First introduced 1987 by Lars Frisen – In HPRP, ring-shaped vanishing optotypes which vary in size are used to assess resolution ability in the central 30° of the visual field – The optotypes used in HPRP are high-spatialfrequency filtered targets where the inner and outer portions of the rings are darker (15 cd/m2), whereas the th center portion of the rings i b i ht (25 cd/m2) t ti f th i is brighter d/ – Parvocellular Color, Form, Long wavelength sensitivity 446
  • 447.
    Latest generation : Ganglioncell VF Analyzer • Hi h P High-Pass R Resolution Perimetry (HPRP) l ti P i t – The space-averaged luminance of the entire ring is equal to the luminance of the photopic background (20 cd/m2) – Th f Therefore, when the edges of the ring cannot b resolved, th h th d f th i t be l d the rings blend into the background, that is, the targets are either resolved (seen) or they are invisible – The target consists of rings of different sizes presented at 50 sizes, locations within the central 26-30° – No stimuli are presented within the central 5° of the visual field – The subject responds when the target is large enough to resolve – E.g : HPRP is with the Ophthimus High-Pass Resolution Perimeter, version 2.0, software version 2.51 (HighTech Vision, Malmö, Sweden). 447
  • 448.
    Examples of visualfield pattern deviation display for SAP, SWAP, FDT, and the small and deep dent display for HPRP in a patient with GON. Each plot shows the location and number of stimulus test locations as designated by either a box or a dot Dot: within normal limits The shading in the dot. limits. boxes denotes the probability of abnormality relative to the internal normative database of each device. Probabilities are shown in the corresponding key. 448
  • 449.
    VF Defect : Chartsand Facts 449
  • 450.
    Source of errorin VF Analyzing • • • • Miosis Lens or media opacities Uncorrected refractive error Spectacles S l – Decrease of sensitivity up to about 1.2 dB per Diopter – Boundary scotoma caused by the frame • Ptosis • Inadequate retinal adaptation • Fatigue Kanski JJ, 2007 450
  • 451.
    Another VF Analyzer • • • • • • • Matrix PULSAR FlickerPerimetry Fli k P i t Motion Detection Perimetry (MDP) Motion Automated Perimetry (MAP) Motion Coherence Perimetry (MCP) Rarebit Perimetry Survey of Ophthalmology, 2007 451
  • 452.
    Endothelial cell loss Trabecular damage / PAS Irisatrophy Primary angle closure Lens damage Ischemic Optic Glaucomatus Neuropathy Optic Neuropathy Damage to ocular tissue in angle-closure glaucoma angle closure Foster PJ 2001 452
  • 453.
    CLASSIFICATION OF GLAUCOMA (JAPANGLAUCOMA SOCIETY, GUIDELINES FOR GLAUCOMA) ANTERIOR CHAMBER ANGLE NORMAL OPEN ANGLE GON NO GVFD NO YES IOP NORMAL ELEVATED NORMAL YES IOP IOP NORMAL ELEVATED NORMAL-TENSION GLAUCOMA (SUSPECT) NORMAL ELEVATED NORMAL-TENSION GLAUCOMA OCULAR HYPERTENSION PRIMARY OPEN-ANGLE GLAUCOMA (SUSPECT) PRIMARY OPEN-ANGLE GLAUCOMA 453
  • 454.
    Steroid-induced glaucoma g • Uncertain •Steroid  excessive deposit of acid mucopolysaccharide or glycosaminoglycan (GAG) • It present in trabecular meshwork  ti t b l h k abnormal function Trans Am Ophthalmol Soc,1977 454
  • 455.
    Newest term ofPOAG and NTG • Developmental and degenerative ocular problems – Degenerative of entire ocular vascular and trabecular meshwork* – Regression failure of hyaloid artery in third trimester of gestation  facilitating the high IOP to directly hits the optic nerve head – Previously “ fragile “ optic nerve head and RNFL y g p * Does not occur in NTG 455
  • 456.
    Glaucoma : Tt Gl Treatment t • • • • • Causes  Trauma, New vessels etc Medical Laser Surgery Others Others* 456
  • 457.
    Gaucoma : Medical Class Dosage IOP decrease Timeto peak effect/ washout 1.  blockers Timolol Maleat bid 20-30% 20 30% 2-3 2 3 hours/1 month Betaxolol bid 15-20% 2-3 hours/1 month bid, tid 20-30% 2 hours/7-14 days 2. Alpha 2 adrenergic agonist Brimonidine 3. Carbonic Anhidrase inhibitor Dorzolamid D l id bid, bid tid 15-20% 15 20% 2-3 hours/48 h 23h /48 hours Brinzolamide bid, tid 15-20% 2-3 hours/48 hours 4. Prostaglandin analogues & Prostamides ostag a d a a ogues osta des Latanoprost qd 25-32% 10-14 hours/4-6 weeks Travoprost qd 25-32% 10-14 hours/4-6 weeks p Bimatoprost q qd 27-33% 10-14 hours/4-6 weeks Unoprostone Tafluprost bid qd 13-18% 18-22% Unknown Unknown 457
  • 458.
    Glaucoma : Pathwaysto IOP reduction 458
  • 459.
    Target IOP g Target IOPmay be defined as a pressure, rather a range of intraocular pressure levels within which the progression of glaucoma and visual field loss will be delayed or halted • Advanced POAG  12 mmHg • Early g y glaucoma  17 mmHg g • NTG  11 mmHg Gumansalangi MNE, 2002 459
  • 460.
    AAO GUIDELINES: TARGETIOP GUIDELINES • Open angle glaucoma with IOP in the mid to high 20s  Target IOP range 1418 mmHg • Advanced Glaucoma  Target IOP is < 15 mmHg • OHT whose IOP > 30 mmHg with no sign of optic nerve damage  Target IOP < 20 mmHg Survey of Ophthalmology, 2003 460
  • 461.
    Factors to beconsidered • • • • • • • • Efficacy: Maximal IOP reduction Minimum required drug Easy to use and compliance Giving flat diurnal curve Ocular tolerability Systemic safety Cost effective Quality of life Gumansalangi MNE, 2002 461
  • 462.
    Glaucoma : Laser •Argon laser trabeculoplasty p y y • Selective laser trabeculoplasty  Primary Glaucoma Therapy? • Laser gonioplasty • Nd:YAG laser iridotomy y • Diode laser cycloablation • Endoscopic cyclo laser photocoagulation 462
  • 463.
    Glaucoma : Surgery • • • • • • • • • • • Inflowprocedures p Vitrectomy Lens extraction Pupil P il reconstruction t ti Iridectomy Trabeculectomy Tubes and Shunting Canaloplasty Viscocanalostomy Deep sclerotomy Crosslinked NaHA  surgery enhancer enhancer* 463
  • 464.
  • 465.
    Glaucoma Devices, Tubesand Shunting • • • • • • • • • • • • Molteno Implant Pressure Ridge Molteno Implant Ahmed Valve Baerveldt Tube Shunt SOLX Gold Shunt iScience Microcatheter Canaloplasty GLAUCOLIGHT C Canaloplasty D i (DORC) l l t Device ExPress Mini-Shunt (Alcon Inc) iStent (Glaukos) Hydrus (Ivantis) Stegmann Canal Expander AqueSys Collagen Tube Implant 465
  • 466.
    Glaucoma : Cilliarybody ablation • Cyclocryo therapy • Ultrasound • Diode laser 466
  • 467.
  • 468.
    Is there moreto glaucoma treatment than l h lowering IOP ? i • Inhibition of activation of Astrocytes • Inhibition of Nitric-Oxide-Syntase 2 (NOS-2) • Reduces nocturnal overdipping – Fludrocortisone 0.1 mg 2 times per week • • • • • Improvement of vascular regulation and autoregulation Combat of oxidative stress Inhibition of Metalloproteinase-9 (MMP-9) Stimulation of Heat Shock Protein (HSP) production Neuroprotection – Memantine  N-Methyl D-Aspartate (NMDA) receptor g antagonist Survey of Ophthalmology, 2007 468
  • 469.
    Lens and cataract L dt t The Pioneer Prof. dr. Istiantoro Sukardi, Sp.M(K) Sukardi, Sp.M(K) 469
  • 470.
  • 471.
    Lens Opacities ClassificationSystem III (LOCS III) 471
  • 472.
    Opt ca oet y ased Cata act C ass cat o Optical Biometry Based – Cataract Classification • No Cataract (NC)  • For Refractive Lens Extraction (RLE) Phacoemulsification Plan • Optical Biometry Examinable Cataract (OBEC)  • For Low Energy Phacoemulsification Plan • For learning Phacoemulsification and for transition to MICS and Femtosecond Laser Cataract Surgery • Optical Biometry Un-examinable Cataract (OBUC)  • For High Energy and More Maneuver Phacoemulsification Plan Pardianto G ESCRS 2010 472
  • 473.
    Paradigm of lenssurgery • Avoid advanced cataract complications  prevents avoidable bli d t id bl blindness • Restores visual function • Nowadays  refractive surgery  p improves visual function  Phacoemulsification or more* Eurotimes, 2009 473
  • 474.
    Refractive Surgery • Opticalsynergy  Sharper vision – Zero spherical aberration – Reduced chromatic aberration – Full visible light transmission – Glistening free – Limited Lens Epithelial Cells (LEC) migration Eurotimes, 2009 474
  • 475.
    Cataract surgery :State of the Art • More comfort, faster and reliable , advanced examination • Minimal invasion • Minimal manipulation • Minimal complication • Better result • Better outcome • More improved visual function 475
  • 476.
    Intraocular materials • • • • • • Sterile Inert I t Nontoxic Non allergenic pH Balanced Long lasting stable 476
  • 477.
    Crystalline Lens vsIOLs • • • • 200 250 200-250 vs 20 mm3 volume 11 vs 12-13 mm overall diameter 4.5 4 5 vs 1 mm thi k thickness 10 vs 5-6 mm front surface radii of curvature • 6 vs 5-6 mm back surface radii of curvature Eurotimes, 2010 477
  • 478.
    Spherical vs AsphericLens Spheric 478
  • 479.
    Spherical vs AsphericLens Aspheric 479
  • 480.
    Spherical vs AsphericLens Changchun Jixiang, 2006 480
  • 481.
    IOL : Biometry •A Scan biometry – Very dense cataract – Use different keratometry analyzer • 3rd and 4th generation formulated biometry  Phakic IOL and post refractive surgery biometry – Partial Coherence Laser Interferometer or Non-contact Optical Coherence Biometry or Laser Interferometry Technique C h Bi t L I t f t T h i • IOL Master 5.0 (Carl Zeiss Meditec AG), • Lenstar LS 900 (Haag-Streit International) • Pentacam HR (OCULUS Optikgeräte GmbH) ( p g ) • IOL Station (NIDEK) – Advanced Immersion A Scan biometry • Aviso (Quantel Medical) 481
  • 482.
    Aviso (Quantel Medical) IOLMaster 500 (Carl Zeiss Meditec AG) Lenstar LS 900 (Haag Streit International) (Haag-Streit 482
  • 483.
    IOL Calculation Formulas •1st Generation – SRK  Sanders, Retzlaf and Kraff • 2nd Generation – Binkhort, Hoffer, SRK II, Holladay • 3rd Generation – SRK/T, Hoffer-Q • 4th Generation – Holladay 2, Haigis, Camellin-Calossi – Double K technique  Post LASIK 483
  • 484.
    IOL calculation formulas •SRK  P = A - (2.5L) - 0.9K – L in millimeter – K in Diopter • Older guidance (Axial length approach) – > 26 mm – 24.4 – 26 mm – 22 – 24 5 mm 24.5 » or  – < 22 mm SRK-T, Optimized Haigis Holladay Holladay 2 Haigis 2, Average of SRK/T, Holladay, Hoffer-Q Hoffer-Q, Optimized Haigis 484
  • 485.
    Reevaluated IOL Calculation: • Less than 22 mm or more than 25 mm axial length • Less than 40.00 D or more than 47.00 D of K Reading • Difference in both eyes : – More than 1.00 D K Reading – More t a 0 3 mm a a length o e than 0.3 axial e gt – More than 1 D IOL Power in target of emmetropia 485
  • 486.
    The IOLs • • • • • 360 360º barrieredge Corrects spherical aberration to essential zero Increases contrast sensitivity Reduces harmful blue lights g p Significant improvement of visual function 486
  • 487.
    IOL: Spheric vsAspheric IOL Spherical aberration correction by Spherical IOL vs Aspheric IOL Alcon, 2010 487
  • 488.
    Lens and Cataract: IOLs Aberration counter Aberration-counter Aspheric IOLs • Acrysof IQ Aspheric Natural IOL (Alcon, Inc) • enVista Glistening-free Aspheric IOL ( g p (Bausch & Lomb Incorporated) • Akreos MI60 Microincision Lens with Aspheric Aberration-Free Optics IOL (Bausch & Lomb Incorporated) • • • • TECNIS 1-Piece Aspheric IOL (Abbott Medical Optics) C-flex and Superflex Aspheric IOL ( y ) p p (Rayner) HOYA’S Aspheric ABC Design IOL (HOYA) Afinity Collamer Aspheric IOL (Staar) y 488
  • 489.
    Multifocal IOL :Refractive • Designed with several optical zones on the intraocular l i t l lens. • These zones provide various focal points, allowing for an improvement in distance, intermediate, and near vision. 489
  • 490.
    Multifocal IOL :Diffractive • Gradual diffractive steps on the intraocular lens implant that create a smooth transition between focal points. • Th IOL also b d i The l bends incoming li ht t th i light to the multiple focal points to increase vision in various lighting sit ations ario s situations. 490
  • 491.
    Apodization • Is thegradual reduction or blending of diffractive step heights. • Distributes the appropriate amount of light to pp p g near and distant focal points  regardless of the lighting situation. • The apodized diffractive optics are also designed to improve image quality and minimize visual di i l disturbances – a significant i b i ifi improvement over traditional multifocal technologies Alcon, 2010 491
  • 492.
    Multifocal : Multifocal*: Accommodative •An accommodative intraocular lens implant only p y has one focal point, but it acts as if it is a multifocal lenses. • Th IOL was designed with a hi The d i d i h hinge similar to the i il h mechanics of the eye’s natural lens. • Using the eye’s muscles the single focal point of eye s muscles, an accommodative intraocular lens can shift to bring objects at varying distances into focus. – Change in SHAPE of the lens in the eye – Change in POSITION of the lens in the eye 492
  • 493.
  • 494.
    Multifocal IOLs • AcrySofReSTOR Diffractive Apodization Aspheric IOL (Alcon Inc) (Alcon, • ReZoom TECNIS Multifocal IOL (Abbott Medical Optics) • TECNIS 1 Diffractive Aspheric 1-piece Multifocal IOL (Abbott Medical Optics) • Acriva Reviol Multifocal IOL (VSY Biotechnology) • AT Lisa (Carl Zeiss Meditec AG) • MF4 (Ioltech  Carl Zeiss Meditec AG) • M-flex (Rayner) ( y ) • Versario (CROMA) 494
  • 495.
    Accommodating IOLs • CrystalensAT-45 Accommodating IOL (C&C Visions) • KH-3500 (Lenstec) • Bi C BioComFold 43A (M h ) F ld (Morcher) 495
  • 496.
    Toric IOLs • AcrySofToric Natural IOL (Alcon, Inc) • Acri.LISAToric IOL (Acri.Tec  Carl Zeiss ( Meditec AG) • AA4203TF (Staar) • MicroSil (H manOptics) (HumanOptics) • T-flex (Rayner) • M-flex-T  Toric Multifocal (Rayner) M flex T 496
  • 497.
    Photochromic IOLs • • • • • Colorless UV-Blockingat night Changes to a yellow outdoor during the day Does not compromise scotopic vision at night Provides additional protection from blue light E.g : MATRIX Acrylic AURIUM (Medennium) 497
  • 498.
    MICS IOL • • • • MI60 (Bauschand Lomb) AT Lisa (Carl Zeiss Meditec AG) AT S Smart 48S (C l Z i M dit AG) t (Carl-Zeiss-Meditec ThinLens UltraChoice 1.0 (Technomed GmbH) • Lentis L-303 (Oculentis GmbH) ( ) • CareFlex (w2o Medizintechnik AG) 498
  • 499.
    Hydrophilic vs HydrophobicIOL • Hydrophilic IOL – – – – Less Uveitis Less Anterior Capsule Contraction Less Glaucoma Less Capsular Block • Hydrophobic IOL – More adhesiveness to posterior capsule – Less PCO • New design  Anterior surface hydrophilic and posterior surface hydrophobic  Bi Flex 1.8 (Medicontur) (M di t ) 499
  • 500.
    Haptic • Three-piece Three piece –Less PCO  if square-edged optic IOL – Less space  if in posterior chamber / sulcus fixation  less glaucoma • One piece One-piece – Less PCO  if design as 360-degree squareedged IOL – Not recommended fixated in the sulcus 500
  • 501.
    Hi-end Operating microscope • Excellentin – – – – – – – – Bright illumination Red reflex Depth perception Outstanding Beam splitter  Assistance, Teaching and Recording Smooth X-Y-(Z) Great i G t in zoom and focus maneuver df UV barrier Blue filter • • • • Carl-Zeiss OPMI Lumera i and Lumera T MÖLLER Hi-R 900 and Hi-R 1000 Leica M844 F40 Alcon LuxOR™ Surgical Microscopes with Q-VUE™ 3-D assistant • Do not forget : How to adjust your microscope microscope. 501
  • 502.
    Cataract surgery :Phacotechnique • 1st Generation – Kelman tecnique  • Can-opener capsulotomy • Anterior chamber • 2nd Generation – Can-opener capsulotomy p p y – Posterior chamber Phaco – Sculpting • 3rd Generation – Continuous Curvilinear Capsulorrhexis (CCC) – In-situ Phaco  Endo-capsular – E.g : Divide and Conquer, Sheperd’s Phaco Fracture Technique, Fine’s Chip and Flip Technique, Fine and colleagues’ Crack and Flip Technique, Nagahara’s Phaco C Ph Cop, Pf iff ’ Q i k Ch and K h’ St Pfeiffer’s Quick Chop d Koch’s Stop and Chop 502
  • 503.
    Cataract surgery :Phacotechnique • 4th Generation – CCC – Supracapsular – E.g : Fine, Parker and Hoffman’s Choo Choo Chop and Flip – Revolution in • • • • • Micro incision  1 7 - 1 8mm 1.7 1.8mm Cooler Phaco Phaco-tip IOLs Improvement in uncorrected post-operative day one visual acuity 503
  • 504.
    Cataract surgery :Anesthesia • Nowadays trend  Topical, and some  add y p , by Viscoelastic-borne intra cameral anesthesia • But please do not forget and keep your ability to perform f – – – – – Akinesia  the absence (or poverty) of movement Retrobulbar Peribulbar Sub-tenon Sub-conjunctiva • In special case  General anesthesia 504
  • 505.
    Cataract surgery :Incision • • • • • Clear Corneal Incision recomended Small to Micro ( ) Micro to 1.6 - 1.8 mm incision (MICS) But  size is not everything Factors to be considered – – – – – Shape and contour of incision Well sealed and water tight Depend on cataract density and hardness Depend on instruments to perform Depend on surgeon ability p g y 505
  • 506.
    Avoid incision leak • • • • • • • • Squareincision Proper size 2-3 2 3 steps direction Avoid incision burns Good t h i G d technique phaco and IOL i h d insertion ti Good tip and cartridge Checking incision at end of surgery Stromal hydration 506
  • 507.
    Limbal relaxing incision •With the rule  CCI and superior limbal relaxing i i i l i incision • Against the rule  temporal CCI and limbal relaxing incision Vajpayee RB 2005 RB, 507
  • 508.
    Cataract surgery :“Peri-phaco” Peri phaco • CCC  Continuous Curvilinear Capsulorrhexis Caps lorrhe is • Tools: – N dl Needle – Forceps –F t Femtosecond Laser  dL • • • • Alcon LenSx (Alcon LenSx Laser Inc) LensAR Laser System (LensAR Inc) Catalys Precision Laser System (OptiMedica) CUSTOMLENS TECHNOLAS (Perfect Vision) EuroTimes, 2010; EyeWorld, 2010 508
  • 509.
    Cataract surgery :“Peri-phaco” Peri phaco • Hydrodissection  Injection of a small amount of fluid into the capsule of the lens to separate the nucleus from cortex • H d d li Hydrodelineation  I j ti of fl id ti Injection f fluid between the layers of the nucleus of the lens using a bl t needle  G ld Ri l i blunt dl Golden Ring 509
  • 510.
    Hydrodissection : Becareful • • • • Posterior pole cataract Traumatic cataract Hard brown cataract Post vitrectomy cataract Rajan M, Mehta C, 2009 510
  • 511.
    Phacomachine and instrumentation • • • • • • • • Wellcontour micro incision Surge free anterior chamber maintenance Cooler phaco tips Smoother vacuum and phaco power Endothelial friendly E d th li l f i dl Reduce dropping nucleus Less edema, less astigmatism Better outcome 511
  • 512.
    Phacomachines a. Peristaltic Pump Apump which fluid is forced along by waves of contraction produced mechanically on flexible tubing 512
  • 513.
    Phacomachines b. Venturi Pump Thispump is driven by compressed gas (nitrogen or air) that is directed through chamber B 513
  • 514.
    Phacomachines c. Diaphragm Pump Aflexible diaphragm A is alternately pushed in and pulled out by a rod connected to an electric motor rotating as indicated 514
  • 515.
    Comparison of pp p pumps Peristaltic Venturi Flow based Vacuum based Vacuum created on occlusion of phaco tip Vacuum created instantly via pump Flow is constant until occlusion Flow varies with vacuum level Drains into a soft bag Drains into a rigid cassette Devgan U, 2008 515
  • 516.
    Phaco Pump Comparison Pump Pro Contra Vacuum e.g.Venturi Less posterior occlusion surge Better for vitreous removal Material comes to tip easily Need source of compressed gas Need rigid cassette Flow Fl e.g. Peristaltic Better f B tt for sculpting l ti No need for compressed air Post P t occlusion surge l i Need occlusion for vacuum to build Siebel BS, 2008 516
  • 517.
    Lens and Cataract: Phacomachines Newest phacomachines : • WHITESTAR SignatureTM System with FusionTM Fluidics and ELLIPSTM Transversal Ultrasound (Abbott Medical Optics) • Th Stellaris MICSTM Vi i E h The St ll i Vision Enhancement S t t System with EQ FluidicsTM Technology (Bausch & Lomb Incorporated) • INFINITI Vision S System with INTREPIDTM Fluidics Management System and the OZil® IP Intelligent Phaco Torsional Handpiece (Alcon, Inc) • The CENTURION® Vision System (Alcon, Inc) • Qube Smart System (CROMA) • Faros OS3 and CataRhex3 (Oertli) 517
  • 518.
    Micro Incision SleeveDevelopment Support smaller incisions – Reduce shaft diameter Optimize performance – Maximize chamber stability – Wound protection – Minimize wound leakage Alcon Inc 518
  • 519.
    Infusion Sleeve Technology Translucence –Maximize visualization Thin Walls – Maximize Flow – Minimize bulk Large Holes – Maximize Flow Smooth Profile – Ease of insertion – MicroSmooth Technology Tight Tolerances – Consistency – Quality Alcon Inc 519
  • 520.
    Older Footswitch Positions 1.Irrigation 2. 2 Irrigation Aspiration + Vacuum 3. Irrigation Aspiration + Vacuum U/S Power 520
  • 521.
    Footswitch Positions 1. 1 Irrigationcan set always ‘On’ 2. Irrigation g Aspiration + Vacuum 3. Irrigation Aspiration + Vacuum U/S Power 521
  • 522.
    Phacodynamics : Fundamentals •Ultrasound (U/S): Repulsive forces  Power (percent) and also  Ph d l Phaco ti time ( (second)  A d) Average U/S, U/S Effective U/S and Absolute U/S • Aspiration Flow Rate: (cc/min); is the magnetic action Rate: in system to ATTRACT lens material at a specific speed. • Vacuum: (mmHg) is negative pressure in system used to HOLD the pieces • Bottle height: (cm)  Estimate IOP (mmHg) = Bottle height X 0.74  now automated by compressor gy technology 522
  • 523.
    Ultrasound: Phaco power •Absolute phaco time (APT) and Effective phaco time (EPT) • Equivalent phaco time at 100% power • APT = total phaco time (seconds) • EPT = phaco time (seconds) X average phaco power (percents) Devgan 2004 523
  • 524.
    Power Delivery • Dutycycle: The ratio of working time to total time of U/S  usually expressed as a percent • P l per second (PPS) A Pulse d (PPS): Amount of pulse t f l those are delivered in one second. 524
  • 525.
  • 526.
    AFR and Vacuum •Aspiration Flow Rate (Attracts) • Vacuum (negative holding pressure) Alcon Inc 526
  • 527.
    ASPIRATION FLOW RATE(AFR) • What does it do? – Attracts material to the tip – Determines how fast material is drawn to the phaco tip Alcon Inc 527
  • 528.
    ASPIRATION FLOW RATE(AFR) • Fluid moving through the tubing toward the collection b i referred t as A i ti Fl ll ti bag is f d to Aspiration Flow, or Aspiration. • Aspiration starts when the pump starts . ASPIRATION FLOW -Pump rotation pushes fluid out TO DRAIN BAG PERISTALTIC PUMP -More fluid moves in -That is Aspiration Flow -Speed of flow is Aspiration Flow Rate -Pump speed controls AFR Alcon Inc 528
  • 529.
    AFR: FOLLOWABILITY • WHATDOES THIS TERM APPLY TO? – The ability to attract material to the tip • WHAT CONTROLS IT? – Aspiration Flow Rate Alcon Inc 529
  • 530.
    VACUUM –Negative Pressure or Negative HoldingForce –Measured in mmHg –Holds material onto the tip –The higher the vacuum the greater the holding force Alcon Inc 530
  • 531.
    Vacuum: OCCLUDE • Occlusionrefers to an obstruction of the phaco tip Alcon Inc 531
  • 532.
    Vacuum: Purchase • Thegrip of the vacuum on the occluding material. • The higher the vacuum the greater the vacuum, purchase. Alcon Inc 532
  • 533.
    Rise Time • WHATIS IT? – The measurement of how fast vacuum builds upon occlusion – Rise Time is directly related to AFR – The faster the AFR the shorter the Rise Time Alcon Inc 533
  • 534.
    COMPLIANCE • WHAT ISIT? “The ability of an object to yield elastically when a force is applied” • WHAT IMPACT DOES IT HAVE? The more compliance, the slower the responsiveness and performance Alcon Inc 534
  • 535.
    NON-COMPLIANCE Non-Compliance is “theability of an object to maintain rigidity when a force is applied”. The more Non-compliant a p fluidic system is, the more responsive it’s performance will be (ie: “True Control”) Alcon Inc 535
  • 536.
    Vacuum: VENTING Vacuum Back to neutral Alcon Inc 536
  • 537.
    Vacuum: REFLUX V • Pushfluid flow •R l Release material that attached on th t i l th t tt h d the phacotip after complete venting process Alcon Inc 537
  • 538.
    Vacuum: SURGE FLUIDIC IMBALANCE • Outflow •Exceeds • Inflow Alcon Inc 538
  • 539.
  • 540.
    ULTRASOUND (U/S) ( ) • Refersto frequencies above the range of human audibility, or above 20,000 vibrations per second second. • In phacoemulsification, the term “ultrasound” is used because the phaco needle moves back and forth in excess of 20,000 times per second  MICS is in 28,500 times per second , p • There are no “sound waves” associated with phacoemusification. Alcon Inc 540
  • 541.
    U/S: FREQUENCY •How FAST thephaco needle moves back and forth Frequency q y WHAT IS THE FREQUENCY RANGE? •The frequency of ultrasonic handpieces is between 27,000 d 60,000 2 000 and 60 000 cycles per second l d Alcon Inc 541
  • 542.
    U/S: STROKE • WHATIS IT? The tip travels 3.5 mils at maximum power Stroke How FAR the phaco tip moves back and forth p p Alcon Inc 542
  • 543.
    U/S POWER • U/SPower is the percent of the maximum stroke length traveled b th phaco ti t k l th t l d by the h tip. • Phaco tip moves in and out in linear fashion. • Some handpieces have a maximum excursion (Stroke) of 3.2 mils , or 3.2 thousands of an inch (0 001 inch) which (0.001 inch), would represent 100% power. • Lower power settings are some portion of the maximum stroke, e.g., 60% would be 1.92 mils of travel. Alcon Inc 543
  • 544.
    PIEZOELECTRIC HANDPIECE • Theforward and back linear (in a straight line) motion of a U/S handpiece is generated by piezoelectric crystals. • Th These crystals, which are l t l hi h located i th t d in the handpiece, vibrate at a known frequency when electricit r ns thro gh them hen electricity runs through them. Alcon Inc 544
  • 545.
    PIEZOELECTRIC HANDPIECE • Motion isgenerated when a tuned, highly refined crystal is deformed by the electrical energy supplied from the console. t l i il to the t h • Th These crystals are similar t th ones i a watch. in • The phaco tip is attached to the vibrating crystals. Alcon Inc 545
  • 546.
    CHATTER • WHAT ISIT? – Fragments rebounding from the tip WHAT CAUSES IT? • Chatter occurs when stroke overcomes Vacuum and AFR Alcon Inc 546
  • 547.
    • • • • • U/S: LOAD WHAT ISIT? Occurs when the tip encounters nuclear material WHAT HAPPENS? Requires more power to maintain stroke Load is constantly changing No Load Load Alcon Inc 547
  • 548.
    CAVITATION WHAT IS IT? •The formation of vacuoles in a liquid by a swiftly moving solid body (an ultrasonic tip) • The collapse of the vacuoles produces energy which will erode solid surfaces Alcon Inc Boat Propeler Example of Cavitation 548
  • 549.
    CAVITATION Kelman tip Implosion f Il i of vacuoles produces: l d Nine (9) ATA of pressure l 5000° F destructive energy release This takes place on a microscopic scale Alcon Inc 549
  • 550.
    TUNING • The methodused to match up the driving frequency of the console with the operating frequency of the phaco handpiece and tip. Alcon Inc 550
  • 551.
    U/S: Power modulation •Continuous – Continuous delivery of power – Phaco is on in position three – Usually increasing ultrasound power with depth into foot position – Used for partial-occlusion sculpting Chang DF, 2004; Oetting T, 2005 551
  • 552.
    U/S: Power modulation •Pulse – Allows surgeon to vary the power with linear control with a fixed number of pulse per second (pps) – Ranges from 1 to 20 pps – With a 50% duty cycle and linear control of power – Phaco pulses with duty cycle on and off – Usually with equal on and off time or 50% duty cycle (time on/cycle time) – Usually the rate (or inverse of duty cycle) is fixed (Hz) – Usually increasing ultrasound power with depth into foot positi Chang DF, 2004; Oetting T, 2005 552
  • 553.
    U/S: Power modulation •Burst – Allows surgeon to vary the number of burst of power per unit time – With Constant amount of power – Duration  varied widely  5-600 ms – Reduce in thermal and exposure time of energy – Bursts of power come with off time that decreases with depth into foot position – Usually when floored in position 3 -- ultrasound power becomes continuous b i – Ultrasound power is fixed Chang DF, 2004; Oetting T, 2005 553
  • 554.
    U/S: Power modulation •Hyperpulse – Uses short on time pulses e.g. 25% on; 75% off – Fixed duty cycle; fixed pulse rate – Usually increasing ultrasound power with depth into foot position Oetting T, 2005 554
  • 555.
    Advantages & Disadvantages ofVarious U/S Modes Mode Advantages Disadvantages Applications Continuous Simple - Repels nuclear material - Hot Sculpting Pulse Less hot - Can repel nuclear material - Choo choo chop - Segment removal Burst B t - L Less h t hot - Holds material well Chopping Ch i Hyperpulse - Followability with long off cycle - Cool with long off y cycle - Sculpting - Bimanual small incision Siebel BS, 2008 555
  • 556.
    U/S: Amount ofPower • Early phacomachine – Available in pedal position 3 – Power level was set on the machine panel • Over a decade –S Surgeon able to vary the power – In LINEAR fashion – By modulating pedal travel in position 3 Chang DF, 2004 556
  • 557.
    Laws of PhacoPhysics  Smaller tips occlude easier  The smaller the tip, the more precise p, p   ultrasonic control The smaller the tip, the easier to p maneuver The larger the tip, the better it holds Alcon Inc 557
  • 558.
    Laser Phacoemulsification • 2940nm Erbium:YAG Laser – Erbium:YAG Phacolase (Carl Zeiss Meditec AG) • Neodymium:YAG Laser – Neodymium:YAG Photon Laser PhacoLysis System (Paradigm Medical) – Dodick Q-Switched Neodymium:YAG laser (ARC GmbH) • Femtosecond Laser – Vi t (TECHNOLAS P f t Vi i ) Victus Perfect Vision) – Alcon LenSx (Alcon Inc)  Rhexis, Incision, Nuclear fragmentation, Limbal Relaxing Incision (LRI) – L LensAR AR – Catalys (OptiMedica) – Femto LDV Z Models (Ziemer-S)* Kohnen T, Koch DD, 2005; Auffarth G, 2010; EyeWorld 2010; Salz JJ, 2010 558
  • 559.
    Femtosecond Laser CataractSurgery • • • • Data collection Docking OCT or S h i fl S Scheimpflug Scan Laser works: – CCC – Lens softening g – Clear corneal incision – Limbal relaxing incision g 559
  • 560.
    Docking and OCTguide scan • Diagram of the optical and mechanical interface between the laser system and the y eye. • The femtosecond laser and OCT beam share the same optical path, p providing an exact g co-registration of the OCT image with the laser segmentation patterns. 560
  • 561.
  • 562.
    Tips in Zonularweakness p • Full dilated pupil • M i t i d b BSS d Maintained by BSS-adrenaline (1 1 000 or 0 5 li (1:1,000 0.5 ml in 500 ml) • Viscoadaptive ophthalmic viscosurgical devices (OVD) • 2 4 to 2.75 mm incision 2.4 2 75 • Large capsulorhexis ( 5mm or more) • Cortical cleaving hydrodissection* • Use a Capsular tension ring (CTR) Chee SP 2009; Kim WS 2009; Pangputhipong P 2009 562
  • 563.
    Tips in Zonularweakness p • • • • Groove long, wide and deep or triangular groove Bevel ti d B l tip downward d Long horizontal chop Utilize Triangular cracking technique  chop both distal corner without any nuclear rotation* • I i ti pole as l Irrigation l low as possible ( b t 70mm – ibl (about 70 75 mm)  reduce any BSS misdirection • Implant Three piece foldable IOL with PMMA Three-piece haptics Chee SP 2009; Kim WS 2009; Pangputhipong P 2009 563
  • 564.
    Small Pupil ManagementDevices • Malyugin’s Ring Pupil Expander • Behler’s Iris Retractor • Iris Hooks 564
  • 565.
    Viscoelastic materials • • • • • • • • Maintains space Spreadsand protects tissues Coats tissues and instruments Non-toxic Non-inflammatory N i fl t Optically clear but visible Neutral effect on IOP Protects the endothelium American Academy of Ophthalmology 565
  • 566.
    Viscoelastic : Rheology • • • • • Viscosity Pseudoplasticity Elasticity Cohesion and Dispersion Rigidity Kohnen T, Koch DD, 2005 566
  • 567.
    Viscoelastic materials • SodiumHyaluronate (SH) – Healon Healon GV Healon 5 (Abbott Medical Healon, GV, Optics) – Provisc (Alcon, Inc) ( , ) – AmVisc Plus (Bausch & Lomb Incorporated) – VisThesia (Ioltech – Carl Zeiss Meditec AG)  Plus 2% Lidocain HCl • Chondroitin sulfate (CS) – Vi Viscoat (Al (Alcon, I ) Inc) – DisCoVisc (Alcon, Inc) Kohnen T, Koch DD, 2005 567
  • 568.
    Viscoelastic materials • Hydroxypropylmethyl cellulose (HPMC) – Ocuvis (CIMA Technology) – OcuCoat (Bausch & Lomb Incorporated) • Colagen IV – Removed from market  world-wide fear of possible prior contamination of human-sourced protein • Polyacrylamide – Formation of microgel  clogged the trabecular meshwork  could not b eliminated  idl h k ld be li i d rapidly removed from the market in Europe and USA Kohnen T, Koch DD, 2005 568
  • 569.
  • 570.
    Cohesive vs Dispersive •C h i  Vi Cohesive Viscoadaptives, Vi d ti Viscouscohesive viscoelastics – – – – – – – Heavy molecular weight High concentration Create and preserve space Displace and stabilize tissues Pressurize the anterior chamber Clear view of posterior capsule Easy to remove – E.g : 2.3% SH  Healon 5 (Abbott Medical Optics (Abbott Medical Optics), SH 1 6%  Amvisc (Bausch and Lomb) Optics) 1.6% Lomb), 1.4% SH  Healon GV (Abbott Medical Optics), SH 1.2%  StaarVisc II (Staar Surgical), and SH 1%  ProVisc (Alcon, ) Inc) Kohnen T, Koch DD, 2005 570
  • 571.
    Cohesive vs Dispersive •Dispersive  Medium viscosity, Very low viscosity Very-low viscosity – Coating tissues – Partition spaces – Prolonged retention – E.g : 3.0% SH  Viscoat (Alcon, Inc), Healon D (Abbott Medical g ( , ), ( Optics), HPMC 2%  Ocucoat (Bausch and Lomb) • Dual Characters  Viscous-Dispersive Viscous Dispersive – Cohesive and Dispersive in one – E.g : • Healon D + G ( bbott Medical Opt cs) ea o GV (Abbott ed ca Optics) • Duovisc (Alcon, Inc) – The proven protection of Viscoat – The ease to removal of ProVisc Kohnen T, Koch DD, 2005 571
  • 572.
  • 573.
    Soft shell technique –Protects compromised corneal endothelium and posterior capsular bag – Injects dispersive viscoelastic materials – Followed by cohesive viscoelastic materials injection – P h di Push dispersive viscoelastic i i l ti materials anteriorly  coating the endothelium – Or  also push dispersive viscoelastic materials i l ti t i l posteriorly  coating the posterior capsular bag  safer in-the-bag IOL implantation 573
  • 574.
  • 575.
    Steroid cataract formation •Glucocorticoids are convalently bound to lens proteins • Resulting in  destabilization of the protein structures • All i f th modification, i : oxidation Allowing further difi ti ie id ti • Leading to cataract Experimental Eye Research, 1997 575
  • 577.
  • 578.
    Retinal Layers American Academyof Ophthalmology 578
  • 579.
    Retinal Layers American Academyof Ophthalmology 579
  • 580.
    Retina : Basic •Strongest j g junction – Ora serrata – Optic nerve head • Retinal vessel – Inner 2/3 by Central retinal artery – Outer 1/3 by Choriocapillaris  also supply • Fovea • RPE – Cilioretina artery • In 50% of persons it supplies 30% parts of inner retina • In 15% of persons it contributes to some of macular circulation 580
  • 581.
  • 582.
    Retina : BloodOcular Barrier • Blood Retinal Barrier – Retinal Blood Vessel  analogous to Cerebral Blood Vessels  maintain Inner Blood-Retina Barrier –I Inner Blood-Retina B i performed b Bl d R ti Barrier f d by • Single Layer of Non Fenestrated Endothelial Cells  TightJunction (zonulae occludens) • Basement Membrane, pericytes (Interupted layer) • Internal Elastic Lamina & Smooth Muscle (Near Optic Head ) – Outer Blood-Retina Barrier performed by RPE in RPE, which adjacent cells are similarly joined by zonulae occludens American Academy of Ophthalmology 582
  • 583.
    Retina : BloodOcular Barrier • Blood Aqueous Barrier –I Inner non-pigmented cilliary epithelium i t d illi ith li – Tight-junctions between epithelial and endothelial cells American Academy of Ophthalmology 583
  • 584.
    RPE : Function • • • • • • • • VitaminA metabolism Maintenance of outer blood-retina barrier g y photoreceptor outer segment p g Phagocytosis of p Absorption of light (reduction of scatter) Heat exchange Formation of basal lamina Production of mucopolysaccharide matrix Active transport of material in and out of the RPE American Academy of Ophthalmology 584
  • 585.
    Clinical Facts • Theouter Blood retinal barrier the RPE barrier, RPE, and the retinal vascular endothelium utilize the same receptor-ligand pairing to control receptor ligand lymphocyte traffic into the retina • The outer Blood retinal barrier is a common site for inflammatory attack, often resulting in breakdown of barrier functions and choroidal neovascularization Penfold PL, Provis JM, 2005 585
  • 586.
    Blue Light toxicityto RPE • Over time  RPE accumulates Fluorescent material  Lipofuscin • Lipofuscin absorbs blue light  Lipofuscin Fluorophore A2E  in presence of Oxygen  generate A2E Epoxides • A2E Epoxides toxic to RPE and induces Apoptosis poptos s • RPE can no longer nourish photoreceptor cells  adversely affect the vision 586
  • 587.
    Fundus : Examination • • • • Opticnerve head Retinal appearance Vascular shape Macula 587
  • 588.
    Fundus : Opticnerve head • • • • • • • • Margin Color Disc, Cup, Disc Cup Rim shape Para papil Vascular change V l h Hemorrhage Myeline Membrane 588
  • 589.
    Fundus : Retina •RNFL • Hard exudates – Intra retinal lipoprotein deposits • Soft exudates  Cotton Wool Spot ( p (CWS) ) – Fuzzy or ill-defined edges as retinal ischemia to infarction  cotton-wool spot • Microaneurysm  around areas of capillary non perfusion • Hemorrhage – – – – Pre-retinal Retinal  Flame-shaped Sub-retinal  Fluids level Roth spot  hemorrhages with white center  Leukemia • Degeneration 589
  • 590.
    Fundus : Vascular •AV ratio • AV crossing – Sallus – Gunn – Banking • Axial reflect – Copper wire – Silver wire • Malformation 590
  • 591.
    Fundus : Macula •Reflect • Malformation : – Edema – Hole – Drusen  deep or dull yellow deposit • Located in the outer retina of posterior pole • Histologically corresponds to abnormal thickening of the inner aspect of Bruch’s membrane • Basal laminar deposits  long-spacing collagen between the plasma membrane and basement membrane of the RPE • B Basal li l linear d deposits  d it deposits of electron-dense granules and it f l t d l d phospolipid vesicles in the inner parts of Bruch’s membrane – Pigment – Cicatrix American Academy of Ophthalmology 591
  • 592.
    American Academy ofOphthalmology 592
  • 593.
    The 1.5 mmMacula Penfold PL, Provis JM, 2005 The central human retina or macula, with an idealized view of its bl d vessels. ith id li d i f it blood l The optic disc (OD) is to the left. The macula is subdivided into the central-most foveola, which is surrounded in turn by the , y 0.35 mm fovea, parafovea and wider perifovea in 5.5 mm of posterior pole. Each is indicated by concentric circles. Blood vessels form a ring outlining the foveal avascular zone, which marks the inner 593 limits of the foveal pit
  • 594.
    Drusen • • • • • • • Drusen – Hard drusen appear clinically as small yellow punctate small, yellow, deposits – Soft drusen  paler, larger deposits Is presence of cellular debris Located in the outer retina of posterior pole, underneath the RPE Histologically corresponds to abnormal thickening of the inner aspect of Bruch’s membrane Consist of extracellular deposit  that aggregate between RPE and Bruch’s membrane Basal laminar deposits  long-spacing collagen between the plasma membrane and basement membrane of the RPE Basal linear deposits  deposits of electron-dense granules and phospolipid vesicles in the inner parts of Bruch’s membrane Penfold PL, Provis JM, 2005 ; Eurotimes 2009 594
  • 595.
    Macula : HRAOCT Spectralis (Heidelberg E i M l HRA-OCT S li (H id lb Engineering) i ) 595
  • 596.
    Simple test formacular function • • • • Colour test Photostress Recovery test Amsler grid g Heyne Retinoscopy 596
  • 597.
    Distribution of photoreceptor cellsand ganglion cells on the g g macula Penfold PL, Provis JM, 2005 597
  • 598.
    The cone cells •Sharp photoreceptor • A human eye can see wavelengths in the range of 380 to 760nm. This range is called the visible region • Trichromatic Theory  3 types of cones, each with a different iodopsin (a photosensitive pigment) • Each type of iodopsin can absorb and respond to a range of wavelengths • Photosensitive pigments  – Erythrolabe  maximum absorption at 565nm (red) – Chlorolabe  maximum absorption at 535nm (green) – Cyanolabe  max. absorption at 440nm (blue) 598
  • 599.
    Color test • • • • Color naming Yarntest Lantern test Plate test – Hardy-Rand-Rittler plates  Red/Green and Bleu/Yellow – Ischihara’s Polychromatic or Pseudoisochromatic plates  Ischihara s Red/Green • Arrangement test  Hue discrimination test • Anomaloscopes test • Panel test  Farnsworth Panel D-15 and FarnsworthMunsell 100-Hue test 599
  • 600.
    Deficient Color Vision •Dichromacy (Color blindness) – Red / Green deficiencies • Protanopes – Confusion  at a point at the red end (right end) of the spectrum l locus – Reds also appear darker to protonopes than to normals • Deuteranopes – Confusion lines  an extraspectral point (off the chart to the lower right, in these coordinates) and their brightness vision is more like that of color-normals – T it Tritanopia and T it i d Tritanomaly  Y ll l Yellow / Bl Blue deficiencies – The third class  Achromacy Birch, 2001 600
  • 601.
    Ischihara’s Pseudo-isochromatic plates p •Standard illumination – Daylight y g – 20-60 foot candles • 75-100 cm reading distance 75 100 • 3-5 seconds observation time per plate • N color contact l No l t t lens wear Deborah Pavan-Langston, 2008 601
  • 602.
    Dark-adaptation test p • TheGoldman-Weekers machine • Used to plot the dark-adaptive curve • In bright light 10 minutes and then all lights are extinguished • Interval 30 seconds  make a measurement of light threshold in one area of visual field • By presenting a gradually increasing light stimulus • U til b l visible t th patient Until barely i ibl to the ti t • The graph of decreasing retinal threshold against time : – Initial steep slope  cone adaptation – Subsequent gradual slope  rod adaptation • Depression of the dark-adaptation  affecting outer retina and RPE, E.g : Retinitis pigmentosa Deborah Pavan-Langston, 2008 602
  • 603.
    Retina : Howto draw the retina • Central  Macula • Ora Serrata – Temporal – Nasal  Thinner • Color : – – – – – Red R d Blue Red with blue margin Brown Black 603
  • 604.
    RD : Basic •RETINAL DETACHMENT (RD) : A SEPARATION OF THE SENSORIC RETINA FROM THE RETINAL PIGMENT EPITHELIUM • RETINAL BREAK : A FULL-THICKNESS DEFECT IN THE SENSORY RETINA 604
  • 605.
    RD : Classification I.RHEGMATOGENOUS R.D. (RRD) ( PRIMARY R D ) R.D. II. NON-RHEGMATOGENOUS R.D. ( SECONDARY R D ) R.D. 1. TRACTIONAL R.D. 2. 2 EXUDATIVE R D R.D. 605
  • 606.
    RD : Classification • MINIMAL –Vitreous haze – Vitreous pigment clumps pg p • MODERATE – – – – • Wrinkling of inner retinal surface Rolled edge of retinal breaks Retinal stiffness Vessel tortousity MARKED full thickness fixed retinal folds – C1, C2, C3 (1,2,3 quadrant(s)) • MASSIVE fixed retinal folds in four quadrant q – D1 wide funnel shape – D2 narrow funnel shape – D3 closed funnel  invisible optic disc American Academy of Ophthalmology 606
  • 607.
  • 608.
    RRD : Principleof management • First : find all breaks • Second : create a chorioretinal irritation surrounding each breaks • Finally : bring the retina and choroid into contact for sufficient time  produce chorioretinal adhesion  permanently close the breaks American Academy of Ophthalmology 608
  • 609.
    RD : Management •Break only : Laser Photocoagulation • With Detachment – Si l Simple • • • • Scleral buckle  Local and Encircling Sub retinal fluid drainage Pneumoretinopexy Cryoretinopexy  Limited due to PVR formation – Vitrectomy 609
  • 610.
    Buckle vs Vitrectomy •Vitrectomy – More expensive* – More equipments and technology – Longer learning curve to perform – Induce more complication – Need specific positioning – S l more diffi lt case Solve difficult 610
  • 611.
    Buckle vs Vitrectomy y •Buckle – Cheaper and faster – Less equipments and technology – Longer learning curve to perform – Less complication – Better mobilization – Need more skill to identifying break location and placing buckle precisely on it – More painful – Myopic shift 611
  • 612.
    Vitrectomy is prefer: When? • • • • • • • • Unclear media Unsolved traction Not indented breaks by buckle Posterior breaks Need of membrane peeling PVR Multiple or spreading breaks Combined with anterior segment surgery 612
  • 613.
    Buckle • Make indentationto close and prevent breaks • Silicone – Band – Tire – Sponge • Sleeve for adjust the tightening • Suture to sclera with non absorbable material 613
  • 614.
    Vitrectomy • Machines  1,000up to 7,500 cuts per minute  face to Microincision Vitroretinal Surgery (MIVS) – Examples : • CONSTELLATION Vision System (Alcon, Inc) • Stellaris PC Phacoemulsification and Vitrectomy System (Bausch & Lomb Incorporated) • Oertli OS3 and Faros Ophthalmic Micro-incision Surgery System (Oertli Instruments) • The Associate 6000 Ophthalmic Microsurgical System (DORC) g y • eva Ophthalmic Microsurgical System (DORC) • The VersaVIT and Core Essentials Vitrectomy Machine System and Vitrectomy Packs (Synergetics) • New  Vitreoretinal Endoscopic – Micro endoscopy for vitrectomy and endophotocoagulation – Examples : p • Endo Optiks • 23 g tapers to 27 g probe and 25 g tapers to 30 g probe IRIDEX EndoProbe 614
  • 615.
    Vitrectomy • Microscope enhancementsystem  Retinal wide angle observation tools – Examples : • • • • • • RESIGHT Fundus Viewing System (Carl Zeiss) MERLIN Surgical Viewing System (Volk) Oculus SDI 4 (OCULUS Optikgeräte GmbH) Oculus BIOM 5 (OCULUS Optikgeräte GmbH) EIBOS 200 (Platinum Medical) SUPER VIEW Wide Angle (Insight Instruments) 615
  • 616.
    Vitrectomy y • Endo Laser –Example : p • PUREPOINT Laser (Alcon, Inc) • Instruments – Example : • 23 and 25+ gauge Micro-Incision Vitrectomy Surgery  MIVS (Alcon, Inc)  ULTRAVIT® High Speed Vitrectomy Probes with Duty Cycle Control • 25+ and 27+ Probe TotalPLUS Paks (Alcon Inc)  7,500 cpm Ultra-High Speed Cutting • Hi-speed 23 and 25 g g NovitreX3000 and p gauge OertliKatalyst (Oertli Instruments) • Intraocular pressure stabilizer  Autoseal PMS (Oertli Instruments) • 27 gauge MIVS system pack (DORCH and Synergetics) • GRIESHABER® Instrumentation (Alcon Grieshaber AG) 616
  • 617.
    Vitrectomy : Illumination • • • • • • Halogen Yellow Dimmer Light Xenon  Bright White Metal Halide  Bright Natural Photon Ph t  G Green Yellow Y ll Light-Emmiting Diode (LED) 29/30 g Chandelier Fiber Optics (Synergetics) 617
  • 618.
    Gas d Liquid Gand Li id Purpose : p 1. MECHANIC MANIPULATION OF RETINA 2. TEMPORARY INTERNAL TAMPONADE OF RETINAL BREAK 3. 3 TO FLATTEN RETINAL DETACHMENT 4. TO MAINTAIN  CLEAR VIEW- RETINA 5. TO MAINTAIN OCULAR TONE 618
  • 619.
    The Gas NONEXPANSILE GASES – AIR(NOT PURE GAS)  20% OXYGENE + 80% NITROGENE  < 5 DAYS – OXYGENE ( O2 ) – CARBON DIOXIDE (CO2 ) EXPANSILE GASES – SULFUR HEXAFLUORIDE (SF6)  2x  10 – 14 DAYS – PERFLUOROPROPANE (C3F8)  4x 55 – 65 DAYS 619
  • 620.
    The Liquid q BSS –PLUS GLUTATHIONE  ANTI OXIDANT SILICONE OIL VISCOSITY  1,000 – 5,300 cSt HEAVY LIQUIDS - PERFLUORODECALIN (C10F18) - SURFACE TENSION 16 – 21.6 dyne/cm - VISCOSITY  2.6 – 8.03 cSt HEAVY SILICONE OIL - MIXTURE OF : - ULTRAPURE POLYDIMETHYLSILOXAN (CH3)3SiO-n-Si(CH3)3 AND - PERFLUOROHEXYLOCTANE (C6F8) 620
  • 621.
  • 622.
    The Laser TO MANAGETHE BREAKS – ARGON GREEN (532 nm) • PREFFERED – KRIPTON RED (647 nm) • HAZY MEDIA • DEEP BURNS • LESS CHANCE OF RNFL DAMAGE – DIODE (810 nm) • VITREORETINAL TRACTIONS 622
  • 623.
    Precaution • Excessive cryoretinopexy Risk of PVR • Heavy laser burn  – Iatrogenic break g – Pain and inflammation – Retinal ede a et a edema • Long time heavy fluid  Toxic to retina • Long time silicone oil  More difficult to manage  Risk of inferior PVR • St id i oil fill d eye  N Steroid in il filled Necrotic retina ti ti 623
  • 624.
    PVR : Classification • GradeA – Vitreous haze – Vitreous pigment clumps – Pigment cluster on inferior retina • Grade B – – – – – • Wrinkling of inner retinal surface Rolled and irregular edge of retinal breaks Retinal stiffness Vessel tortousity Decreased mobility of vitreous Grade CP 1-12 – Posterior to equator : focal, diffuse or circumferential full thickness folds – Sub retinal strands • Grade CA 1-12 – – – – Anterior to equator : focal, diffuse or circumferential full thickness folds Sub retinal strands Anterior di l A t i displacement t Condensed vitreous with strands American Academy of Ophthalmology 624
  • 625.
    Diabetic Retinopathy (DR) Basicof disease – Hyperglicemia  EPO, IGF  PKCβ, VEGF – Basal membrane thickening – Pericyte death – Mild endothel proliferative (Microaneurysm) with plasma leakage Ong SG, 2009 625
  • 626.
    Diabetic Retinopathy (DR) Basicof disease – Lost of intramural pericytes – Compromised blood-retinal barrier by defect in the p y junction between abnormal vascular endothelial cells – Increased vascular permeability  dot and blot hemorrhages, hemorrhages edema and hard exudates – Extensive capillary closure in tripsin-digest flat p p preparations of the retina – Retinal rendered ischemic by capillary closure elaborates VEGF  stimulates neovascularization American Academy of Ophthalmology 626
  • 627.
    Diabetic Retinopathy (DR) Mullercells – – – – – – Uptake glutamate  toxic to neurotransmitter Maintain the synaps  release of neurotrophic agents y p p g Control extracellular ion concentration Regulate water transport out of retina  Aquaporin 4 Responsive to VEGF  Express VEGFR1 Responsive to Glucocorticoids  Only one*  Express Glucocorticoid receptors Ong SG, 2009 627
  • 628.
    DR : Basic Haematologicand biochemical abnormalities – Increased platelet adhesiveness – Increased erytrocyte aggregation – Abnormal serum lipids – Defective fibrinolysis – Abnormal level of growth hormone – Ab Abnormal serum and whole blood viscosity l d h l bl d i it American Academy of Ophthalmology 628
  • 629.
    DR : Highlight 1.No Diabetic Retinopathy 2. Non 2 N proliferative Di b ti R ti lif ti Diabetic Retinopathy th A. Background Diabetic Retinopathy B. Preproliferative Diabetic Retinopathy 3. Proliferative Diabetic Retinopathy 4. Diabetic maculopathy Deborah Pavan-Langston, 2008 629
  • 630.
    DR : Nonproliferative Non-proliferative • • • • • Dilated veins Dot d blot intra ti l hemorrhages D t and bl t i t retinal h h Microaneurysms Hard exudates Edema and CWS Deborah Pavan-Langston, 2008 630
  • 631.
    Progression from NPDRto PDR • Diffuse intra retinal hemorrhages and mycroaneurysms in 4 quadrants y y q • Venous beading in 2 quadrants • IRMA in 1 quadrant American Academy of Ophthalmology 631
  • 632.
    DR : Pre-proliferative Preproliferative • Intra retinal hemorrhages • Microaneurysm • Intra retinal microvascular abnormalities (IRMA)  dilated vessel within the retina • Venous beading • Widespread capillary closure • 10-50% develop to proliferative within a year Deborah Pavan-Langston, 2008 632
  • 633.
    DR : Proliferative •New vessel on surface the retina and optic nerve head  usually attached of posterior hyaloid of vitreous body • C Cycatrical stage  vitreous hemorrhages ti l t it h h and traction retinal detachment Deborah Pavan-Langston, 2008 633
  • 634.
    Diabetic maculopathy • Resultfrom increased vascular permeability bilit • With or without hard exudates • Less commonly  result from ischemia due to closure of foveal capillaries p • May NOT be seen in early background DR Deborah Pavan-Langston, 2008 634
  • 635.
    DME : Typeof Thickening • Uniform speckled – Extra cellular fluid  Vasogenic mechanism • Cystic – Swollen of Muller’s cells  Toxic mechanism – Not extra cellular fluids Ong SG, 2009 635
  • 636.
    DME : Clinicalvariations • Vasogenic – Localized leakage from microaneurism • Toxic - Non vasogenic – Leakage from poorly identifiable sites – Massive leakage • Mechanical – Vitromacular tractions – Epiretinal membrane (ERM) • T id - VEGF mediated Toxid di t d – Perpheral ischemia  VEGF over expression Ong SG, 2009 636
  • 637.
    DR : CSME ClinicallySignificant Macular Edema • Thickening of the retina at or within 500 µm of center of the macula • Hard exudates at or within 500 µm of center of the macula • A zone of retinal thickening one disc area or larger  any p of which is one disc diameter g y part of center of the macula American Academy of Ophthalmology 637
  • 638.
    DR : CSME AmericanAcademy of Ophthalmology 638
  • 639.
    DR : CSME AmericanAcademy of Ophthalmology 639
  • 640.
    DR : CSME AmericanAcademy of Ophthalmology 640
  • 641.
    DR : Highrisk PDR • Mild Neovascularization on disc (NVD) with vitreous hemorrhages • Moderate to severe NVD  larger than ¼ to ⅓ disc area with or without vitreous hemorrhages • M d t N Moderate Neovascularization at elsewhere l i ti t l h (NVE) ½ disc area or more with vitreous hemorrhages American Academy of Ophthalmology 641
  • 642.
    DR : Highrisk PDR • At least 3 of : – Vitreous or pre retinal hemorrhages – New vessels (NV) – Location of new vessel on or near optic disc – Moderate or severe extent of new vessels American Academy of Ophthalmology 642
  • 643.
    DR : Approach • • • • • • • Reduceblood sugar Monitoring Hba1c Laser photocoagulation L h t l ti Steroids Anti-VEGF Rapamycin (Sirolimus)* (Sirolimus) Surgery Ong SG 2009; Blumenkranz, 2009; Eurotimes 2009 643
  • 644.
    DR & DME:Clinical Trial Update • • • • • • • N acetylcarnosine N-acetylcarnosine Eye Drops Nepafenac Eye Drops Fenofibrate Oral F fib t O l Dextromethorphan Oral Danazol Oral Ranibizumab (Advance Clinical Trial) Dexamethasone Implant Retinal Physician 2013 644
  • 645.
    DR : Laserrationale Retina • • • • • • Thinning of retina Destruction of ischemic retina Reduction of VEGF release Proliferation f d th li l ll P lif ti of endothelial cells Increase blood flow Improve auto regulation Ong SG, 2009 645
  • 646.
    DR : Laserrationale RPE • • • • Destruction of RPE  new growth Increase transmission of metabolism Increase Oxygen transmission yg Improve “pump” Ong SG, 2009 646
  • 647.
    DR : Laserrationale Bruch s Bruch’s membrane • Altered permeability • Lipid destruction Choriocapillary • Destruction of choriocapillary Ong SG, 2009 647
  • 648.
    DR : Laser GridLaser Photocoagulation g • Macular application  500 µm up to 3000 µm from foveal center • Excluded  area of PMB • Grid Lens / +78 and +90 D Lens • Start at 100mW power  increments of 10-20mW 10 20mW • 50-100 µm spot size • 0.100 second or less duration • Spots spaced at least one burns apart • Supplemental treatment considered at least 3-4 month after initial coagulation  up to 300 µm 648
  • 649.
    DR : Laser FocalL F l Laser Ph t Photocoagulation l ti • Grid Lens / +78 and +90 D Lens • Start at 100mW power  increments of 1020mW • 50-100 µm spot size • 0.100 second or less duration • Attempt to whiten or darken microaneurysms 649
  • 650.
    Laser : PRP Pan-RetinalPhotocoagulation / Scatter Laser Photocoagulation • NVD or / and NVE • PRP L Lens • Start at 180mW power  increase gradually to achieve the end point • 500 µm spot size • 0.100 to 0.200 second duration • 1800 total applications pp • 1 – 1.5 burns width apart • 3 sessions complete  10 days to weeks apart • Usually inferior half of retina coagulated first Usually, 650
  • 651.
    DR : Laser •Poor visual outcome after photocoagulation associated with : – Diffuse macular edema with center involved – Diffuse fluorescein leakage – Macular ischemia  extensive perifoveal capillary non perfusion – Hard exudates in the fovea – Marked Cystoid Macular Edema (CME) American Academy of Ophthalmology 651
  • 652.
    DR : Laser •Side effect and complication – Paracentral scotomata – Transient increased edema  decreased vision – Choroidal Neovascularization (CNV) – Subretinal fibrosis – Scar expansion p – Inadvertent foveolar burns American Academy of Ophthalmology 652
  • 653.
    Laser in Retina:Nowadays • • • • • • • • Highly focused Adjustably patterned Burn effectively  Speed and accuracy Surrounding area safety OCT guided with high transparency Navigated and tracked Real time information and comfort for patient Better result and less side effect 653
  • 654.
    DR : IVTAConsideration • Edema refractory to Laser photocoagulation treatment • Proximity of leakage to the fovea • Difficult to laser or more exacerbate of edema  High risk PDR, Cataract with DME • Hard exudates with heavy leak close to fovea • Extreme exudation Ong SG, 2009 654
  • 655.
    DR : IVTAto Muller s cells Muller’s • M ll ’ cells are t Muller’s ll target of St id t f Steroids treatment • Increase in Adenosin mediated fluid resorption • Reducing the cystic thickening DME Ong SG, 2009 655
  • 656.
    DR : Steroids •Slow released injectable non-erodible non erodible intravitreal steroids • Fluocinolone Acetonide  Medidur (Bausch & Lomb)  18 to 36 months • Oral treatment – Danazol  Optina (Ampio Pharmaceuticals) Cousins SW, 2009; Retina Today 2012 , ; y 656
  • 657.
    Vitreous hemorrhages • Majorcause – Diabetic retinopathy (39-54%) – Retinal break without detachment (12-17%) – Posterior vitreous detachment (7.5-12%) ( ) – Rhegmatogenous retinal detachment (7-10%) – Retinal NV following BRVO or CRVO (3.5-10%) (3.5 10%) American Academy of Ophthalmology 657
  • 658.
    DR: Vitrectomy Indications AmericanAcademy of Ophthalmology 658
  • 659.
    Central Serous Chorio-Retinopathy(CSCR) • Sensory detachment of the sensory retina, resulting from S d t h t f th ti lti f – Altered barrier function – Deficient pumping function at level of the RPE and may also involving the choriocapillaris p • • Preferentially in 30-50 years old healthy men Sudden onset of – – – – • Blurred and dim vision Micropsia Mi i Metamorphopsia Decreased color vision FFA – Expansile dot  most common • Focal hyperfluorescent leak from RPE • Appear in early phase • Increase in size and intensity as angiogram processes – Smokestack • Leakage of fluorocein into sub retinal fluid pocket • Produce a pattern of sub retinal pooling of dye – Mushrooms Umbrella Mushrooms, American Academy of Ophthalmology 659
  • 660.
    Infrared CSCR :HRA OCT Spectralis (Heidelberg Engineering) 660
  • 661.
    Sub retinal fluidin elderly CSCR CNV associated with AMD Pin point leak relative to a large area of sub retinal fluid on FFA Sub retinal fluid corresponds closely to area of leakage on FFA Multifocal RPE abnormalities - Small serous PED Large drusen Absence of blood and significant lipid Presence of blood and significant lipid American Academy of Ophthalmology 661
  • 662.
    CSCR : Laserindication • Persistent serous detachment 3-4 months 34 • Recurrences in eye with visual deficit from previous episodes • Presence of permanent visual deficit from previous episodes in fellow eye • Development of chronic signs  – Cystic changes – Widespread RPE abnormalities • Occupational American Academy of Ophthalmology 662
  • 663.
    Retina : AMD InternationalClassification (1995) ( ) • Age-related maculopathy ( Ageg p y (ARM) ) – Drusen • Small, intermediate, large • Hard, soft, confluent Hard soft – Hyper or hypopigmentation of RPE • Age-related macular degeneration (AMD) Age– Exudative – N -exudative NonNon d ti Koh A, 2005 663
  • 664.
    AMD : Exudative •Choroidal Neovascularisation (CNV) • Pigment E ith li l D t h Pi t Epithelial Detachment (PED) t • Glial/scar tissue (disciform scar) Koh A, 2005 664
  • 665.
    AMD : Non-Exudative NonExudative • RPE hypopigmentation >175 m diameter (Geographic atrophy) (G hi t h ) Koh A, 2005 665
  • 666.
    AMD : Signs • • • • • • • GreenishGreenish-grayor Yellow-green lesion YellowPigmented halo around lesion Subretinal hemorrhage S b ti l h h Hard lipid exudates Sensory retinal detachment RPE detachment Cystoid edema Koh A, 2005 666
  • 667.
    AMD : Symptoms • • • • • • • Monocularvision loss p p Metamorphopsia Decreased contrast sensitivity Scotoma Decreased color vision Micropsia Nowadays level of vision early detection and monitoring  ForeseeHome (NOTALVISION) Koh A 2005, Retina Today 2013 667
  • 668.
    AMD : RF,IF, AF, FA, ICGA Red Free Infrared Fluorescein Angiography Autofluorescence ICG Angiography HRA Spectralis (Heidelberg Engineering) 668
  • 669.
    AMD : HRTand OCT HRT3 Heidelberg Engineering Cirrus HD OCT (Carl Zeiss Meditec AG) 669
  • 670.
    CNV : Morphology •Vascular • Hypervascular • Fib Fibrovascular l Cousins SW 2009 SW, 670
  • 671.
    CNV : Diversecell types • • • • • • • Endothelial Smooth muscle cells Pericytes Myofibroblasts RPE cells ll CD34 progenitor cells Macrophages Cousins SW 2009 SW, 671
  • 672.
    CNV : FFA Classic(Type 1) CNV • • Bright area of fluorescence surrounded by hypofluorescent margin in early phase Leakage of fluorescein at boundaries of bright area in late phase Koh A, 2005 672
  • 673.
    CNV : FFA Occult(Type 2) CNV • Fibrovascular PED – Irregular elevation of the RPE – Stippled fluorescence within 1 to 2 minutes – Persistent staining or leakage in late phase frames • Late Leakage Undetermined Source – Leakage at level of RPE –A Areas of leakage d not correspond t an area of fl k do t d to f classic CNV or fibrovascular PED in early or mid phase frames to account for leakage Koh A, 2005 673
  • 674.
    Occult (Type 2)CNV Hagerman GS 2008 H GS, 674
  • 675.
    CNV : ICG •Components p – Subretinal fibrovascular complex – Intrachoroidal “Feeder Artery” – Intrachoroidal “Draining Vein” • Patterns – Capillary pattern – Arteriolar pattern p – Mixed pattern Cousins SW, 2009 675
  • 676.
    Occult CNV • Morethan one lesion • Sub RPE low flow and poor defined vascularity • High flow arteriolarized • Atypical polypoidal choroidal vasculopathy • Retinal angiomatous p g proliferation Cousins SW 2009 SW, 676
  • 677.
    AMD : MajorRisk Factor • Molecular Biology : – H Gene (Known as CFH of HFI)  Located ( ) on Human Chromosome Iq31 – Less of Particular Non-Coding SNP Variant (Allele A)  Found in Intron 6 of the Serping 1 Gene Eurotime, 2009 E ti 677
  • 678.
    AMD : Approach •Laser photocoagulation • Signal  Anti VEGF OSI Eyetech (Pegabtanib)  Selective y g ) VEGF165 Inhibitor – Lucentis® Genentech (Ranibizumab) – Avastin™ Genentech (Bevacizumab) – Macugen® g – ALG-1001Allegro Ophthalmic (Anti Integrin Oligo Peptide)  Signaling and Regulating Cousins SW 2009; Eurotimes 2009, Retina Today 2013 678
  • 679.
    AMD : Approach •Signaling pathway  Steroids – Anecortave – Triamcinolone • Formation  PDT – Verteporfin dye (Visudyne) p y ( y ) • Liposome-encapsulated Benzoporphyrin • Maximum absorption  light near 689 nm wavelength – Others : • Tin Ethyl Etiopurpurin (SnET2, Purytin) • Lutetium (Lu-Tex) Cousins SW 2009; Eurotimes 2009, Retina Today 2013 679
  • 680.
    AMD : Approach •E10030 – A ti PDGF Aptamer (Ophthotech)  Synthetic Anti A t RNA molecules  bind protein similar to antibody • • • • • Implantable Miniaturized Telescope (MT)* p p ( ) The Lipshitz Macular Implant (LMI)* The IOL-VIP System* Gene Therapy  Small interfering (si)RNA* Membrane Differential Filtration (MDF)  Rheopheresis  Dry AMD* AMD Eurotimes, 2009, 2011 680
  • 681.
    AMD : Approach •I t Integrin P tid Therapy i Peptide Th • ALG-1001 • Topical Therapies*: – – – – – ATG3 (coMentis) OT-551 (Othera Ph OT 551 (Oth Pharm) ) TG100801 (TargeGen) Pazopanib (GlaxoSmithKline) OC-10X (OcuCure) Eurotimes, 2010; Retina Today 2012 681
  • 682.
    AMD : Approach pp •Brachytherapy • Source of radiation is placed close to the surface of targeted therapeutic area • Beta radiation targeted at abnormal or leaking vessels • Stereostatic Radiotherapy  Oraya Therapy (Oraya Inc) (O I ) Retina Today, 2011, 2012 682
  • 683.
    Dry AMD :Approach y pp • Anti oxidants – Vitamin C, Vitamin E, Beta-Carotene, Zinc and Copper – Lutein and Zeaxanthin – Omega 3 fatty acid • • • • • Visual cycle inhibition Anti inflammatory agents Complement inhibitor Targeting amyloid Neuroprotector Retina Today, 2011 683
  • 684.
    Response to Anti-VEGF AntiVEGF • C ill Capillary-dominated CNV  W ll d i t d Well response • Mixed CNV  variable response depends on  Ratio of feeder artery caliber and length to capillary area • Arteriolarized CNV  Poor response p Cousins SW, 2009 684
  • 685.
    Remember • • • • PDT induces hypoxiain tissue yp PDT induces formation of oxygen free radical After 1 day  Strong VEGF expression After 1 month PDT increases expression of – CD 34 ( marker of endothelial cell) – CD 105 ( marker of activated endothelial cell) – KI-67 ( marker of proliferation ) Eurotimes, 2009 685
  • 686.
    PDT : Postprocedure • Inflammatory cells observed y – – – – – Monocytes Macrophages Platelets Mast cells Leukocytes • Release angiogenic factors  VEGF, bFGF IL 1β, IL-2, • Release cytokines  IL-1β, IL 2, TNFα • Release vasoactive mediators  Thromboxane, TNFα, Histamine Koh A, 2009 686
  • 687.
    Remember • Fundus fluoresceinangiography remains an g g p y indispensable tool in diagnosis and management of AMD • Indocyanine green angiography is useful in certain situations • Optical coherence tomography is very popular because of ease of use and interpretation, b f f di t t ti particularly useful for follow-up follow• Newer tec ques suc as S O a g og ap y e e techniques such SLO angiography and autofluorescence not so essential for clinical practice Koh A, 2005 687
  • 688.
    Wet AMD: ClinicalTrial Update • • • • • • • • • • Proton Beam Irradiation Slidenafil Zeaxanthin Oral (Advance Clinical Trial) Aflibercept Intravitreal injection Squalamine Lactate Eye Drops Ranibizumab ( (Advance C Clinical Trial) ) LFG316 Intravitreal injection AGN-150998 AGN 150998 Intravitreal injection ESBA 1008 Microvolume injection E10030 Intravitreal administration Retinal Physician 2013 688
  • 689.
    Occult CNV AFand OCT : HRA OCT Spectralis (Heidelberg Engineering) 689
  • 690.
    Polypoidal Choroidal Vasculopathy(PCV) • Also as "idiopathic p yp p polypoidal choroidal vasculopathy") p y) • A distinct form of choroidal neovascularization (CNV) • Disorder characterized by vessel networks and polypoidal lesions • Specifically, an inner choroidal vascular abnormality with two distinct components: – A network of branching vessels predominantly external to the choriocapillaris, and – Aerminal aneurysmal dilatations Nakashizuka H, 2008; Cousins SW, 2009 690
  • 691.
    Polypoidal Choroidal Vasculopathy(PCV) • Sometimes clinically seen as reddish-orange y g spheroidal, or polypoidal, vascular lesions. • Location  Peripapillary, Sub foveal, Juxtafoveal, E J f l Extra f foveal l • Formation  Single, Cluster (more than 2 polyps in a group) or String (more than 3 polyps in a line ) S e µ • Size  in µm • Area  Single, Multiple Nakashizuka H, 2008; Cousins SW, 2009 691
  • 692.
    Polypoidal Choroidal Vasculopathy(PCV) • • • (A) Color fundus photograph showing a white fibrin-like lesion (arrow) adjacent to subretinal h b ti l hemorrhage h (arrowhead) and serous retinal detachment in the macula. (B) Fluorescein fundus angiography showing granular hyperfluorescence in the early phase (arrow). (C) IGA showing polypoidal lesions resembling grape clusters Nakashizuka H, 2008 692
  • 693.
    Polypoidal Choroidal Vasculopathy(PCV) • • • (A) Color fundus photograph shows orange lesions (arrow) surrounded by a white lesion. These findings are consistent with PCV (i.e., a polypoidal lesion accompanied b fib i ) i d by fibrin). (B) Fluorescein fundus angiography showing two small round hyperfluorescent lesions near the fovea (arrow) and a hyperfluorescent lesion indicating pigment epithelial detachment (arrowhead). (C) IGA showing polypoidal lesions corresponding to hyperfluorescent lesions on fluorescein fundus angiography. Nakashizuka H, 2008 693
  • 694.
    PCV : Management •Focal laser photocoagulation • PDT • Anti VEGF Cousins SW 2009 SW, 694
  • 695.
    Macular hole • • A, StandardStratusOCT image of the normal human macula. Most of the major intraretinal layers can be visualized in the Stratus OCT image and correlated with intraretinal anatomy. B, Ultrahigh-resolution optical coherence tomography (Cirrus HD OCT?) image of normal human macula. Ultrahigh-resolution OCT has an improved ability to visualize smaller structures such as the external limiting membrane (ELM) and ganglion cell layer (GCL) INL = inner nuclear layer; IPL = inner plexiform layer; IS/OS = (GCL). photoreceptor inner and outer segment junction; NFL = nerve fiber layer; ONL = outer nuclear layer; OPL = outer plexiform layer; RPE = retinal pigment epithelium 695 Fujimoto J, 2006
  • 696.
    Macular hole :Lamellar • Lamellar hole. A, Fundus photograph depicting the direction of optical , p g p p g p coherence tomography (OCT) scans. StratusOCT (B) and ultrahighresolution OCT (UHR-OCT) (C) images. D, Two-times magnification of the UHR-OCT image in the region of the hole. ELM = external limiting membrane; GCL = ganglion cell layer; INL = inner nuclear layer; IPL = inner plexiform layer; IS/OS = photoreceptor inner and outer segment junction; NFL = nerve fiber layer; ONL = outer nuclear layer; OPL = outer plexiform layer; RPE = retinal pigment epithelium. 696 Fujimoto J, 2006
  • 697.
    Macular hole :Stage 1 • Stage 1 macular hole. A, Fundus photograph depicting the direction of g , p g p p g optical coherence tomography (OCT) scans. Stratus OCT (B) and ultrahighresolution OCT (UHR-OCT) (C) images. D, Two-times magnification of the UHR-OCT image in the region of the hole. ELM = external limiting membrane; GCL = ganglion cell layer; INL = inner nuclear layer; IPL = inner plexiform layer; IS/OS = photoreceptor inner and outer segment junction; NFL = nerve fiber layer; ONL = outer nuclear layer; OPL = outer plexiform layer; PR OS = photoreceptor outer segment; RPE = retinal pigment 697 epithelium. *Henle’s fibers of the OPL. Fujimoto J, 2006
  • 698.
    Macular hole :Stage 2 • Fujimoto J, 2006 Eccentric stage 2 macular hole. A, Fundus photograph depicting the hole before surgery and the direction of optical coherence tomography (OCT) scans. B C t h B, C, Stratus OCT (B) and ultrahighresolution OCT (UHR-OCT) (C) images of the hole before surgery. D, Two-times g magnification of the UHR-OCT image in the region of the hole. E, Fundus photograph depicting repair of the hole after surgery. F, G, StratusOCT (F) and UHROCT (G) images of the repair of the hole after surgery H Twosurgery. H, Two times magnification of the UHROCT image in the region of the hole repair. ELM = external limiting membrane; GCL = ganglion cell layer; INL = inner nuclear layer; IPL = inner plexiform layer; IS/OS = photoreceptor inner and outer segment junction; NFL = nerve fiber layer; ONL = outer nuclear layer; OPL = outer plexiform layer; PR OS = photoreceptor l h t t outer segment; RPE = retinal pigment epithelium. 698
  • 699.
    Macular hole :Stage 3 • Stage 3 macular hole. A, Fundus photograph depicting the direction of g , p g p p g optical coherence tomography (OCT) scans. B, C, Stratus OCT (B) and ultrahigh-resolution OCT (UHR-OCT) (C) images. D, Two-times magnification of the UHR-OCT image in the region of the hole. ELM = external limiting membrane; GCL = ganglion cell layer; INL = inner nuclear layer; IPL = inner plexiform layer; IS/OS = photoreceptor inner and outer segment junction; NFL = nerve fiber layer; ONL = outer nuclear layer; OPL = outer plexiform layer; PR OS = photoreceptor outer segment; RPE = retinal pigment epithelium. Fujimoto J, 2006 699
  • 700.
    Macular hole :Stage 4 • Fujimoto J, 2006 Stage 4 macular hole. A, Redfree fundus photograph depicting the direction of optical g p y (OCT) ) coherence tomography ( scans. B, C, Stratus OCT (B) and ultrahigh-resolution OCT (UHR-OCT) (C) images of the hole before surgery. D, Twotimes magnification of the UHROCT image in the region of the hole. E, Fundus photograph depicting repair of the hole after surgery. F, G, StratusOCT (F) and UHR-OCT (G) images of the repair of the hole after surgery. H, Two-times H Two times magnification of the UHR-OCT image in the region of the hole repair. ELM = external limiting membrane; GCL = ganglion cell layer; INL = inner nuclear layer; IPL = inner plexiform layer; IS/OS = photoreceptor inner and outer segment junction; NFL = nerve fiber layer; ONL = outer nuclear layer; OPL = outer plexiform layer; PR OS = photoreceptor outer segment; RPE = retinal pigment epithelium. 700
  • 701.
    Hole Form Factor‘HFF’ HFF Pullifiato, 1999; Ullrich S, 2002 701
  • 702.
    Hole Form Factor‘HFF’ HFF • ‘HFF’ > 0,9 • ‘HFF’ < 0,5 • Higher ‘HFF’    80% success rate 25% success rate Better visual outcome Pullifiato, 1999; Ullrich S, 2002 702
  • 703.
    Vitreo Macular Vitreo-Macular Adhesion(VMA) • Symptomatic VMA is which  the vitreous gel adheres i an abnormally strong manner t th dh in b ll t to the retina • VMA can lead to vitreomacular traction (VMT) and subsequent loss or distortion of visual acuity • Anomalous posterior vitreous detachment (PVD) is linked to several retinal disorders including macular pucker, macular hole, age-related age related macular generation (AMD), macular edema, and retinal tears and detachment Retina Today 2012; Retina Physician 2012 703
  • 704.
    Vitreo Macular Vitreo-Macular Adhesion(VMA) • Approach  Pars Plana Vitrectomy (PPV) is used to surgically induce PVD and release the traction on the retina for selected cases • PPV may result in incomplete separation separation, and it may potentially leave a nidus for vasoactive and vasoproliferative substances, or it may induce development of fibrovascular membranes Retina Today 2012; Retina Physician 2012 704
  • 705.
    Vitreo Macular Vitreo-Macular Adhesion(VMA) • Approach pp – Ocriplasmin 2.5mg/ml, a vitreolysis agent  JETREA (TromboGenics) – ALG-1001 (Allegro) ALG 1001 • Pharmacologic vitreolysis has the following advantages g y g g over PPV: It induces complete separation, creates a more physiologic state of the vitreomacular interface, prevents the development of fibrovascular membranes membranes, is less traumatic to the vitreous, and is potentially prophylactic Retina Today 2012; Retina Physician 2012 705
  • 706.
    CME • Intraretinal edemacontained honeycomb-like cystoid spaces • Abnormal perfoveal retinal capillary permeability • FFA  because of Henle’s fiber layer  Flowerpetal pattern • Irvine-Gass syndrome – – – – High as 60% after ICCE Lower when posterior capsule remains intact Occurs 6-10 weeks post operatively Uncomplicated cases  95% spontaneous resolution after 6 months American Academy of Ophthalmology 706
  • 707.
    Hypertensive retinopathy • Grade0 • Grade 1 • Grade 2 • Grade 3 • Grade 4 No changes Barely detectable arterial narrowing Obvious arterial narrowing with focal irregularity Grade 2 plus retinal hemorrhages and or exudates Grade 3 plus disc swelling p g American Academy of Ophthalmology 707
  • 708.
    CRAO • • • • Sudden Severe Painless Retina R ti opaque, edematous, thi k t nerve fib l d t thickest fiber layer and ganglion cell layer in the posterior pole • Cerry-red spot  orange reflex  intact choroidal vasculature beneath the fovea  stands out in contrast to surrounding opaque neural retina • Iris neovascularization 18% in 1-12 weeks after 1 12 onset with mean time 4-5 weeks American Academy of Ophthalmology 708
  • 709.
    BRVO In BRVO, theblockage occurs in one of the smaller branch vessels th t connect b h l that t to the central retinal vein. Allergan 709
  • 710.
    BRVO : Causeof poor vision • • • • • • Macular edema Macular pigmentation Epi ti l E i retinal membrane (ERM) b Macular ischemia Vitreous haemorrhage Tractional retinal detachment Yeo KT, 2009 710
  • 711.
    CRVO • Non-ischemic – Milder form • • • • • Milddilatation and tortuosity of central retinal veins y Dot and flame hemorrhages Macular edema  decreased visual acuity Mild optic disc swelling FFA  prolongation of circulation time with breakdown of permeability but minimal areas of non perfusion – Sometimes referred as partial, perfused or venous stasis retinopathy • Ischemic – – – – – 80% CRVO progress to be Marked venous dilatation at least 10 disc areas Cotton wool spot Decrease visual acuity FFA  • Retinal capillary non perfusion on posterior pole  non perfused, complete or hemorrhagic • Widespread capillary non perfusion – Iris neovascularization 60% in 3-5 months after onset American Academy of Ophthalmology 711
  • 712.
    CRVO : Approach HypoxiaInduced yp VEGF Increased Hydrostatic y Pressure Increased Hydrostatic Pressure Rheopheresis* Grid Laser Inflammatory Vascular y Leak Increased Hydrostatic Pressure Cousins SW, 2009 712
  • 713.
    CRVO In CRVO, theblockage occurs in the central retinal vein, which is the main drainage line for blood leaving the retina Allergan 713
  • 714.
  • 715.
  • 716.
    CRVO : Anti-VEGFand Steroids Anti VEGF • Anti-VEGF* • Intra Vitreal Injection  Preservative-free Triamcinolone • Slow-released Drug Delivery System – Fluocinolone  Retisert (Bausch & Lomb)  ( ) 30 months – Dexamethasone  • Posurdex (Allergan) • Ozurdex (Allergan) Cousins SW, 2009; EuroTimes, 2010 716
  • 717.
    Retinal Vascular Disease: Surgery • CRAO  Decompression • BRVO  Arteriovenous Sheatotomy (AVST)  Reduce compression artery-venous  p y – Persistent CME – ERM with Vitreous traction – Significant retinal ischemia  more than 5 discdiameter of capillary non-perfusion with or without NV –M Macular i h i l ischemia • CRVO  Radial Optic Neurotomy (RON) Yeo KT, 2009 717
  • 718.
    ROP : Indirectophthalmoscopy • • • • Stage 1: Demarcation line Stage 2: Ridge : height, width, volume Stage 3 N St 3: New vessels growing out of ridge l i t f id Stage 4: Partial retinal detachment – 4 a. Extra fovea – 4 b. Involving fovea g • Stage 5: Total retinal detachment with funnel American Academy of Ophthalmology 718
  • 719.
    Zone and clockhours 719
  • 720.
    Stage 1: St 1 Demarcation Line Stage 2: Ridge Stage 3: Neo Vascularization 720
  • 721.
    ROP : Screening g Indirectophthalmoscopy • All infants with a birth weight of ≤ 1500 g • All infants with a gestational age of ≤ 28 weeks • Infants over 1500g if unstable clinical co rse o er nstable course • Timing: 4-6 weeks after birth or 31 to 33 weeks after conception • Treat < 72 hours after diagnosis of threshold disease New approach  RetCam Di it l I N h Digital Imaging (Cl it ) i (Clarity) 721
  • 722.
    ROP : Treatment •Laser photocoagulation • C th Cryotherapy • Retinal detachment surgery American Academy of Ophthalmology 722
  • 723.
    Intravitreal Antibiotics (/ 0 1 ml ) 0.1 • • • • • • Gentamycin G t i Vancomycin Amikacin Chlorampenicol Amphotericin B Ceftazidime Cefta idime 0.1 0 1 mg 1.0 mg 0.4 mg 1.0 mg 5.0 µg 2.0-2.25 2 0 2 25 mg American Academy of Ophthalmology 723
  • 724.
    Intravitreal Steroids (/ 0.1 ml ) 01 • Dexamethasone • Triamcinolone 0.4 mg 4 mg American Academy of Ophthalmology 724
  • 725.
    Consideration : Anatomy •Limbus identification • Lens existence – Ph ki  3 5 – 4 mm Phakic 3.5 – Aphakic / Pseudophakic  3 mm • Cilliary body  2.5 mm • Widest Pars plana and Ora  Temporo p p inferior  Safest area 725
  • 726.
    Retina : VEGFSession • VEGF is – Survival factor – Neuro protector – Fenestration • New vessels  Endothelial tubes Eurotimes, 2009 726
  • 727.
    Angiogenesis factors • • • • • VEGF bFGF Angiopoietin A i iti PGE2 Erythropoietin Cousins SW 2009 SW, 727
  • 728.
    The VEGF • Asub-family of growth factors sub family • More specifically of platelet-derived growth factor family of cystine-knot growth factors. cystine knot • They are important signaling proteins involved in both of – Vasculogenesis (the de novo formation of the embryonic circulatory system) – Angiogenesis (the growth of blood vessels from pre-existing vasculature) 728
  • 729.
    The VEGF :Production • VEGFxxx production can be induced in cells that p are not receiving enough oxygen. • When a cell is deficient in oxygen  it produces Hypoxia Inducible Factor (HIF)  a transcription factor. • HIF stimulates the release of VEGFxxx  among other functions (including modulation of th f ti (i l di d l ti f erythropoeisis). • Circulating VEGFxxx t e b ds to VEGF C cu at g G then binds G Receptors on endothelial cells  triggering a Tyrosine Kinase Pathway  leading to angiogenesis 729
  • 730.
    The VEGF Type Function VEGF-A • Angiogenesis •Migration of endothelial cells • Mitosis of endothelial cells • Methane mono oxygenase activity • αvβ3 activity • Creation of blood vessel lumen • Creates lumen • Creates fenestrations • Chemo tactic for macrophages and granulocytes • Vasodilatation (indirectly by NO release) VEGF-B Embryonic angiogenesis VEGF-C Lymph angiogenesis VEGF-D Needed for the development of lymphatic vasculature surrounding lung bronchioles PlGF Important for Vasculo genesis, Also needed for angiogenesis during ischemia, inflammation, wound healing, and cancer. 730
  • 731.
    VEGF A • • • • • Located onChromosome 6 Consist of 8 exons and 7 introns Diffusible Tightly bound to intracellular matrix Isoforms – – – – A121 A165 A185 A206 Eurotimes, 2009 731
  • 732.
    VEGF 165 • Moderatedifusible • Potent inducer of angiogenesis  –N Neovascularization l i ti – Inflammation – Increase permeability Eurotimes, 2009 732
  • 733.
    AMD : Intravitrealinjections Drug Structrure Dosage Bevacizumab (Avastin)) Complete p immunoglobulin 2.5 mg/0.1 ml g Ranibizumab (Lucentis Antibody fragment 0.3–0.5 mg/0.1 ml Pegaptanib (Macugen) Aptamer (oligonucleotide) 0.3–1.0 mg/0.1 ml Williamson TH, 2008 733
  • 734.
    Potential Methods 1. Adult 1. Phakic : 4 mm 2. Aphakic : 3.5 mm 3. 3 Pseudophakic : 3.5 mm 35 2. Infant  1 – 1.5 mm Krieglstein GK, Weinreb RN, 2005 734
  • 735.
    Retinal Artery Occlusion:Approach • Vasodilators: Increase blood oxygen content – Sublingual isosorbide mononitrate – Systemic pentoxifyline – Carbogen inhalation – Hyperbaric oxygen Retinal Physician 2013 735
  • 736.
    Retinal Artery Occlusion:Approach • Reduction retinal edema – IV methylprednisolone (suspected areteritic CRAO) • IOP reducers – Acetazolamide – Mannitol – T i l anti glaucoma Topical ti l – Paracentesis Retinal Physician 2013 736
  • 737.
    Retinal Artery Occlusion:Approach • Dislodge the emboli – Ocular massage – Nd:YAG laser embolectomy Retinal Physician 2013 737
  • 738.
  • 739.
  • 740.
    The optic nerve • Intraocular – 1.0 mm length – 1 5 X 1 75 mm diameter 1.5 1.75 – Supplied by retinal arterioles and branches of posterior ciliary arteries • Intra orbital – 25 mm length – 3-4 mm diameter – Supplied by intraneural branches of central retinal artery • Intra canalicular – 4-10 mm length – various diameter – Supplied by Ophthalmic artery • Intra cranial – 10 mm length – 4-7 mm diameter – S Supplied b b li d by branches of i t h f internal carotic and ophthalmic artery l ti d hth l i t American Academy of Ophthalmology 740
  • 741.
    Optic nerve :Intra ocular • Surface • Prelaminar • Laminar – Scaffold for optic nerve axons – Point of fixation for central retinal artery and vein – Reinforcement of posterior segment of the g p g globe • Retrolaminar American Academy of Ophthalmology 741
  • 742.
    Optic disc A. Surface B.Pre Laminar C. Laminar D. Retro Laminar 742
  • 743.
    Vascularization Surface : branchesof central retinal artery Prelaminar and laminar : posterior cilliary artery Retrolaminar : central retinal artery and y posterior cilliary artery anastomosis 743
  • 744.
    Euro ophthalmic Euro-ophthalmic examination • • • • • • • • History Visualacuity Color vision Pupil reactions Ocular O l motility tilit Discs Visual fields Advanced intracranial examination Cullen JF, 2007 744
  • 745.
    Neurologic and imaging: Indication • • • • • • • • Progressive visual loss more than 4 weeks No recovery of vision and fields after 10 weeks Head or periocular pain for more than 4 weeks Patient older than 50 year Quadrantic or Hemianopic fields defect Development of field defect in fellow eye Atypical features History of paranasal sinus disease Kumar SM 2007 745
  • 746.
    Neuro imaging Neuro-imaging :Which? • • • • • Brain Anterior visual pathway p y Pituitary area Orbit + Coronal view ? Base of skull Cullen JF, C ll JF 2007 746
  • 747.
  • 748.
    Visual cortex • Theterm visual cortex refers to – The primary visual cortex  Striate cortex or V1 – Extrastriate visual cortex  V2, V3, V4, and V5. • The primary visual cortex is anatomically equivalent to Brodmann Area 17 or BA17 748
  • 749.
    Visual pathway andVF defects Miller-Keane 2003 749
  • 750.
    Intracranial hypertension andVF defects d f (a) Enlarged blind spot. (b)Nasal step. (c) Biarcuate scotoma. (d)Severe visual field constriction Kedar, Gathe and Corbett 2011 750
  • 751.
    The pupillary lightreflex pathway p p y g p y 751
  • 752.
    Afferent pupillary pathway •Light stimulates p g photoreceptors p • Signal conveyed to a special set of ganglion cells  send nerve impulses through the axons in similar topographic distribution • Carrying signal to optic nerve • Decussation occurs at the optic chiasm • Afferent fibers NOT enter lateral geniculate bodies • BUT instead exit and pass the brachium of of the superior colliculus  its synapse on the protectal olivary nuclei (pontine olivari and sublentiform nuclei) • This nuclei project bilaterally to Edinger-Westphal nuclei Kourouyan and Horton, 1997 752
  • 753.
    Efferent pupillary pathway •Efferent parasympathetic response p y p p – The Edinger-Westphal nuclei send fiber to join the cranial nerve III – Follow that course on dorsomedialsurface of the nerve – After coursing through the cavernous sinus, fibers emerge to enter orbit with the inferior oblique branch of cranial nerve III – Fibers synapse at ciliary g g y p y ganglion – Enter the eye through short posterior ciliary nerves to distribute fiber to choroid, ciliary body and iris Kourouyan and Horton, 1997 753
  • 754.
    Efferent pupillary p pp y pathway y • Efferent sympathetic response – This believed to start in the hypothalamus and project in an uncrossed fashion with synapses in mesencephalon and pons – These neurons project to and synapse upon intermediolateral cell column from C8-T2 in spinal cord – These exit the spinal cord and p p pass through stellate g g g ganglion to synapse in the superior cervical ganglion – Fibers go with internal carotic artery – Enter the cavernous sinus – G with cranial nerve VI Go ith i l – Enter superior orbital fissure with cranial nerve V – Go with the nasociliary branch of cranial nerve V – Pass through the ciliary ganglion without synapsing – Pass through the long ciliary nerves – Terminate the dilator muscle – Some fibers diverge in the superior orbital fissure to innervate Muller’s muscle Kourouyan and Horton, 1997 754
  • 755.
  • 756.
    RAPD: Grading Scale g • Grade1+: – A weak initial pupillary constriction f ll k i iti l ill t i ti followed b greater redilation d by t dil ti – Minimally detectable • Grade 2+: – An initial pupillary stall followed by greater redilation – Pupil fails to constrict or dilate slightly when the light swings to weaker eye • Grade 3+: – An immediate pupillary dilation – Pupils dilate or “escape” readily • Grade 4+: – No reaction to light – Amaurotic pupil – Non reactive mydriatic pupil Kumar SM 2007; Uhwi 2011 756
  • 757.
    RAPD • • • • • Dark D k room Brightlight  torch 2 eyes Patient fixation is at distance 2-3 seconds per eye  longer may create an p y g y iatrogenic RAPD • Check by your self  do not rely on others Burton B, Golnik K, 2010 757
  • 758.
    Cause of light-neardissociation • Unilateral – – – – Afferent conduction defect Adie pupil HZO Aberrant degeneration of the cranial nerve III • Bilateral – – – – – – – Neurosyphilis Type I diabetes T di b t Myotonic distrophy Parinaud dorsal midbrain syndrome Familial amyloidosis Encephalitis Chronic alchoholism Kanski JJ, 2007 758
  • 759.
    Anisocoria • Good light reaction – – Physiologic Horners Horner’s Syndrome • • • • • Sympathetic chain disruption Miosis, Ptosis, Anhydrosis Anisocoria worse in the dark Dilatation Lag Poor light reaction – Adie’s tonic • • • • • • – – – Post ganglionic parasympathetic  usually idiopathic No ptosis, No ophthalmoplegia Mydriatic pupil Segmental iris contraction Slow (tonic) redilation Light – Near dissociation 3rd nerve palsy Pharmacologic Sphincter damage • • • Trauma Surgery Herpes Zoster Burton B, Golnik K, 2010 759
  • 760.
    Papilledema : Walsh& Hoyt’s • Early E l manifestations if t ti – – – – • Late L t manifestations if t ti – – – • As the papilledema continues to worsen, the nerve fiber layer swelling eventually obscures the normal disc margins and the disc becomes grossly elevated. Venous congestion develops, and peripapillary hemorrhages become more obvious, along with exudates and cotton-wool spots. The Th peripapillary sensory retina may d i ill ti develop concentric or, occasionally, radial f ld k l ti i ll di l folds known as Paton lines. Choroidal folds also may be seen. Chronic manifestations – – • Disc hyperemia Subtle edema of the nerve fiber layer can be identified with careful slit lamp biomicroscopy and direct ophthalmoscopy. This most often begins in the area of the nasal disc. A key finding occurs as the nerve fiber layer edema begins to obscure the fine peripapillary vessels. vessels Small hemorrhages of the nerve fiber layer are detected most easily with the red-free (green) light. Spontaneous venous pulsations that are normally present in 80% of the individuals may be obliterated when the intracranial pressure rises above 200 mm water. If the papilledema persists for months, the disc hyperemia slowly subsides, giving way to a gray or pale disc that loses its central cup. With time, the disc may develop small glistening crystalline deposits (disc pseudodrusen). Atrophic manifestations – – Blurred-border and pale disc Atrophic vessels Giovannini J, 2005 760
  • 761.
  • 762.
    Papilledema : LarsFrisen’s Scale • Stage 0 – Normal disc with blurring of nasal and temporal disc; no obscuration of the vessel and the cup is maintained. p • Stage 1 – C shaped blurring of the nasal, superior and inferior borders. Usually the temporal margin is normal • Stage 2 – Elevation of the temporal margin • Stage 3 – Elevation of the entire disc with obscuration of the retinal vessels at the disc margin • Stage 4 – Complete obliteration of the cup and obscuration of the vessels on the surface of the disc. • Stage 5 – Dome shaped appearance with all vessels being obscured Lars Frisen, 2004 762
  • 763.
  • 764.
  • 765.
  • 766.
  • 767.
  • 768.
  • 769.
    Differentiating Papilledema fromPseudopapilledema Papilledema Pseudopapilledema Physiologic cup usually present Central cup often absent, disc diameter small Vessels arise normally Vessels from central apex of disc Arterioles bifurcate Anomalous branching, trifurcation Hyperemia due to dilation of the disc capillaries Absence of superficial capillary telangectasia C shaped blurring of RNFL in peripapillary region Disc margins irregular with pigmentary derangement Diffuse elevation of the disc Irregular elevation, refractile masses which glow Peripapillary NFL radial hemorrhage Rare 'blot' subretinal hemorrhage Dilation of the retinal veins No venous dilation Exudates in chronic situations p No exudates or cotton-wool spots Not usually familial Familial Absence of SVP SVP usually present Lars Frisen, 2004 769
  • 770.
    Optic Neuropathies p p • • • • Trauma ocular,orbit and skull • Single or multiple nerve defect Metabolic • Early diabetic  Insufficient in vascular to nourish the optic nerve Toxic • Methanol, Ethambutol, Isoniazid Neuritis • Primary inflame • Secondary inflame • Giant Cell Arteritis • Multiple Sclerosis • t th and paranasal sinus i fl teeth d l i inflammation or nearby ti ti b tissue inflammation 770
  • 771.
    AION : Symptoms • • • • • Giantcell arteritis Sudden, painless, non progessive visual loss Initially unilateral may rapidly bilateral unilateral, Older than 60 years, Women greater than Men Antecedent or simultaneous headache jaw headache, claudication or chewing pain, scalp or hair co b g tenderness, proximal muscle a d jo t combing te de ess, p o a usc e and joint ache, anorexia, weight loss and fever may occur Will’s Eye Manual 771
  • 772.
    AION : Signs g •Critical – Aff Afferent pupillary defect ill d f – Devastating worse visual loss – Pale swollen disc with flame shape hemorrhages  Pale, atrophy – Erythrocytes Sedimentation Rates, C Reactive Protein and platelets may be markedly increased • Other – Visual field defect  altitudinal, involving central field – Non pulsatile temporal artery – CRAO an cranial nerve palsy may occur Will’s Eye Manual 772
  • 773.
    NAION : Symptoms •Sudden, painless, non progressive visual loss of moderate degree • Initially unilateral, may become bilateral • 45 65 years, commonl younger than 45-65 ears commonly o nger AION Will’s Eye Manual 773
  • 774.
    NAION : Etiology •Idiopatic – Arteriosclerosis – Diabetes – Hypertension – Hyperhomocystinemia – Anemia – Sl Sleep apnea  risk f t i k factor – Relative nocturnal hypotension Will’s Eye Manual 774
  • 775.
    NAION : Riskfactors • • • • • Hypertension Hyperlipidemia H li id i Diabetes mellitus Smoking Obesity Deborah Pavan-Langston, 2008 775
  • 776.
    NAION : Signs g •Critical – Afferent pupillary defect – Pale, swollen disc involving only a segment of the disc with flame shape hemorrhage – Normal Erythrocytes Sedimentation Rates – Non-progressive  sudden decrease of VA and VF, which stabilized – Progressive  sudden decrease of VA and VF, followed with another decrease of VA and VF • Other – Visual field defect  altitudinal, involving central field – Reduced color vision proportional to decrease in acuity Will’s Eye Manual 776
  • 777.
    AION PION ON Symptoms Sudden i S ddvisual l l loss, often ft on awakening Sudden i S dd visual l l loss, often ft on awakening Rapid loss of vision over R id l f i i several days to 1 week VA Can be good if central field maintained Can be good if central field maintained Good to no perception of light CV Normal in unaffected field Normal in unaffected field Disproportionate loss of color vision Pupils Relative afferent pupil defect Relative afferent pupil defect Relative afferent pupil defect VF Most commonly inferonasal loss, or altitudinal defects, but other patterns possible More commonly central scotoma seen Central visual field loss relatively common, nerve fiber bundle defects also possible Disc -Hyperemic disc swelling in early phase -Pallor developing 3-6 weeks after onset -However arteritic AION usually causes chalky white disc infarction from onset -Disc appear normal at onset -Pallor develops about 6 weeks after onset -Hyperemic disc swelling in early phase -Pallor developing from about 6 weeks after onset Cullen JF, 2007 777
  • 778.
    Acquired optic atrophyin childhood • • • • • • • Craniopharyngioma Optic nerve / Chiasmal glioma Retinal degenerative di R ti l d ti disease Hydrocephalus Optic neuritis Post papil edema Hereditary Cullen JF, 2007 778
  • 779.
    Optic Pit • Oftenappear as small, hypopigmented, y pp yp p g yellow or whitish, oval or round excavated defects. • Most often within the inferior temporal portion of the optic cup cup. • Approximately 20 to 33 percent are found centrally, with an average size of 500µm (onethird disc diameter). thi d di di t ) • Typically, optic pits occur unilaterally (85 pe ce t) percent). • The optic disc in these patients appears larger than normal, and 60 percent of discs with optic pits also have cilioretinal arteries arteries. 779
  • 780.
  • 781.
    Optic Disc Drusen p •The classic appearance involves bilaterally elevated optic discs with irregular or "scalloped" margins, a small scalloped or nonexistent cup, and unusual vascular branching patterns that arise from a central vessel core. • Often there are small, refractile hyaline deposits visible , y p on the surface of the disc and/or in the peripapillary area. • Most often manifests on the nasal disc margin, but can yp be found within any part of the nerve head. • In younger patients, the disc elevation tends to be more pronounced and the drusen less calcific, making them less visible ophthalmoscopically, and hence offering a more challenging diagnostic dilemma. • Unlike true disc edema, its very rarely presents with juxtapapillary nerve fiber edema, exudate, or cotton-wool spots. t 781
  • 782.
    Optic Drusen :Pathophysiology • There is no histopathological correlation between drusen of the optic nerve head and retinal drusen; the former represent acellular l i t d concretions, often partially t ll l laminated ti ft ti ll calcified, possibly related to accumulation of axoplasmic derivatives of degenerating retinal nerve fibers. • Optic disc drusen are globules of mucoproteins and mucopolysaccharides that progressively calcify in the optic disc. • They are thought to be the remnants of the axonal transport system of degenerated retinal ganglion cells. • Optic disc drusen have also been referred to as congenitally elevated or anomalous discs discs, pseudopapilledema, pseudoneuritis, buried disc drusen, optic nerve head drusen and disc hyaline bodies. • They may be associated with vision loss of varying degree 782
  • 783.
  • 784.
    VF Defects inOptic neuropathies • Central scotoma – – – – • Demyelination y Toxic and nutritional Leber disease Compression Enlarged blind spot – Papil edema – Congenital anomalies – AIBSE (Acute Idiopathic Blind Spot Enlargement)  with flashing light ( p p g ) g g seen, normal retina, normal imaging – AZOOR (Acute Zonal Occult Outer Retinopathy)  with flashing light and other field loss, normal retina, normal imaging • Respecting horizontal meridian p g – Anterior Ischemic Optic Neuropathy – Glaucoma – Disc drusen Kanski JJ, 2007; Burton B, 2010 784
  • 785.
    Unexplained visual loss •Miss the real diagnosis • Munchausens – Factitious disorder, or mental illness  repeatedly acts as has a physical or mental disorder when – People with factitious disorders act this way because of an inner need t be seen as ill or i j d not t achieve a concrete d to b injured, t to hi t benefit • Hypochondriac – Health phobia or health anxiety – Excessive preoccupation or worry about having a serious illness • Hysteria (Conversion disorder) – Exacerbation of symptoms during psychological stress – Relief from tension (primary gain) – Gain of outside support or attention (secondary gains) • Malingering Burton B, Golnik K, 2010 785
  • 786.
    Nystagmus • Clinician’s notes –Amplitude – Frequency – Direction of gaze that induces nystagmus – Null point  Gaze location where nystagmus at least evident p y g • Concerns – Congenital or acquired – Specific lesion location – True nystagmus or nystagmoid movements (saccadic oscillations) • Characteristics – I it conjugate  symmetrically affecting both eyes Is j t t i ll ff ti b th – Slow or fast, equal speed or different speed – Movement  horizontal, vertical, torsional or mixed American Academy of Ophthalmology 786
  • 787.
    Nystagmus : Type • • • • • • Latentnystagmus Pendular nystagmus Congenital motor nystagmus Spasmus nutan Acquired pendular nystagmus Acquired jerk nystagmus – Gaze paretic nystagmus – Vestibular nystagmus Deborah Pavan-Langston, 2008 787
  • 788.
    Nystagmus : Othernystagmus form • • • • • • • • Endgaze (physiologic) nystagmus Upbeat nystagmus Downbeat motor nystagmus Rotary nystagmus Dissociated nystagmus ssoc a ed ys ag us Seesaw nystagmus Optokinetic nystagmus Other nystagmoid-like oscillations – Ocular myoclonus – Ocular bobbling – Ocular flutter  One plane of ‘Back to Back Saccades’ without inter saccadic interval – Opsoclonus  Multi directional of ‘Back to Back Saccades’ without inter saccadic interval Deborah Pavan-Langston, 2008 788
  • 789.
    Nystagmus : Medicaltreatment y g • Cyclopentolate 1% – One drop bid  Latent nystagmus  60 % reduce the amplitude, p y g p velocity and frequency – With occlusion  improve visual acuity • Baclofen – 5 mg po tid starting dose  acquired periodic alternating nystagmus – Dosage increased every 3 days  80 mg maximum per day • Botulinum A – Dampened acquired nystagmus and oscillopsia – 66%  improve visual acuity • Other drugs – – – – Gabapentin/Memantine  dampen nystagmus/oscillopsia Clonazepam  downbeat nystagmus Carbamazepin  SO myokymia Propanolol  Opsoclonus Deborah Pavan-Langston, 2008 789
  • 790.
    Nystagmus : Opticaltreatment • Glasses or contact lenses – Decrease nystagmus in bilateral aphakia • Stimulating accommodative convergences – Overcorrecting with minus lenses  dampening nystagmus at distance fixation – Improve visual acuity p y • Galilean arrangement – Stabilizing retinal images • Base-out prisms – Promote covergence and dampen nystagmus in Congenital motor nystagmus • Fresnel stick-on prisms – Displace image at null p p g point in Congenital motor nystagmus g y g – Vertically correct head position in Vertical nystagmus and Acquired downbeat nystagmus – Combination prisms  help in Oblique head turns Deborah Pavan-Langston, 2008 790
  • 791.
    Nystagmus : Surgicaltreatment • Kestenbaum Anderson procedures – Recession of horizontal muscles – The versions are blocked • F d operation Fade ti – Acts like recession  by creation of a more posterior attachment t i tt h t – Reducing the area of contact Kumar SM 2007 791
  • 792.
    Optic Ataxia • • • • • • Is lackof coordination between visual inputs and hand movements, resulting in inability to reach and grab objects objects. Optic ataxia may be caused by lesions to the posterior parietal cortex. p parietal cortex is responsible for combining and p g The posterior p expressing positional information and relating it to movement. Outputs of the posterior parietal cortex include the spinal cord, brain stem motor pathways, pre-motor and pre-frontal cortex, basal ganglia and the cerebellum cerebellum. Some neurons in the posterior parietal cortex are modulated by intention. Optic ataxia is usually part of Balint's syndrome, but can be seen in isolation ith injuries to the i l ti with i j i t th superior parietal l b l as it represents i i t l lobule, t a disconnection between visual-association cortex and the frontal premotor and motor cortex. 792
  • 793.
    Visual Agnosia • Isan inability of the brain to make sense of or make use y of some part of otherwise normal visual stimulus • Typified by the inability to recognize familiar objects, people or faces. • This is distinct from blindness, which is a lack of sensory input to the brain due to damage to the eye, optic nerve, or primary visual systems in the brain such as the optic radiations or primary visual cortex. • Visual agnosia is often due to damage, such as stroke, in the i th posterior occipital and/or t t i i it l d/ temporal l b ( ) i th l lobe(s) in the brain. 793
  • 794.
  • 799.
    Uvea and Immunology In Iremembrance: b dr. Muhammad Anie, Sp.M 799
  • 800.
    Choroid : Layers •Th choriocapillaris The h i ill i • Small vessels • Large vessels 800
  • 801.
    Uveitis • How toavoid complication – Fi t  C l l i agents First Cycloplegic t • Complication – Acute  Cell – Chronic  Synechiae 801
  • 802.
    U ets Uveitis Non-granulomatous Onset O Granulomatous Acute A Chronic Hidden Chi – Hidd Pain Marked +/- Photophobia Marked Mild Moderate Obvious Marked Mild Keratic precipitate White - smooth Big – grey / Mutton fat Pupil Small - irregular Small – irregular (vary) Posterior synechiae +/- +/- Iris nodule +/- +/- Anterior uvea Anterior and posterior uvea Often +/- Blur vision Circumcorneal injection Predilection Recurrent Vaughan DG, 2000 802
  • 803.
    Flare and Cell •Flare  Resulting of extra protein in the aqueous • Cell  White Blood Cell in the aqueous – Hallmark of Iritis – Ob Observed under Hi h M d d High-Magnification Slit L ifi ti Lamp examination by 1 X 3 mm field of light – If its clustering on corneal endothelium  it l t i l d th li Keratic Presipitate 803
  • 804.
    Grading anterior chambercells g Grade Cells in field 0 0 0.5+ 0 5+ (Trace) 1-5 15 1+ 6-15 2+ 16-25 3+ 26-30 26 30 4+ > 50 Kanski JJ, 2007 804
  • 805.
    Grading anterior chamberflare g Grade Description 0 Nil (Completely Absent) 1+ Faint (Barely Present) 2+ 2 Moderate (Iris and lens detail clear) 3+ Marked (Iris and lens detail hazy) 4+ Intense (Fibrinous exudates) Kanski JJ, 2007 805
  • 806.
  • 807.
  • 808.
    HLA Immunogenic test g •Specific ocular inflammatory : – – – – – – – – – Acute anterior uveitis : HLA-B27, HLA-B8 Adamantiades-Behçet disease : HLA B-51 Birdshot retinopathy : HLA A29 HLA-A29 Multiple sclerosis, uveitis and optic neuritis : DR2 Ocular pemphigoid :HLA-B12, DQw7 :HLA B12, Presumed ocular histoplasmosis : HLA-B7, DR2 Reiter syndrome : HLA-B27 Sympathetic ophthalmia :HLA-A11, DR4, Dw53 VKH disease : DR4, Dw53, DQw3 Deborah Pavan-Langston, 2008 808
  • 809.
  • 810.
    Lipid mediators :Basic activities 810
  • 811.
    Vasoactive amine • Containingamino groups • Breakdown of amino acids. Many natural neurotransmitters like epinephrine epinephrine, norepinephrine, dopamine, serotonine, histamine • Acts on the blood vessels to alter vascular permeability or t cause vasodilation. bilit to dil ti 811
  • 812.
    Cytokines • Small secretedproteins which mediate and regulate p g immunity, inflammation, and hematopoiesis. • Produced de novo in response to an immune stimulus. • Generally (although not always) act over short distances and short time spans and at very low concentration. • Act by binding to specific membrane receptors, which then i th signal th cell via second messengers, often l the ll i d ft tyrosine kinases, to alter its behavior (gene expression). y g g • Responses to cytokines include increasing or decreasing expression of membrane proteins (including cytokine receptors), proliferation, and secretion of effector molecules. 812
  • 813.
    Selected Immune Cytokinesand Their Activities* Cytokine Producing Cell Target Cell GM-CSF Th cells progenitor cells Function** growth and differentiation of monocytes and DC Th cells IL-1 monocytes macrophages B cells DC co-stimulation B cells maturation and proliferation IL-2 Th1 cells IL-3 Th cells NK cells NK cells activation various IL-1 inflammation, acute phase response, fever activated T and B cells cells, NK cells growth, proliferation, growth proliferation activation Th2 cells growth and differentiation mast cells growth and histamine release activated B cells IL-4 stem cells proliferation and differentiation IgG1 and IgE synthesis macrophages h T cells MHC Cl Class II proliferation 813
  • 814.
    IL-5 Th2 cells IL-6 monocytes macrophages Th2 cells stromalcells activated B cells proliferation and differentiation IgA synthesis activated B cells differentiation into plasma cells plasma cells stem cells various antibody secretion differentiation acute phase response IL-7 marrow stroma thymus stroma y stem cells differentiation into progenitor B and T cells IL-8 macrophages endothelial cells neutrophils chemotaxis IL-10 IL 10 Th2 cells macrophages B cells cytokine production activation differentiation into CTL (with IL-2) macrophages B cells activated Tc cells NK cells activation IFN- leukocytes various viral replication MHC I expression IFN- fibroblasts various viral replication MHC I expression IL-12 814
  • 815.
    various macrophages IFN- Th1 cells, Tc cells,NK cells Viral replication MHC expression activated B cells Th2 cells macrophages Ig class switch to IgG2a proliferation pathogen elimination MIP-1 macrophages monocytes, T cells chemotaxis MIP-1 lymphocytes monocytes, T cells chemotaxis monocytes, macrophages chemotaxis activated macrophages activated B cells TGF- IL-1 synthesis IgA synthesis T cells, monocytes various TNF macrophages, mast cells, NK cells macrophages proliferation CAM and cytokine expression cell death phagocytes TNF- tumor cells phagocytosis, NO production tumor cells cell death Th1 and Tc cells 815
  • 816.
    Reactive Oxygen Intermediate •Including both radicals and non-radicals. non radicals. • Constantly formed in the human body and have been shown to kill bacteria and inactivate proteins, and have been p implicated in a number of diseases. • Produced by inflammatory phagocytes to p cancer development. • Important signals controlling cell growth and cell death 816
  • 817.
  • 818.
    Immune Systems Systems exhibit fascinating complexity and y g p y interrelationships that allow them to fine-tune immune reactions to almost any antigen, or molecule that p stimulates an immune response • Humoral immunity – Deals with infectious agents in the blood and body tissues – Managed by B-cells (with help from T-cells) • C ll Cell-mediated immunity  di t d i it – Deals with body cells that have been infected. – Managed by T-cells. 818
  • 819.
    Immune Systems :Humoral y • The humoral system of immunity is also called the antibody-mediated system because of its use of specific immune-system structures called antibodies. • Activation phase – The first stage in the humoral pathway of immunity is the ingestion (p g y (phagocytosis) of foreign matter by special blood cells called macrophages. ) g y p p g – The macrophages digest the infectious agent and then display some of its components on their surfaces. – Cells called helper-T cells recognize this presentation, activate their immune response, and multiply rapidly • Effector phase – Involves a communication between helper-T cells and B-cells. – Activated helper-T cells use chemical signals to contact B-cells, which then begin to multiply rapidly as well B cell descendants become either plasma cells or B well. B-cell memory cells. – The plasma cells begin to manufacture huge quantities of antibodies that will bind to the foreign invader (the antigen) and prime it for destruction. – B memory cells retain a "memory" of the specific antigen that can be used to y y p g mobilize the immune system faster if the body encounters the antigen later in life. These cells generally persist for years. 819
  • 820.
    Immune Systems :Cell-Mediated • • • • • • • • The cell-mediated immune response involves cytotoxic T-cells, or killer-T cells. Body cells that have been infected by foreign matter often present components of that material on their surfaces. Killer-T cells recognize these displays and respond by ingesting or otherwise destroying the infected cell. Killer-T cells are also important in the body's defenses against parasites, fungi, protozoans, and other larger cells that might have found their way into the body. The killer T cells recognize these large invaders by their foreign killer-T proteins and then destroy them. Killer-T cells also produce T memory cells which "remember" a specific protein or antigen. The Th combination of T ll and B ll memory assures the b d of bi ti f T-cell d B-cell th body f familiarity with any antigens or foreign agents that have been present in the body within the last few years. p g g y y A response to an agent against which the body has already formed memory cells is called a secondary response. All other responses are primary responses. 820
  • 821.
    Inflammatory cascade: Steroidsvs NSAID Cervantes-Coste G et al 2009 821
  • 822.
    Retinal arteritis • Causes –SLE – Polyarteritis nodosa – Churg-Strauss – Microscopic polyangitis – Frosted branch angitis – S hili Syphilis – Herpetic viruses Retinal Physician 2011 822
  • 823.
    Retinal phlebitis • Causes –Sarcoidosis – Paraviral – Toxoplasmosis – Birdshot – HIV – E l di Eales disease Retinal Physician 2011 823
  • 824.
    Mixed retinal vasculitis •Causes – Multiple sclerosis – Behçet’s disease Behçet s – Wegener’s granulomatosis Retinal Physician 2011 824
  • 825.
    Non infectious uveitis:Approach • ANTIMETABOLITES – Methotrexate (MTX) – Azathioprine (AZA) – Mycophentolate Mofetil (MMF) Retinal Physician 2013 825
  • 826.
    Non infectious uveitis:Approach pp • BIOLOGIC RESPONSE MODIFIERS – Adalimunab – Interferon 2a – Anakinra • ALKYLATING AGENTS – Cyclophosphamide – Clorambucil – Mycophentolate Mofetil (MMF) Retinal Physician 2013 826
  • 829.
    dr. Bakri AbdusSyukur, Sp.M Orbit and Tumor 829
  • 830.
    The orbit • 7bones make the bony orbit : – Frontal – Zygomatic – Maxillary – Ethmoidal – Sphenoid –L i l Lacrimal – Palatine American Academy of Ophthalmology 830
  • 831.
    The orbit :Margin g • Superior by frontal bone, interrupted p y , p medially by Supraorbital notch • Medial above by frontal bone • Medial bellow by – P t i l i l crest of l i l b Posterior lacrimal t f lacrimal bone – Anterior lacrimal crest of maxillary bone • Inferior by maxillary and zygomatic bone • Laterally by zygomatic and frontal bone American Academy of Ophthalmology 831
  • 832.
    The orbit :Roof • Orbital plate of frontal bone • L Lesser wing of sphenoid b i f h id bone American Academy of Ophthalmology 832
  • 833.
    The orbit :Medial wall • • • • Frontal process of maxilla Lacrimal bone L i lb Orbital plate of ethmoid Lesser wing of sphenoid American Academy of Ophthalmology 833
  • 834.
    The orbit :Lateral wall • Formed by – Zygomatic – Greater wing of sphenoid • Lateral orbital tubercle of Whitnall – Check ligament of the lateral rectus muscle – Suspensory ligament of the eyeball – Lateral palpebral ligament – Aponeurosis of the levator muscle American Academy of Ophthalmology 834
  • 835.
    The orbit :Floor • Formed by – Maxillary – Palatine – Orbital plate of zygomatic • Very fragile to orbital blunt trauma American Academy of Ophthalmology 835
  • 836.
    The Orbit :Superior orbital fissure • Above the ring – Lacrimal nerve of V-1 – Frontal nerve of V-1 – Cranial nerve IV • Within the ring (Heads of 4 rectuses) – – – – – Superior and inferior division of cranial nerve III Nasociliary b N ili branch of cranial nerve V 1 h f i l V-1 Sympathetic root of ciliary ganglion Cranial nerve VI Superior ophthalmic vein • Bellow the ring – Inferior ophthalmic vein American Academy of Ophthalmology 836
  • 837.
    The orbit :Cavernous sinus • Posterior to orbital apex • Lateral to the sphenoidal air sinus and pituitary fossa • Structures located within are : – Internal carotic artery that that, – Surrounded by sympathetic carotid plexus – Cranial nerves III, IV and VI – Ophthalmic and maxillary divisions of cranial nerve V American Academy of Ophthalmology 837
  • 838.
    Orbital surgical space • • • • Subperiorbital Extra E t conal l Intra conal Episcleral American Academy of Ophthalmology 838
  • 839.
    Retinoblastoma • Most commonprimary intraocular malignancy of p y g y childhood • 30-40% occurs bilaterally – If associated with ectopic intracranial retinoblastoma  Trilateral retinoblastoma  pineal gland and para sellar region • Most abnormal finding – Leukocoria (50-62%) – Strabismus (20%) • Esotropia : Exotropia  50:50 – Redness, painful, glaucomatous, decreased vision, etc American Academy of Ophthalmology 839
  • 840.
  • 841.
    Basalioma • • • • • • • • Basal cell carcinoma Mostcommon eye lid malignancy  90-95% y g Lower eyelid margin  50-60% Near medial canthus  25-30% Upper eyelid  15% Lateral canthus  5% Most common  Nodular Less common  Morpheaform of Fibrosing type  more aggressive American Academy of Ophthalmology 841
  • 842.
    Basalioma : Managements •Localized to the adnexa – 3-5mm excision from macroscopic margin  frozen section • Invasion to the orbit – Exenteration – Radiation therapy • Only a palliative treatment • Generally be avoided for periorbital lesions • Invasion to intracranial or paranasal sinuses – Palliative 842
  • 843.
    Squamous Cell Ca •40 times less common than basalioma  biologically more aggressive • Metastasize through : – Lymphatic transmission – Bl d b Blood-borne t transmission i i – Direct extension  often, along nerves American Academy of Ophthalmology 843
  • 844.
    Squamous Cell Ca: Eyelid • Localized to the adnexa – 6 7 mm excision f 6-7 i i from macroscopic margin  f i i frozen section ti • Invasion to the orbit – Without regional lymphatic nodes involvement • Exenteration • Radiation therapy – With regional lymphatic nodes involvement • Exenteration • Lymphatic nodes disection  joint surgery • Radiation therapy • Invasion to intracranial or paranasal sinuses or far metastasizing – Palliative 844
  • 845.
    Squamous Cell Ca: Conjunctiva • 1-2 mm diameter of tumor 12 – 6-7 mm excision from macroscopic margin – 70 degree subzero cryotherapy • 2-5 mm diameter of tumor – If excision not available  Enucleation or f Excenteration • M More than 5 mm diameter of t th di t f tumor – Excenteration 845
  • 846.
    Sebaceous Adeno Ca • • • • Highlymalignant and potentially lethal tumor Tarsal plate  meibomian glands Eyelash  Glands of Zeis Or, Or sebaceous glands of caruncle eyebrow or caruncle, facial skins • Patient commonly older than 50 years of age American Academy of Ophthalmology 846
  • 847.
    Sebaceous Adeno Ca: Managements • Less than 1 mm diameter of tumor – wide excision f id i i from macroscopic margin  f i i frozen section ti • More than 1 mm diameter of tumor – Without regional lymphatic nodes involvement • Exenteration – With regional lymphatic nodes involvement • Exenteration • Lymphatic nodes disection  joint surgery • Radiation therapy • Invasion to intracranial or paranasal sinuses or far metastasizing – – – – Exenteration and joint surgery if possible Lymphatic nodes disection  joint surgery Radiation therapy py Palliative 847
  • 848.
    Malignant melanoma • 5%of cutaneous cancers • 1% of eyelid malignancies • Develop de novo or from preexisting melanocytic nevi or lentigo maligna • Four clinicopathologic forms – Lentigo maligna – Nodular – Superficial spreading – Acro-lentiginous Acro lentiginous American Academy of Ophthalmology 848
  • 849.
    Malignant melanoma :Managements • Localized – Incision biopsy – 6-7mm full thickness excision from macroscopic margin  frozen section • Invasion to the orbit – Without regional lymphatic nodes involvement • Exenteration • Radiation therapy • Cytostatic agent and immune therapy – With regional lymphatic nodes involvement • Exenteration • Lymphatic nodes disection  joint surgery • Cytostatic agent and immune therapy • Invasion to intracranial or paranasal sinuses or far metastasizing – – – – Exenteration and joint surgery if possible Lymphatic nodes disection  joint surgery y p j g y Cytostatic agent and immune therapy Palliative 849
  • 850.
    Epithelial tumors ofLacrimal gland • 50% of epithelial tumor  malignant p g • Types – Pleomorphic adenoma (Benign mixed tumor) – Malignant mixed tumor – Adenoid cystic carcinoma • Half of the carcinomas • Grow in tubules, solid nest or cribiform Swiss cheese pattern Swiss-cheese • Management – – – – – Percutaneous biopsy Permanent section Radical orbitectomy High dose radiation with surgical debulking Palliative Palliati e American Academy of Ophthalmology 850
  • 851.
    Secondary orbital tumor •Lung  40% in male • Breast  68 % in female • Leukemia – – – – Ocular involvement  80% Choroid is more often affected Also found in retina, optic disc and vitreous Retinal hemorrhages and pseudo Roth spots are common American Academy of Ophthalmology 851
  • 852.
    Thyroid orbitopathy :Classification Class Mnemonic Suggestion 0 N No physical signs or symptom 1 O Only signs 2 S Soft tissue involvement 3 P Proptosis o 3 mm o more op os s of or o e 4 E Extra ocular muscle involvement 5 C Corneal i C l involvement l t 6 S Sight loss (due to optic nerve) Werner, 1963 852
  • 853.
    Thyroid orbitopathy :Classification • Soft tissue involvement – 0 : Absent – A : Minimal – B : Moderate – C : Marked Werner, 1963 853
  • 854.
    Thyroid orbitopathy :Classification • Proptosis of 3 mm or more – 0 : Absent – A : 3 – 4 mm – B : 5 – 7 mm – C : 8 mm or more Werner, 1963 854
  • 855.
    Thyroid orbitopathy :Classification • Extra ocular muscle involvement – 0 : Absent – A : Limitation of motion at extremes of gaze – B : Evident restriction of motion – C : Fixation of globe g Werner, 1963 855
  • 856.
    Thyroid orbitopathy :Classification • Corneal involvement – 0 : Absent – A : Punctate lesions – B : Ulceration – C : Necrosis or perforation p Werner, 1963 856
  • 857.
    Thyroid orbitopathy :Classification • Sight loss (due to optic nerve) – 0 : Absent – A : 20/20 – 20/60 – B : 20/70 – 20/200 – C : Worse than 20/200 Werner, 1963 857
  • 858.
    Staging of Disease •Rundle’s Curve – Disease Activity – Active (Dynamic) Stage  Proptosis and Lid retraction – Static (Partial regression) Stage  Stable disease with littl i di ith little improvement t – Inactive (Burnt out) Stage  Spontaneous relative i l ti improvement t Sanjeev Y, 2010 858
  • 859.
    Disease Activity (EUGOGO) Proptosis Diplopia Neuropathy Mild 19-20mm Intermittent Subclinical Moderate 21 23 21-23 mm Inconstant 6/9 -6/12 6/12 Marked > 23 mm Constant (Primary) (P i ) 6/12 and worse • Severe disease – 1 Marked – 2 Moderate – 1 Moderate + 2 mild Sanjeev Y, 2010 859
  • 860.
    Auto antibodies Auto-antibodies • Anti-TSH.R •A tit id P Antityroid Peroxidase id Sanjeev Y, 2010 860
  • 861.
    Blow out fracture: Signs • Major signs – Enophthalmos – Diplopia – Hypoesthesia • Also – Positive forced duction test – Cloudiness and fluid level in the maxillary sinus 861
  • 862.
    Le Fort fractures • LeFort I – Low transverse maxillary fracture above the teeth – No orbital involvement • Le Fort II – Pyramidal configuration – Nasal, lacrimal and maxillary bones  medial orbital floor • Le F t L Fort III – Disjunction of craniofacial bones – Suspended only by soft tissues – Orbital floor, medial and lateral orbital walls are i bit l ll involved l d American Academy of Ophthalmology 862
  • 863.
    Painful ophthalmoplegia • Think Life saving first  Infection ?? – Orbital cellulitis • Tumor • Tolosa-Hunt-Syndrome – High dose steroids usually produce rapid and dramatic resolution 863
  • 864.
    Painful blind eye • • • • Think Life saving first  infection ?? Relieving the pain immediately Cryo-therapy ? Enucleation  Last choice that strongly to be avoided • Remember : – Incisional intra ocular surgery strictly contra indicated in blind eye and in eye with severe decreased vision. 864
  • 865.
  • 866.
    What is blindness? •WHO classification of visual impairment Criteria Normal Vision 6/6 to 6/18 Visual impairment (1) <6/18 to 6/60 Severe visual impairment (2) <6/60 to 3/60 Blind (3) Blind (4) Totally blind (5) < 3/60 Or Visual Field 5 10 5-10º 1/60 Or Visual Field < 5º No light perception 866
  • 867.
    Legal Blindness • Bestcorrected of visual acuity both eyes 20/200 or less (USA) • Or, Visual fields in both eyes of less than 10 degree centrally (USA) Deborah Pavan-Langston, 2008 867
  • 868.
    Decreased vision percentage Distancevision 20/20 20/25 20/40 20/50 20/80 20/100 20/160 20/200 20/400 Decrease (%) 0 5 15 25 40 50 70 80 90 Vaughan DG 868
  • 869.
    Decreased vision percentage Nearvision 1 2 3 6 7 11 14 Decrease (%) 0 0 10 50 60 85 95 Vaughan DG 869
  • 870.
    Trachoma • Initially Chronic follicular conjunctivitis • Marked on upper tarsal plate • Pannus – Usually pronounced on upper half of the cornea – Corneal infiltrates – Superficial vascularization • Art line – Transverse band of scar  Fine linear – Occurring on superior tarsal conjunctiva • Herber pits – Regression of the follicles formation – Locate at the limbus – Sharply defined depression at the base of the pannus American Academy of Ophthalmology 870
  • 871.
    Trachoma : WHO SIGN DEFINITION TF TrachomaFollicullar 5 or more follicles on superior tarsal conjunctiva TI Trachoma Intense Pronounced inflammatory thickening of the upper tarsal conjunctiva  obscures more than ½ the normal deep tarsal vessels TS Trachomatous T h t Scarring The presence of scarring in the tarsal conjunctiva TT Trachomatous Trichiasis At least one eyelash rubbing on the eyeball CO Corneal opacity Easily visible corneal opacity over the pupil American Academy of Ophthalmology 871
  • 872.
    Trachoma : MacCallan •Trachoma I – Immature follicles on upper tarsal plate – Including in central area – Without scarring • Trachoma II – Mature follicles on upper tarsus  necrotic or soft – Obscuring tarsal vessels – Still without scarring • Trachoma III – Follicle presents on tarsus – Definite scarring of the conjunctiva • Trachoma IV – No follicles on tarsal plate – Marked scarring of the conjunctiva 872
  • 873.
    Vitamin A deficiency Xerophthalmia(WHO 1996) • • • • • (XN) (X1A) (X1B) (X2) (X3A) • (X3B) • • (XS) (XF) : Nyctalopia : Conjungtival xerosis : Conjungtival xerosis + Bitot spot : Corneal xerosis : Keratomalacia or corneal ulceration with < 1/3 corneal involvement : Keratomalacia or corneal ulceration with > 1/3 corneal involvement : Corneal scar : Xerophthalmia fundus American Academy of Ophthalmology 873
  • 874.
    Fortified topical antibiotics •Fortified Tobramycin (or Gentamycin) – Inject 2 ml of 40mg/ml Tobramycin – Directly into a 5 ml – 0 3% Tobramycin 0.3% ophthalmic solution – This gives a 7 ml fortified Tobramycin  approximately 15 mg/ml – Refrigerate – Expires after 14 days Will’s Eye Manual, 2004 874
  • 875.
    Fortified topical antibiotics •Fortified Vancomycin – Add non preservative sterile water to 500 mg of Vancomycin dry powder to form 10 ml of solution – This provides a strength of 50 mg/ml solution – To achieve a 25 mg/ml solution  take 5 ml of 50 mg/ml solution – Add 5 ml sterile water – Refrigerate – Expires after 4 days Will’s Eye Manual, 2004 875
  • 876.
    Fortified topical antibiotics •Fortified Cefazolin – Add non preservative sterile water to 500 mg of Cefazolin dry powder to form 10 ml of solution – This provides a strength of 50 mg/ml solution – Refrigerate – Expires after 7 days Will’s Eye Manual, 2004 876
  • 877.
    Fortified topical antibiotics •Fortified Bacitracin – Add non preservative sterile water to 50,000 50 000 U of Bacitracin dry powder to form 5 ml of solution – This provides a strength of 10,000 U/ml solution – Refrigerate g – Expires after 7 days Will’s Eye Manual, 2004 877
  • 878.
    Intracameral Antibiotics • Glycopeptide –Vancomycin  Use Millipore powder filter • Cephalosporins – Cefuroxime – Cefazolin • Fluoroquinolones – Gatifloxacin – Moxifloxacin EyeWorld 2009 878
  • 879.
    Intravitreal antibiotics (/ 0 1 ml ) 0.1 • • • • • • Gentamycin G t i Vancomycin Amikacin Chlorampenicol Amphotericin B Ceftazidime Cefta idime 0.1 0 1 mg 1.0 mg 0.4 mg 1.0 mg 5.0 µg 2.0-2.25 2 0 2 25 mg American Academy of Ophthalmology 879
  • 883.
  • 884.
  • 885.
  • 886.
    Laser : Type •GAS ION LASERS - Argon, Krypton • SOLID STATE LASERS - R b C t l Nd YAG Ruby Crystal, Nd:YAG • LIQUID LASERS -D e Dye • DIODE LASERS 886
  • 887.
    Laser for Eye •Photocoagulation  Proteindenaturating processes – Argon Blue Green – Argon Green – Krypton Red – Diode – Tunable Dye – Frequency Doubled Nd:YAG –X Xenon Arc A 887
  • 888.
    Laser for Eye •Photodisruption  Cutting by optical break down  10,000° K – Q-switched Frequency Doubled Nd:YAG Laser 888
  • 889.
    Laser for Eye •Photodecomposition  Carving  C tti th molecular b d Cutting the l l bond – UV short wavelength – Excimer (Excited Dimmer) Laser 889
  • 890.
    Laser for Eye •Photoevaporation  Infra Red – CO2 Laser –H l i Holmium:YAG L YAG Laser Shorter Long Wavelength – Erbium:YAG Laser Laser 890
  • 891.
    MODERN LASERS • ContinuousWave ( CW ) p accurate selection of power & emission time • Efficiency - lower power and energy consumption - lower space consumption - lower cost - long term use 891
  • 892.
    The Lasers • • • • • integrepro multicolorlaser (ellex) PUREPOINT Laser (Alcon Inc) MicroPulse Fovea-Friendly Laser (IRIDEX) VISULAS 532s VITE (Carl-Zeiss) (Carl Zeiss) PASCAL (Pattern Scan Laser) Photocoagulator (OptiMedica, now: TopCon) • Novus Varia multicolor photocoagulator (Lumenis) • MC-500 Vixi Multi-Colour Laser (NIDEK) MC 500 Multi Colour • Vitra Multispot Laser (Quantel Medical) 892
  • 895.
    Laser on Retina Myteacher, my mentor, my friend: dr. dr Tjuk Suparjadi Sp M Suparjadi, Sp.M 895
  • 896.
    Laser on Retina: Photocoagulation • L Lenses – PRP Lens – Goldmann 3 mirror Lens • 59°, 67°, 73° –F Focal and G id L l d Grid Lens – +78 and +90 D Lens – PDT Lens 896
  • 897.
  • 898.
    LASER ON RETINA •GREEN LASER : 532 nm Produced by : - Gas ( Argon ) - Diode Pumped Solid State (DPSS) F Frequency doubled Nd YAG d bl d Nd:YAG 898
  • 899.
    LASER ON RETINA: Argon g • 514 nm and 532 nm wavelength • Clear media  safe and proven effective • Indications : – DR – Veins occlusions – CNV – Retinal breaks 899
  • 900.
    LASER ON RETINA: Dye Yellow • • • • • 577 nm wavelength Better than Argon for microaneurism Preferred for Coats disease Not acceptable in hemorrhage Macula  absorbed by haemoglobin, unabsorbed b M l b b db h l bi b b d by Xanthophil 900
  • 901.
    LASER ON RETINA: Krypton Red • • • • • • • 647 nm wavelength Less absorption by blood Hazy media Deep b D burns Less NFL damage Not preferable for Coats disease and Retinal angioma Indications : – – – – DR with vitreous hemorrhage Veins occlusions with vitreous hemorrhage Vitreoretinal tractions CNV  General Peripapillary, Near PMB with pre-retinal General, Peripapillary PMB, pre retinal membrane 901
  • 902.
    LASER ON RETINA: Diode • • • • • • 810 nm wavelength Deep burns Less NFL damage Less absorbed by blood Not preferable for Coats disease and Retinal angioma Indications : – – – – DR with vitreous hemorrhage Veins occlusions with vitreous hemorrhage Vitreoretinal tractions CNV  General, Peripapillary, Near PMB, with pre-retinal membrane b 902
  • 903.
    HOW to OPERATE •TECHNICAL SPECIFICATION p 1. Laser Specification 2. Electrical Requirement 3. Visualization - Slit Lamp - Aiming Beam - Laser Safety Eye Wear MPE = maximum permissible exposure 903
  • 904.
    How to selectthe mode • Type of Laser : Wavelength • Power : 0 3 - 1 7 W ( DPSS ) 0.3 1.7 0.5 - 4.0 W ( Gas ) • S t Size: 50 - 2000 um Spot Si • Exposure time : 0.01 - 4.0 s ( DPSS ) 0.01 - 1.0 s ( Gas ) • Pulse Interval : 0.1 - 1.0 s 904
  • 905.
    Nice to know •Xantophyl, Oxyhaemoglobin and Melanin • Indirectly mechanism • Exposure time : < 0 1 sec : mechanical effect 0.1 h i l ff t > 0.1 sec : thermal effect • Energy Density  inversely proportional to the focal spot size 905
  • 906.
    Applications • Diabetic retinopathy –Non-perfusion – Edema – Neovascularization • • • • • • Venous occlusion Retinal breaks Retinal degeneration Retinal vasculitis CSCR AMD • G id Grid • Focal • Pan retinal 906
  • 907.
    Applications : GridLPC • Grid Laser Photocoagulation • Macular application  500 µm up to 3000 µm from foveal center • Excluded  area of PMB • Grid Lens / +78 and +90 D Lens • Start at 100mW power  increments of 10-20mW • 50-100 µm spot size • 0.100 second or less duration • S t spaced at least one burns apart Spots d tl t b t • Supplemental treatment considered at least 3-4 month after initial coagulation  up to 300 µm 907
  • 908.
    Applications : FocalLPC Focal Laser Photocoagulation • • • • • Grid Lens / +78 and +90 D Lens Start at 100mW power  increments of 10-20mW 50-100 µm spot size 0.100 second or less duration Attempt to whiten or darken microaneurysms 908
  • 909.
    Applications : PRP Pan-RetinalPhotocoagulation / Scatter Laser Photocoagulation • • • • • • • • • NVD or / and NVE PRP Lens Start at 180mW power  increase gradually to achieve the end point 500 µm spot size 0.100 to 0.200 second duration 1800 total applications 1 – 1.5 burns width apart 3 sessions complete  10 days to weeks apart Usually, inferior half of retina coagulated first y, g 909
  • 910.
    Applications : Others • • • • • • • • ROP Retinoblastoma Coatsdisease Vitreolysis Retinal cavernosus hemangioma Choroidal hemangioma Optic Disc Pit – Maculopathy Idiopathic Juxtafoveal Retinal talengiectasis 910
  • 911.
    Chorioretinal burn intensity •Light – Barely visible retinal blanching • Mild – Faint white retinal burn • Moderate – Opaque, dirty white retinal burn • Heavy – Dense-white retinal burn 911
  • 912.
    Laser on Retina: PDT • • • • • Systemic administration Use photosensitizing drugs Followed b li ht application F ll d by light li ti Particular wavelength to affected tissue Incite a localized photochemical reaction 912
  • 913.
    Laser on Retina: PDT • CW beam  500 - 590 µm of low thermal energy laser • Extend at least 500 µm beyond lesion margin y g • 50 J/cm2 laser energy • 600 mW/cm2 dose rate • 15 minutes after start the infusions 913
  • 914.
    Laser on Retina: PDT • Liposome-encapsulated Benzoporphyrin  Verteporfin dye (Visudyne) – Maximum absorption  light near 689 nm wavelength • Others : – Tin Ethyl Etiopurpurin (SnET2, Purytin) – Lutetium (Lu-Tex) 914
  • 915.
    Laser on Retina: PDT • 30 ml Verteporfin via 10 minutes infusion pump injection, plus • 5 ml D5W injected simultaneously via Y tube • Filtered by 1.2 um filter to venflon catether into Cubiti vein 915
  • 916.
    Laser on Retina: TTT • Transpupillary Thermotherapy – Alt Alternative th ti therapy f S bf for Subfoveal CNV l – Rise intralession temperature of 4-9° C • • • • • Infra Red Diode laser 810 nm Within 72 hours of recent FFA Diode-coated Diode coated Volk QuadrAspheric Lens 0.8 mm, 1.2 mm, 2.0 mm, 3.0 mm spot size 200 – 600 mW power W 916
  • 919.
  • 920.
    A Tribute to Prof.dr. Ratna Kentjana, Sp.M(K) Prof. d MNE G P f dr. MNE. Gumansalangi, S M(K) l i Sp.M(K) 920
  • 921.
    ALT • Argon LaserTrabeculoplasty 921
  • 922.
    ALT : Aims •I Increase aqueous outflow tfl • By burning the trabecular meshwork • By applying a low energy of laser 922
  • 923.
    ALT : Mechanism •Absorption of laser by Pigmented TM • Produces thermal energy • Shrinkage of collagen of trabecular lamellae – Probably opens un intratrabecular space in untreated region – Trabecular tightening  pulling meshwork centrally  opens Schlemm’s canal • Attract phagocytes that clean up debris • Allows aqueous to flow better 923
  • 924.
    ALT : Preparations •CW Argon laser : – Bichromatic Blue-Green – Monochromatic Green • Krypton Red • Frequency doubled Nd:YAG laser q y • Diode – Lesser pain – Lesser PAS – Lesser disruption of Blood Aqueous Barrier • Gonio lens 924
  • 925.
    ALT : Protocol 1.Pre-Treatment ● Alpha-adrenergic antagonist (Apraclonidine 1%) and topical anesthetic 2. Treatment ● G i i Gonioprisms ● Focus aiming beam to target the entire height of TM ● 180° or 360° of TM can be photocoagulated in single or two sessions ● Goniolens rotated clockwise and make 25 burns for each 90° 3. Post-Treatment ● ● ● ● Alpha-adrenergic antagonist Topical steroid or NSAID for 3 to 5 days (optional) 1 hour IOP check after treatment Regular follow-up routine 925
  • 926.
    ALT : Indications • • • • POAG Exfoliationsyndrome Pigmentary glaucoma Glaucoma in aphakia and pseudophakia 926
  • 927.
    ALT : Contraindications • • • • • • Closedor Extremely narrow angle Corneal haze and diminished aqueous clarity Vitreous in anterior chamber Neovascular glaucoma Active uveitis Poor responsiveness glaucoma  Congenital glaucoma and Angle recession glaucoma 927
  • 928.
    ALT : Complications • • • • • • ElevatedIOP Progressive visual fi ld l P i i l field loss Iritis PAS Hemorrhage Corneal complications 928
  • 929.
    SLT • Selective LaserTrabeculoplasty 929
  • 930.
    SLT : Mechanism •Uses specific wavelength • Absorption of laser by Pigmented TM  selective t l ti targets  no d t damage on N Nonpigmented TM Non thermal • Produces Photothermolysis  Non-thermal • Trabecular tightening • Allows aqueous to flow better 930
  • 931.
    SLT : Preparations •532nm Wavelength Q-switched frequency doubled Nd:YAG laser (Neodymium: Yytrium-Aluminum-Garnet) • 63 635nm W Wavelength Di d l l h Diode laser • Goldmann, Thorpe or Latina lens (0° magnification) ifi ti ) 931
  • 932.
  • 933.
    SLT : Protocol 1.Pre-Treatment ● Alpha-adrenergic antagonist and topical anesthetic 2. Treatment ● G ld Goldmann, Th Thorpe or Latina lens (0° magnification) L ti l ifi ti ) ● Focus aiming beam to target the entire height of TM ● Set laser to 0.8 mJ (average) and then increase in 0.1 mJ steps until champagne bubbles appear approximately 50%-70% of the time 50% 70% ● Approximately 50 shots are placed onto the TM in the same pattern as ALT 3. Post-Treatment 3 P T ● ● ● ● Alpha-adrenergic antagonist Topical steroid or NSAID for 3 to 5 days (optional) 1 hour IOP check after treatment Regular follow-up routine 933
  • 934.
    SLT is notALT Spot size comparison: ALT 50µm SLT 400µm ALT SLT ALT SLT 50 micron SPOT SIZE 400 micron 500 – 1,000 mW 720 – 1,200 mW ENERGY OUTPUT 0.8 – 1.5 mJ 10 ms PULSE DURATION 3 ns 60,000 mJ/cm2 FLUENCE 600 mJ/cm2 934
  • 935.
    SLT is notALT The SLT technique is much less traumatic to the eye than ALT ALT, and evokes a gentle response of the auto-immune system to begin clearing the TM without the coagulative damage of ALT. TM tissue after ALT TM tissue after SLT 935
  • 936.
    SLT : Processes SLTis a non-thermal treatment which uses short pulses of relatively low energy 532nm light to target and irradiate only the melanin-rich cells in the trabecular meshwork (TM); the laser pulses affect only these melanin-containing cells, and the surrounding structure of the TM is unaffected. During the procedure approximately 50 confluent spots are applied along the meshwork in order to treat a 180° angle. Animation 936
  • 937.
    1. SLT isselective SLT selectively targets only the melanin-rich cells of the trabecular meshwork. 2. SLT is non-thermal The short pulse duration of SLT is below the thermal relaxation time of the TM tissue, thereby eliminating the incidence of thermal damage. 3. SLT is repeatable SLT treatment can be repeated without causing harm or further p complications. 937
  • 938.
    SLT : Indications OpenAngle Glaucoma • • • • POAG OHT Pigmentary Glaucoma Pseudo-exfoliative glaucoma Poorly compliant to drug therapy Intolerant or unresponsive to drug therapy I l i d h Failed ALT (either 180˚ or 360˚) Inflammatory glaucoma Patients currently undergoing drug therapy who wish to use SLT in conjunction with glaucoma medications 938
  • 939.
    SLT represents awhole new approach to managing open-angle glaucoma Compliance issues minimized Gentle, non-invasive treatment SLT does not cause thermal damage of the trabecular meshwork No systemic side effects SLT can be used in conjunction with medicine to enhance the overall IOP lowering effect IOP-lowering Non-penetrating glaucoma surgery is not compromised as with ALT The latest in ‘Primary Glaucoma Therapy Primary Therapy’ 939
  • 940.
    ALPI • Argon LaserPeripheral Iridoplasty 940
  • 941.
    ALPI : Aims • • • • • Laserenergy placed near iris root Separate Iris from TM S t Ii f For PACG Reopening of closed angle Widening of narrow angle 941
  • 942.
    ALPI : Preparations •532nm Wavelength Q-switched frequency doubled Nd:YAG laser (Neodymium: Yytrium-Aluminum-Garnet) • Ab h Abraham contact lens +55 to +66 D l 66 942
  • 943.
    ALPI : Indications •Plateau iris syndrome • Unbreakable attack of angle close glaucoma  laser iridotomy not possible • Phacomorphic glaucoma • Adjunct to laser trabeculoplasty • R t ti peripheral i i stuck Retracting i h l iris t k • Rare case of nanophthalmos 943
  • 944.
    ALPI : Contraindications • • • • Advancedcorneal edema / opacity Flat anterior chamber Extensive PAS Creeping angle glaucoma  not effective ALPI : Complications • • • • Iritis Corneal endothelial burns Hemorrhage Transient IOP rise 944
  • 945.
    Nd:YAG Laser Iridotomy •R li Relieve th pupillary bl k the ill block • 532nm Wavelength Q-switched frequency doubled Nd:YAG laser (Neodymium: Yytrium-Aluminum-Garnet) • Abraham contact lens +55 to +66 D 945
  • 946.
    Nd:YAG Laser Iridotomy •Indications : – PACG : • A t / Sub acute angle closure Acute S b t l l • Creeping angle closure – Fellow eye of ACG – Non-pupillary block angle closure • Plateau iris • Forward lens position – Narrow or closed angle 946
  • 947.
    Nd:YAG Laser Iridotomy y •Complications : – – – – – – – – – Corneal epithelial / endothelial burns Iritis Pigment dispersion Hemorrhages g Lens opacities Retinal burns Raised IOP Posterior synechiae Monocular di l i M l diplopia 947
  • 948.
    Laser for Glaucomaand Others • • • • • Nd:YAG Laser C Nd YAG L Capsulotomy l Diode Laser Cyclophotocoagulation Endoscopic Cyclo Photo Coagulation Nd:YAG Laser Iridolenticular Synechiolysis Cyclophotocoagulation – – – – • Transpupillary CP Endo CP Nd:YAG Trans-scleral CP  Contact and Non-contact Diode laser CP (DLCP) Excimer Laser Trabeculotomy (ELT) – 308 nm X Cl l XeCl laser, power 35 55 mJ/mms spot size 200 um, d ti 10 35-55 J/ t i duration sec, freq 20Hz • Excimer Laser Assisted Deep Sclerotomy – Argon Fluoride XL 193 nm at 180 mJ x sq cm fluence g q 948
  • 949.
    Laser for RefractiveSurgery • • • • • • PRK LASIK Epi LASIK SBK LASEK LaserACE 949
  • 950.
    LASIK : Woodcarving • W dC Wood Cornea • Equipment  Laser • Carver  Ophthalmologist 950
  • 951.
    Argon Fluorine (ArF) • • • • • • 193nm Above th h ld t b k molecular b d Ab threshold to break l l bond Ablative photodecomposition Neighboring tissue <10º C (Cold laser) Minimal collateral damage Maximal accuracy & precision 951
  • 952.
    Solid State UV213 • • • • • 213 nm DPSS Nd YAG P l Nd:YAG Pulzar 21 (C t Vi ) (CustomVisc) Less absorbed by neighboring tissue Much better penetrating Less sensitive to environmental factor 952
  • 953.
    Solid State UV210 • • • • • 210 nm DPSS L LaserSoft (K t S ft (Katana T h l i ) Technologies) Less inflammations Less pain Faster visual recovery 953
  • 954.
    Lasik • Pre Lasik –General Examination – Mapping  Topography and pachymetry, Aberration measurement and collecting data – Making algorithm for laser treatment • Durante – Flapping  Micokeratome or Femtosecond – Eye-tracked Laser treatment – Recovery management • Post Lasik 954
  • 955.
    Corneal Topography, Corneal Pachymetryand Aberrometry System 955
  • 956.
    Femto and ExcimerLaser System 956
  • 957.
    Pre Lasik • Topography- Keratometry • Ab Aberrometry t 957
  • 958.
    Topography 3 types – Placido-basedsystems Placido– Elevation-based systems Elevation– Interferometric system y Bausch and Lomb 958
  • 959.
    Topography Provide topography ofthe cornea, like a map Bausch and Lomb 959
  • 960.
    ORBSCAN II z Combinationof : • Placido based-system • Scanning slit imaging (elevation based system) Bausch and Lomb 960
  • 961.
    Reflective and Slit-ScanTechnologies • • • One image, one surface. Angle-dependent specular A l d d t l reflection. Measures slope (as a function of distance). f ti f di t ) • • • Multiple images, multiple surfaces Omni-directional diffuse backscatter Triangulates elevation Ti l t l ti The overwhelming advantage Placido reflective systems is that they can measure curvature curvature. Bausch and Lomb 961
  • 962.
    How corneal shaperelates to shape factor 962
  • 963.
    LASIK  Fitthe cornea Data surface (cornea) Fit-zone Reference surface (Best Fit Sphere) ( p ) Bausch and Lomb 963
  • 964.
    3D Corneal Topography BFS BFS: Reference surface (Best Fit Sphere) Bausch and Lomb 964
  • 965.
    Major points • • • • • Anterior Elevation PosteriorElevation Pachymetry Thickness Keratometry - Surface Curvature Statistics and Data • • • • • • • • Sim K Steep and Flat Axis White to White Pupil diameter Thinnest point Anterior Chamber Depth (ACD) Angle Kappa g pp Kappa Intercept Bausch and Lomb 965
  • 966.
    Anterior Elevation Map CurvatureM C Map Posterior Elevation Map Statistics d D S i i and Data Pachymetry Map P h M Bausch and Lomb 966
  • 967.
    Elevation (f El ti (froma reference surface) f f ) Max Red • High • Anterior to the reference surface (+) reference f (-) level l l • Low • Posterior to the reference surface Min Blue Bausch and Lomb 967
  • 968.
    Elevation Map Reading •Warmer colors are above “sea level” sea level • G Green i “ is “sea l level” ( t h with a l” (match ith sphere that best matches the cornea) • Cooler colors are below “sea level” • Both Anterior and Posterior are read in the same way y Bausch and Lomb 968
  • 969.
    Eye #1 Highest Point LowestPoint Bausch and Lomb 969
  • 970.
    Eye #1 Highest Point LowestPoint Bausch and Lomb 970
  • 971.
    Pachymetry Maps • Warmercolors are THINNER • Cooler colors are THICKER Pre-Op Pre Op eyes are usually thinnest in the temporal and inferior quadrant Bausch and Lomb 971
  • 972.
    Thickness Min Red (+) • Thin (+ +) •Thi k Thick Max Blue Bausch and Lomb 972
  • 973.
  • 974.
    Pachymetry map y y p • Thinnestpoint  obtain from data sheet Bausch and Lomb 974
  • 975.
    Pachymetry map • Orbscanpachymetry measurements  5% to 8% more compared to ultrasonic – Orbscan measures from epithelium to endothelium – Ultrasonic pachymetry : Stroma Bausch and Lomb 975
  • 976.
    High and Lowis not always directly related to Steep and Flat High Tissue is usually flatter, but not always g y , y Low Tissue is usually steeper, but not always Color coded in elevation map >< curvature map (keratometric) Ablation requires Elevation Data because tissue that needs to be removed is high Bausch and Lomb 976
  • 977.
    Color-coded scales Colors : –Warm (red, orange, yellow) for steeper portions of cornea – Green denotes intermediate portions – Cool (blue, dark blue) depict flatter portions Bausch and Lomb 977
  • 978.
    Surface Curvature S rfaceC r at re (+ +) Max Red • Sharp • Fast bend • Short radius • Flat • Slow bend • Long radius (+) Min Blue Bausch and Lomb 978
  • 979.
  • 980.
    Orbscan topography priorto refractive surgery • • • • • • • • • • • Ultrasound pachimetry > 475 µm Residual bed thickness (RBT) > 250 - 300 µm Posterior elevation < 50 µm Posterior bed fit sphere < 50 D Anterior/Posterior Radii-Ratio 1.21 – 1.27 Irregularity (3mm) < 1.5 D Irregularity (5mm) < 2 0 D 2.0 Peripheral-Central Pachimetry < 20 µm SimK (Max) < 47 D Astigmatism variance between eyes < 1.0 D Symetric bowtie EyeWorld 2009; Joo CK 2009 980
  • 981.
  • 982.
    Keratoconus Refractive surgery makesearly diagnosis of corneal abnormalities more important Bausch and Lomb 982
  • 983.
    Close-Fitting Reference Surfaces Topographicmaps of terrestrial landscapes are displayed in the form of constant-elevation contours, measured from the “mean sea level” of the earth. mean sea-level earth Data surface (cornea) Reference surface (sphere) Corneal topography differs from terrestrial topography in that the reference surface is not some fixed “mean sealevel”, but is movable. Bausch and Lomb 983
  • 984.
    Close-Fitting Reference Surfaces Forth F the cornea, a reference surface (typically, a sphere) i f f (t i ll h ) is constructed by fitting the reference surface as close as p possible to the data surface. Data surface (cornea) Fit-zone Reference surface (sphere) A best-fit minimizes the square difference (always a p positive number) between the two surfaces, but only within ) , y a specified region known as the fit-zone. Bausch and Lomb 984
  • 985.
    Elevation Topology: CentralHill Bausch and Lomb Sharp center Flat periphery The normal cornea is prolate meaning that meridional curvature prolate, decreases from center to periphery. Prolateness of the normal cornea causes it to rise centrally above the reference sphere. The result is a central hill. f h Th lt i t l Immediately surrounding the central hill is an annular sea where the cornea dips below the reference surface. In the far periphery, the prolate cornea again rises above the reference surface, producing peripheral highlands. 985
  • 986.
    Elevation Distortion Bausch andL b B h d Lomb Spherical reference surface Post Lasik profile Relative elevation p profile As an example of distortion, consider the corneal surface following p g myopic lasik correction. It is centrally flattened by the surgery. To see surface features, elevation must be measured with respect to some reference surface. This relative elevation peak is NOT the highest point on the cornea. This apparent central "concavity" does NOT exist. 986
  • 987.
    Normal Post LASIKAnterior Elevation Bausch and Lomb Lower in the Center - OD Lower in the Center - OS 987
  • 988.
    Elevation (sphere) Elevation (sphere) Theseare pre-op (left) and post-op (right) elevation maps of a myopic with-the-rule astigmatic eye corrected with LASIK. y p g y The post-operative central “sea” is not a concavity but a central flattening. The ring of relatively highest terrain is not absolutely higher (more anterior) than the “sea” bottom near the map center. 988
  • 989.
    Abnormal Post LASIKPosterior Elevation Bausch and Lomb Abnormally High but High & De centered - Poor Vision De-centered Centered - Moderately Good Vision • Diplopia at night 989
  • 990.
    Normal Band Scale Bauschand Lomb Accentuates anomalies 990 Filters small irregularities
  • 991.
    Normal B dS l N l Band Scale • Elevation Maps (Anterior & Posterior) – + 0.25 microns of Best Fit Sphere • Total Cornea Power – 40 to 48 Diopter • Pachymetry – 500 to 600 microns Bausch and Lomb 991
  • 992.
    Posterior Keratoconus The normalband scale on the left indicates very small changes on the anterior corneal surface and a relatively small area of corneal steepening above 48 D. These findings are indicative of milder disease than the contra-lateral contra lateral eye but probably represents an earlier forme fruste of keratoconus. Bausch and Lomb 992
  • 993.
    The CRS-Master How dyou plan your t t H do l treatments ? t Wavefront Patient Data Microkeratome Refraction Corneal C C l Curvature t Pachymetry • Modern refractive excimer surgery is based on a complex data set • I must take into account not only wavefront data, b all It k i l f d but ll relevant parameters of each individual patient. Bausch and Lomb 993
  • 994.
    Aberrometry • Collecting aberrationdata • Make algorithm for laser treatment • Minimizing aberration post surgery Bausch and Lomb 994
  • 995.
    Aberration : Category •Two categories of aberrations commonly are used to describe vision errors, including: – Lower-order aberrations consist primarily of nearsightedness and farsightedness (defocus), as well as astigmatism. They make up about 85 percent of all aberrations in an eye. – Higher-order aberrations comprise many varieties of aberrations. Some of them have names such as coma, trefoil p , y and spherical aberration, but many more of them are identified only by mathematical expressions (Zernike polynomials). They make up about 15 percent of the total number of aberrations in an eye. • Order refers to the complexity of the shape of the wavefront emerging through the pupil — the more complex the shape the higher the order of aberration shape, aberration. Vessel M, 2008 995
  • 996.
    Aberration : WhatExactly y • A higher-order aberration is a distortion acquired by a wavefront of light when it passes through an eye with irregularities of it refractive components (t i l iti f its f ti t (tear fil film, cornea, aqueous humor, crystalline lens and vitreous body • Abnormal curvature of the cornea and crystalline lens may contribute to the distortion acquired by a wavefront of light. • Serious higher order aberrations also can occur from higher-order scarring of the cornea from eye surgery, trauma or disease. • Cataract clouding the eye's natural lens also can cause eye s higher-order aberrations. Aberrations also may result when dry eye diminishes your eye's tear film, which p g y helps bend or refract light rays to achieve focus Vessel M, 2008 996
  • 997.
    Aberration : Howto diagnose • • • • Higher-order aberrations are identified by the types of distortions acquired by a wavefront of light as it passes through your eye. Because light travels in bundles of rays a common way of rays, describing an individual wavefront involves picturing a bundle of light rays. The tip of each light ray in the bundle has its own point. We create the wavefront or wavefront map by drawing lines perpendicular to each point point. The shape of a wavefront passing through a theoretically perfect eye with no aberrations is a flat plane known, for reference, as piston (see next chart). The measure of difference between the actual wavefront shape and the ideal flat shape represents the amount of aberration in the wavefront. Because no eye is absolutely perfect (emmetropic), a wavefront passing through an eye acquires certain three-dimensional, distorted shapes. S f more th 60 diff h So far, than different shapes, or aberrations, h t h b ti have been identified. Significant amounts of aberrations can pose vision problems y y y because they interfere with the eye's ability to see clear and distinct images (focus). Vessel M, 2008 997
  • 998.
    Aberration : Visualquality • The impact of higher-order aberrations on vision quality depends on various factors, including the underlying cause of the aberration. • People with larger pupil sizes generally may have more problems with vision symptoms caused by higher-order aberrations, particularly in low lighting conditions when the pupil opens even wider. il id • But even people with small or moderate pupils can have significant vision problems when higher-order aberrations are caused by conditions such as scarring of the eye's surface eye s (cornea) or cataracts that cloud the eye's natural lens. • Also, specific types and orientation of higher-order aberrations have been found in some studies to affect vision quality of q y eyes with smaller pupils. • Large amounts of certain higher-order aberrations can have a severe, even disabling, impact on vision quality. Vessel M, 2008 998
  • 999.
    Aberration : Symptoms •An eye usually has several different higher-order aberrations i t hi h d b ti interacting ti together. • Th f Therefore, a correlation between a l ti b t particular higher-order aberration and a specific symptom cannot easily be drawn drawn. • Nevertheless, higher-order aberrations are generally associated with double vision vision, blurriness, ghosts, halos, starbursts, loss of contrast and poor night vision vision. Vessel M, 2008 999
  • 1000.
    TERMS OF WAVEFRONT SO O Aberrometry Provideinformation, h P id i f i how b d the bad h Aberrations of the rays inside the eye gy  Wavefront technology 1000
  • 1001.
    What is Wavefront? •Wavefront Technology is the latest generation of laser vision correction. • Light travels in a flat uniform beam. • When there is nothing disturbing it, such as light going through space, it is perfectly flat without error. • This pattern of a straight beam of light is called a wavefront. • As light g g goes through objects, the light beam becomes g j , g distorted or becomes more like a wave. • When light enters the eye, the light rays become distorted because of the many components of the eyes optical system. • Some of these components include the cornea, lens and aqueous fluid, although the greatest amount of distortion occurs when light enters th h li ht t through th cornea. h the 1001
  • 1002.
    What is Wavefront? Perfectbeam Imperfect beam p Wavefront E e Wa efront in Eye 1002
  • 1003.
    How does WavefrontWork? • As the light rays touch the retina, the Wavefront Analyzer measures the amount of distortion that has occurred prior to the light entering the eye and after going through the eye. • As with the diagram the simulation grid would be diagram, considered the ideal or perfect optical grid. • This grid is projected on to the back of the eye and is measured. measured • The measurement is compared to the original grid producing what is called a wavefront map. • This wavefront map calculates the specific aberrations of the cornea precisely measuring each section of the cornea to provide the most accurate p and detailed information about our vision. 1003
  • 1004.
    How does WavefrontWork? • Once the information is collected, it is , transferred to the laser. • The laser then does a customized treatment that is i specific to the patient and i not b ifi h i d is based on d general guidelines of treatment. • No two wavefront maps are identical therefore a identical, customized treatment is specific to that patient, enhancing the opportunity for superior quality of vision, reduced or eliminated night vision and improved uncorrected visual acuity. 1004
  • 1005.
    Why wavefront technology? To reshape corneal surface to compensate for optical t f ti l aberrations Real eye: rays do not intersect retina Ideal eye: all rays intersect in image plane Determine actual shape p of wavefront Bausch and Lomb retina 1005
  • 1006.
    Wavefront methods • Hartman-Shack •Tscherning • Optical Path Difference (OPD) Scan Deborah Pavan-Langston, 2008 1006
  • 1007.
    Measurements & Terminology • • • • • • Zernikepolynomials Point S P i t Spread F d Function (PSF) ti Root Mean Square (RMS) Strehl Ratio Diffraction Convolution Bausch and Lomb 1007
  • 1008.
    Zernike polynomials • Prof.Frits Zernike Groningen, Holland Awarded Nobel prize in Physics 1953 • The complex shape of wavefront is approximated by a sum of function to give a special geometrical mode ti l d Bausch and Lomb 1008
  • 1009.
  • 1010.
  • 1011.
  • 1012.
    3 common higherorder aberrations g most patients suffer from 3rd 3rd 4th Bausch and Lomb 1012
  • 1013.
    Aberrations of theeye Bausch and Lomb 1013
  • 1014.
    Aberrations of theeye Bausch and Lomb 1014
  • 1015.
    Understanding Aberrations Second Order Myopia Cylinder BowlShape Saddle Shape Third Order Fourth Order Coma Trifoil Sph Aber Bump & Dip Napoleon’s Hat Sombrero Plant Stand 1015 Bausch and Lomb Quadrafoil
  • 1016.
    Understanding Aberrations g Coma (3rdorder) ( ) Spherical Aberration (4th order) Bausch and Lomb 1016
  • 1017.
    Point Spread Function(PSF) Normal eye Monocular Diplopia Bausch and Lomb 1017
  • 1018.
    Point Spread Function(PSF) Bausch and Lomb 1018
  • 1019.
    Root Mean Square(RMS) • Single value • Measure the magnitude of a set of number • Example : – Set of no : -2 +5 -6 +4 -1 – Average = 0  not informative – We want to know the variation, disregard the signs  average = 3.6 g g Bausch and Lomb 1019
  • 1020.
    Root Mean Square(RMS) Another way to know the variation : 1. Square all values 2. 2 Take average of the squares 3. Square root of average Smaller RMS = Less aberrations General agreement : RMS < 0.38 plano LASIK Bausch and Lomb 1020
  • 1021.
    Strehl Ratio • Ametric calculated from : Actual A t l peak PSF k Diffraction-limited peak PSF Results closer to 1  less aberration Bausch and Lomb 1021
  • 1022.
    Strehl ration H eye Strehlratio  H dl Diffraction limited PSF Aberration free H dl Actual PSF with aberrations Bausch and Lomb H eye 1022
  • 1023.
    Diffraction • Diffraction causeslight to bend perpendicular to the direction of the diffracting edge • Spreading of light waves as they p p g g y pass through a g small opening. (Christiaan Huygens, 1678) • Cause the light imaged not as a single sharp g g g p point  AIRY DISK • Smaller apertures generates more diffraction Bausch and Lomb 1023
  • 1024.
    Convolution • Method toportray blur, using PSF in every p p y , g y point of object to stimulate retinal image Bausch and Lomb 1024
  • 1025.
    Wavefront Analyzers • • • • • Zywave (Bausch& Lomb Incorporated) ( ) CRS Master (Carl Zeiss Meditec AG) WaveScan (Abbott Medical Optics) g p y (WaveLight, Alcon) g ) Allegro Topolyzer Vario ( MAXWELL (Ziemer) 1025
  • 1026.
    Glare • Glare canbe described as “extreme brightness” from the presence of excessive visible light. • Glare can be distracting and even dangerous and can occur day or night in a number of ways. • Gl Glare can cause you to squint, resulting i eye t i t lti in strain and eye fatigue. In extreme cases, glare can even result in temporary blindness blindness. 1026
  • 1027.
    • Distracting glare –Distracting glare can be caused by car headlights or streetlights at night. – It can also be as simple as light being reflected off the front of your lenses making it difficult for others to see your eyes. ff f – Similarly, it may be from light reflected off the back – or inside – of your lenses so that you see the distracting reflection of your own eyes of objects behind you in your forward field of vision. – As a result, this kind of glare may cause eye fatigue, annoyance and distraction. 1027
  • 1028.
    • Discomforting glare –Glare can be caused by everyday, normal sunlight conditions. – D Depending upon one’s li ht sensitivity, thi glare can di ’ light iti it this l be discomforting regardless of weather or time of day. – It can be present in any level or intensity of light, or when moving from one lighting condition to another. – Discomforting glare often causes squinting and eye fatigue 1028
  • 1029.
    • Disabling glare –Straylight – This type of glare comes from excessive, intense light that can occur when you face directly into the sun. – Disabling glare can block vision because the intense light can g y g cause significantly reduced contrast of the retinal image. – The latent effects can last well beyond the time of exposure. – It can occur by light scattering from IOL edge, glistenings or calcifications. calcifications 1029
  • 1030.
    • Blinding orreflected glare – This comes from light reflected off smooth, shiny g , y surfaces such as water, sand or snow. – It can be strong enough to block vision. – Reflected light is polarized and requires polarized lenses to reduce it optimally. 1030
  • 1031.
    All being measuredto make an an… Eye of the Thief Eye of the Eagle 1031
  • 1032.
    Another Pre-LASIK examination PreLASIK • Understand the Cornea  Measuring the biomechanical g properties of the cornea • Is to quantify various corneal conditions by means of a measurable and repeatable metric. • Low Corneal Hysteresis (CH) demonstrates that the cornea is less capable of absorbing (damping) the energy of the air pulse. pulse • The differences in CH between normal and compromised corneas are highly evident, and lead some experts to theorize that normal eyes exhibiting t t th i th t l hibiti significantly lower than average CH may be at risk of developing corneal disorders in the future. 1032
  • 1033.
    How does itwork? • The Ocular Response Analyzer utilizes a rapid air impulse, and an advanced electro-optical system to record two applanation pressure d l i measurements; one while the cornea is moving inward, inward and the other as the cornea returns returns. • Due to its biomechanical properties, the cornea resists the dynamic air puff causing delays in the inward and outward applanation events, resulting in two different pressure values 1033
  • 1034.
    How does itwork? • The average of these two p g pressure values provides a repeatable, Goldmann-correlated IOP measurement (IOPG). • Th difference b The diff between these two pressure h values is Corneal Hysteresis (CH); a new measurement of corneal tissue properties that is a result of viscous damping in the corneal tissue. • The ability to measure this effect is the key to understanding the biomechanical properties of the cornea. 1034
  • 1035.
    How does itwork? Ocular Response Analyzer (Reichert) 1035
  • 1036.
    How does itwork? • The CH measurement also provides a basis for two additional new parameters: CornealCompensated Intraocular Pressure (IOPCC) and Corneal Resistance Factor (CRF). IOPCC is an Intraocular Pressure measurement that is less affected by corneal properties than other ff t d b l ti th th methods of tonometry, such as Goldmann (GAT). (GAT) CRF appears to be an indicator of the overall “resistance” of the cornea 1036
  • 1037.
    Standard vs CustomizedLASIK STANDARD CUSTOMIZED • No data necessary y • Correct defocus only (Sphere & Astigmatism) y () • Contrast sensitivity (-) • Use aberration data • Correct both defocus and High order aberration • Contrast sensitivity (++) 1037
  • 1038.
    Aberrometer Zywave Complete WavefrontAnalysis Zylink  Generation of optimized Laser Treatment OrbScan IIz Corneal architecture Laser System 1038
  • 1039.
    Eye registration The integratedprocedure • Ease of Use: Fully automated imaging with online data quality check WASCA WASCA MEL 80 Wavefront Acquisition Reference Image Surgical Image 1039
  • 1040.
    Microkeratomes • • • • • • Hansatome (Bausch &Lomb) Moria Evolution 3E (Moria) Gebauer SL (Gebauer Medizin) G b (G b M di i ) Zyopic XP (Bausch & Lomb) ML7 (Med Logics Inc) (Med-Logics, Amadeus II (AMO, Inc  Ziemer) • Make ‘Hinged Flap’ • Take 110 – 180 um corneal thickness 1040
  • 1041.
  • 1042.
    Some kind ofolder microkeratomes : A Hansatome (Ba sch & Lomb); A. (Bausch Lomb) B. LSK-one (Moria); C. Amadeus (Abbott Medical Optics); D. MK-2000 (Nidek) 1042
  • 1043.
  • 1044.
    Femtosecond Laser • Afemtosecond is one millionth of a nanosecond or 10-15 of a second and is a measurement used in laser technology • Procedure of laser corneal flap making – Increased accuracy and predictability for corneal flap thickness – Faster – Better visual outcomes 1044
  • 1045.
    Femtosecond Laser • Range ofuses – Flap creation  • • • • • IntraLase FS (Abbott Medical Optics) CUSTOMFLAP TECHNOLAS (Perfect Vision) FEMTO LDV CrystalLine(Ziemer) VisuMax (Carl Zeiss Meditec AG) WaveLight FS200 (Alcon Inc) g ( ) – Presbyopia surgery  INTRACOR TECHNOLAS (Perfect Vision) – CUSTOMSHAPE TECHNOLAS (Perfect Vision) • • • • • • Astigmatic Keratotomy (AK) Limbal Relaxing Incisions (LRIs) Penetrating and Lamellar Keratoplasty (PK/LK) Endothelial Keratoplasty (FL-EK) Intrastromal segment insertion  ring implantation (ICRS) Cross-linking – Even for glaucoma patient and Cataract surgery 1045
  • 1046.
    Femtosecond Laser • Pulseof energy – Low  Less than 1 µJ – High  1 µJ and above • Pulse of frequency – Low  Bellow 80 kHz – High  Above 100 kHz 1046
  • 1047.
    Femtosecond Laser • Highpulse energy and Low pulse frequency – IntraLase FS (Abbott Medical Optics) – TECHNOLAS (Perfect Vision) • Low pulse energy and High pulse q y frequency – FEMTO LDV CrystalLine(Ziemer) – VisuMax (Carl Zeiss Meditec AG) su a (Ca e ss ed tec G) 1047
  • 1048.
    Femtosecond : TheIntraLase FS The IntraLase laser produces tiny bubbles to be able to lift up the surface of the cornea The ability to precisely place the bubbles up to the edge of cornea enables an exact preparation of the flap The corneal flap is opened up in order to treat the deeper layers of cornea f EuroEyes, 2008 1048
  • 1049.
    Another “Flaps” Flaps • HingedFlap  – Lasik – Epi-Lasik  Epi-K (Moria) – SBK  One Use-Plus SBK (Moria) • Smaller flap diameter  8 5 mm 8.5 • 100-115 microns flap thickness • 50% fewer fibers being cut than a 150 microns flap • Epithelial Scrubber  PRK – Amoils Epithelial Scrubber 1049
  • 1050.
  • 1051.
    Decentered ablations :Causes • • • • • • • Saccadic eye movements Improper head alignment Cyclotorsion Pupil shift p Centroid shift Eye rolling Technical misalignment of the laser beam 1051
  • 1052.
  • 1053.
    Cyclotorsion • • • • Eye rotates 3.7°+ 2.3° y Some until 9.1° 60% counter clockwise counter-clockwise 40% clockwise 1053
  • 1054.
  • 1055.
    JUST FOR YOUAND SAFETY Iris structure i finger print fi i •Safe S f •Compensate pupil center shift & cyclotorsion 1055
  • 1056.
    SAFETY • Adapted formedical use from military technology utilized for high l tili d f hi h level security control l it t l 1 out of 3,493..E24 or 1 out of 3 493 000 000 000 000 000 000 000 t f 3.493.000.000.000.000.000.000.000 There are not more than 10.000.000.000 people or 20.000.000.000 20 000 000 000 eyes on earth th 1056
  • 1057.
    Eyetracker : Ability y y •Not all eyetrackers are created equally. • The new generation e etracker has a sampling rate ne eyetracker faster than 200 Hertz. • The reason why this is so important is because your eye can twitch at a rate of 60 Hz Hz. • If the eye twitches faster or at the same speed as the eyetracker then the eyetracker may not be able to get the appropriate readings of the movement of the eye eye. • In turn, the laser may not be able to place the right pulse of the laser in the appropriate section of the cornea because of the lack of information. information • What is also extremely important is the ability of the laser to react to the information being sent to it from the eyetracker. eyetracker 1057
  • 1058.
    Eyetracker : Ability y y •What is also extremely important is the ability of the laser to react to the information being sent to it from the eyetracker. t k • The response time of the laser must be very fast to ensure that each laser pulse is placed exactly on the appropriate part of the cornea cornea. • Even if the laser can sample the movement of the eye 1000 times but the laser reacts slowly to this information, the result is that the laser may be placing pulses on areas of the cornea based on old information. • The best example of the relationship between the eyetracker and the laser is to try and imagine throwing a ball at a moving object that is going 200 miles an hour. • Although we can see the moving object, our reflexes are too slow to adjust to the constant changes of the moving object. 1058
  • 1059.
    Eyetracker : Ability •As a result, every time you throw the ball you are , y y y missing the moving object. Slow or older lasers work on the same principle. • Al h Although the eyetracker can see the eye h h k h moving, it is too slow to react and may miss the targeted area of the cornea cornea. • Eyetracker with the ability to react between 4 to 8 ms  optimizes the ability of each pulse being placed on the appropriate spot on the cornea reducing erroneous misplaced pulses of the laser more common on older laser technology 1059
  • 1060.
  • 1061.
    Laser ablation • • • • Extremely pec se ab a o s e e y precise ablations Disrupting molecular bonds Vaporising material Without generating heat 1061
  • 1062.
    ArF Laser (Photoablation) •Laser energy ArF = 6.0 eV • Tissue inter-molecular bond = 3.5 eV • Ablation  Cut the bond Laser 6.0 eV 3.5 eV 1062
  • 1063.
  • 1064.
  • 1065.
    Beam Size andProfile • A small diameter laser beam or also known as spot p size is very important for both accuracy and smoothness. • An ideal beam size is approximately 1mm or less. less • If the size of the laser beam is larger the result is that the beam is too large to make fine adjustments throughout the cornea. • Imagine filling a fishbowl with marbles compared to filling is with sand. • The marbles allow gaps while the sand contours and fills the fishbowl exactly. 1065
  • 1066.
    Beam Size andProfile 1 mm vs 2 mm 1066
  • 1067.
    Laser Beam Profile •Gaussian Beam • Flat Top • T Truncated Gaussian Beam t dG i B 1067
  • 1068.
    Gaussian Beam • Energynot well homogene distributed • Hi h energy on central Higher t l • Lower energy on peripheral Energy Ablation Threshold Heat sensation 1068
  • 1069.
    Gaussian Beam • Advantage: Smoother ablation profile • Disadvantage : Heat sensation Energy Ablation threshold Absorbed as heat 1069
  • 1070.
  • 1071.
    Flat Top Beam p •Homogen energy distribution • No heat • Less smooth ablation profile Energy Ablation threshold 1071
  • 1072.
    Truncated Gaussian Beam •Bausch & Lomb Combine all benefits of Gaussian Beam + Flat Top Beam • Smooth ablation surface • No heat no residual energy heat, Energy Ablation threshold 1072
  • 1073.
    Gaussian Beam Flat TopBeam Truncated Gaussian Beam u c ed G uss e 1073
  • 1074.
    Laser treatment • WaveLightEX500 (Alcon Inc) • VISX Star S4 IR Advanced CostumVue (Abbott Medical Optics) • MEL 80 and MEL 90 (Carl Zeiss Meditec) (Carl-Zeiss • TECHNOLAS Perfect Vision – SUPRACOR is a new corneal approach to treating pp g presbyopia with TECHNOLAS Excimer Workstation 217P • • • • Z LASIK (Ziemer) ( ) Pulzar ZI (CustomVisc) LaserSoft (Katana Technologies) Schwind Amaris (Schwind Eye-Tech) 1074
  • 1075.
  • 1076.
    Rinse and Flclosing Ri d Flap l i Animation 1076
  • 1077.
    Special Laser VisionCorrection • Reduce aberrations • Improve contras sensitivity – Scotopic – Intermediate Mesopic – Photopic • Improve reading speed • Improve the ability to special task force  p y p Astronauts and Fighter-Pilots – NASA, US Navy Aviation and US Air Force – Using : • iDesign Advanced WaveScan (Abbott Medical Optics) • 5th Generation Femtosecond IntraLase FS  iFS Advanced Femtosecond Laser (Abbott Medical Optics)  10 seconds only • VISX Advanced CustomVue Technology (Abbott Medical Optics) 1077
  • 1078.
    Once more :Lasik 1078
  • 1079.
    Flap & StromalThickness Analysis 1079
  • 1080.
    Presby LASIK y • MonovisionLASIK • Pseudo-accommodative cornea  PAC Nidek EC 5000 Excimer Laser (Nidek Co Ltd) • Aspheric-multifocal cornea  VISX CustomVue STAR S4 IR Aspheric (Abbott Medical Optics) • Lens Femtosecond laser treatment  100 microns thi k i thickness th t corresponds t 2 3 that d to 2-3 Diopters  INTRACOR (TECHNOLAS Perfect Vision) 1080
  • 1081.
    Non LASIK PresbyLaser Illuminating LaserACE • Bladeless microsurgical procedures • Ablate scleral tissue  Restoring Eye’s natural Eye s accommodative ability • VisioLite Er:YAG Ophthalmic laser system  LaserACE (ACE Vision Group, USA) • Laser ablations made in 3 Scleral critical zones EyeWorld, June 2008 1081
  • 1082.
    Laser : MiscellaneousApplication • Femtosecond laser assisted Descemet stripping Endothelial keratoplasty (FS-DSEK) • Laser suturolysis • Bleb remodeling Go opu ctu e • Goniopuncture • Laser in DCR Lids, • Lids Trichiasis and Punctal occlussion 1082
  • 1083.
    Laser : MiscellaneousApplication • Deep sclerotomy • Anterior hyaloidotomy • Persistent pupilary membrane removal • Lysis of vitreous strand 1083
  • 1084.
    Laser Phacoemulsification • 2940nm Erbium:YAG Laser – Erbium:YAG Phacolase (Carl Zeiss Meditec AG) • Neodymium:YAG Laser – Neodymium:YAG Photon Laser PhacoLysis System (Paradigm Medical) – Dodick Q-Switched Neodymium:YAG laser (ARC GmbH) • Femtosecond Laser – Vi t (TECHNOLAS P f t Vi i ) Victus Perfect Vision) – Alcon LenSx (Alcon Inc)  Rhexis, Incision, Nuclear fragmentation, Limbal Relaxing Incision (LRI) – L LensAR AR – Catalys (OptiMedica) – Femto LDV Z Models (Ziemer-S)* Kohnen T, Koch DD, 2005; Auffarth G, 2010; EyeWorld 2010; Salz JJ, 2010 1084
  • 1085.
  • 1086.
    Acknowledgement • All MyTeachers in Department of Ophthalmology, Airlangga University, Medical School, 1913 • All My Friends in Laser and Advanced Eye Care Team of Sumatera Eye Center • All My Teachers from IOA/Perdami, InaSCRS, ESCRS, Euretina, APAO, APACRS, ASCRS, EuCornea, AAO, IIRSI, ICO, AIOS, Cicendo Eye Hospital Bandung, Jakarta Eye Center, SN Feodorov MSC Moscow, Yale Eye Center and Yale School of Medicine, Beijing Tongren Hospital, Mitsui Hospital Tokyo, and Singapore National Eye Center 1086
  • 1087.
    And also specialthanks to • • • • • • • • • Alcon, Inc Bausch & Lomb Incorporated and TECHNOLAS Abbott Medical Optics Carl Zeiss Meditec AG Heidelberg E i H id lb Engineering i OCULUS Optikgeräte GmbH Haag Streit Ziemer Allergan g © May 20, 2008 – 2014 See also: gedepardianto blogspot com gedepardianto.blogspot.com Any suggestions : gedepardianto@yahoo.com 1087
  • 1088.
    Main references • AmericanAcademy of Ophthalmology, Basic and Clinical Science Course • Kanski JJ Clinical Ophthalmology JJ, • Deborah Pavan-Langston, Manual of Ocular Diagnosis and Therapy • Will’s Eye Manual y • Vaughan DG, General Ophthalmology • Kohnen T, Koch DD, Cataract and Refractive Surgery • Journal of Cataract and Refractive Surgery, Ophthalmology, g y, p gy, American Journal of Ophthalmology, British Journal of Ophthalmology, Clinical Ophthalmology • ESCRS, EUROTIMES • ASCRS EyeWorld USA ASCRS, E W ld • APACRS, EyeWorld Asia-Pacific • Retina Today • Retina Physician 1088
  • 1089.
    Support Team • Sightfor a Lifetime.TM • Bi h Bring hope t th li ht TM to the light. • ACT-G.TM 1089
  • 1090.
    Sail across PacificOcean of the 150 years of Gold Rush in California ,USA, 1999 USA © 2008-2014. 100 tahun Kebangkitan Nasional… KRI Dewaruci : Duta antar bangsa dan lambang kejayaan bangsa bahari