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The document provides a comprehensive overview of key concepts in ophthalmology, including refractive errors like myopia, hyperopia, and astigmatism, along with their causes and corrective measures. It covers cataracts, their types, management, and surgical options, as well as corneal diseases and their treatments. Additionally, it discusses the anatomy and physiology of the lens and cornea, along with diagnostic techniques and complications associated with various conditions.
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OPHTHALMOLOGY QUICK REVISION NOTES
OPTICS
+ Total Power- 58 - 60D
+ 2/3rd is by Air-Cornea interface: most
important refractive surface: 45D
EMMETROPLA - Absence of refractive error
AMETROPLA - Presence of refractive error
BDO:
91 Qo)
1, Myopia
+ Short sightedness without the use of glasses.
+ Eyeball is longer in size
+ Concave lenses , mirus lenses (Diverging lenses)
2. Hyperopia
+ Long sightedness
+ Eyeball is smaller in size
+ Convex lenses, Plus lenses
3. Astigmatism
+ Refractive error whichis different indifferent
direction .
+ Cylindrical lenses
Refractive errors can be caused by
+ Axial - Change in eyeball size
+ Curvature - Curvature of the cornea is
different, Corrected by refractive surgery
+ Index - Change in the refractive index of the
lens , Age related Nuclear Cataract > Myopic
shift.
DOC in May!
+ Positional ~ Change in the position of the lens
‘Anteriorly / Posteriorly
MYOPIA
+ High Myopia ~ Refractive error is > 6 D
+ Pathological Myopia ~ Changes in the retina of
the eye.
Different pathological changes:
+The Myopic Fundus
+ Temporal myopic crescent ~ seen at the optic
disc on the temporal side
+ Thinning of retina
+ Macular degeneration - Foster fuch spots
(Hyperpigmentation / Hemorrhage).
+ Tessellated Fundus- Tigroid fundus, Underlying
choroidal vessels are visible,
ing &+ Patients are predisposed to Retinal
Detachment in High myopia -> Peripheral
Retinal degeneration: Lattice degeneration
+ Stophyloma~ (Bulging of the outer coat of eye)
MCC of Posterior staphyloma - High Myopia ®
+ Pseudo Popillitis
Types of Hypermetropia :
75
Ophthalmology
Equatorial
choroiditis
Staphyloma - seen after recurrent
Anterior Staphyloma - seen after corneal ulcer
perforation where there is pseudo cornea formation.
iliary Staphyloma - At the ciliary body, outbulging
of the outer coat
Intercalary Staphyloma - At the root of Tris.
HYPERMETROPIA
ype
+ Able to see far object without accommodation
+ Not able to see near object
+ Asthenopia
+ Eyeball size is smaller
+ Predisposed to Angle closure Glaucoma?
+ Silk shot retina
| TOTAL HYPERMETROPIA |
Latent hypermetropia
Manifest hy
ypermetropia
Tone of ciliary muscles | Facultative hypermetropia
Absolute hypermetropia
foconeedatve oor |
DOC in MayKing &Cerebellum Quick Revision Notes
ASTIGMATISM
Type of Astigmatism:
‘There are two types of astigmatism
1, Regular astigmatism 2 Primary Axes; Steepest 2. Irregular astigmatism - seen in corneal Scar or
& Flattest seen in keratoconus,
Ne
ZI
No Regular
Astigmatism Astigmatism
RETINOSCOPY
+ Differentiate b/w the types of refractive
error.
+ Reflected light from the retina appears like a
streak of light.
Movement of reflected light at the retina with
respect to Retinoscopy
fig Anan telnet aed 9 etrwzoe
projects eon tina he eye urge
DOC in MayKing &“motor tn
1. Against / Opposite movement ~ Myopia »-1 D
2. With / same movement - Myopia < -1 D or
Emmetropia = 0 or Hypermetropia = + value
3. No movement = Myopia = -1D
7
Ophthalmology
letoscoic
ace
rest Ey
is
spherical err Astron
(tatoos spo ‘chem
‘rat menos)
Refractive error = Retinoscopy value - 1/distance -
Cycloplegic used
+ For atropine- 1
+ Cyclopentolate- 0.75
+ Homatropine- 0.5
+ Tropicamide- 0.25
Mydeiasis ycloplegia
brug % Maximal Hours | Recovery Maximal Hours | Recovery Deys
Anteopine 10 30-40 7-10 doys 13 72
Homatrapine 10 40-60 1-3 days 05-1 13
Cyclopentolete 05-1 30-60 1 days 05-1 1
Tropicamide 05-1 20-40 3-6 hours we a4
Phenylephrine 05-1 20-60 3-6 hours None None
APHAKIA + Traumatic extrusion of lens
“Aphoki erly means absence of crstaling PEER ACTIVE CORRECTION
+ From an ophthalmological point of view, aphakia
is the absence of lens in the pupillary area,
Causes of aphakia:
+ Congenital aphakia
+ Surgical aphakia- removal of lens as in cataract
extraction
+ MC- Surgical aphakia : Findirgs- Tridodonesis ,
Deep Anterior chamber , Jet black Pupil . #10-
+11 correction , Jack in the Box phenomena ,
Rovsing Ring Scotoma
+ Aphakia due to absorption of lens- sometimes
seen in children after trauma
OPTIONS
+ Cornea based surgeries -
~ LASIK - Excimer laser used- 198rm, ArF
used?
- SMILE surgery- femtolaser used, argon
glass laser
+ Lens based surgeries - phakic TOL
Criteria for choosing Candidate:
~ Pt> 18 age
~ Stable refractive error
~ No coexisting diseases
DOC in MayKing &7
Cerebellum Quick Revision Notes
LENS
EMBRYOLOGY AND ANATOMY OF
LENS
le ae de
~ 2
~
+ Eye~Neuroectoderm - 3rd Wk of gestation
+ Lens - Surface ectoderm
+ Biconvex structure.
+ 15-17 Dof total eye
+ Copsule » Cortex > Nucleus
+ Oldest fibres are in the centre of the lens
+ Anterior surface : has Epithelium
+ Posterior surface - devoid of ary epithelium
+ Equatorial region ~ new lens fibres are being
formed
+ Pre equatorial region - Thickest Lens capsules
Physiology of Lens:
+ avascular structure
+ Nutrition supplied by Aqueous
+ Metabolism is mostly anaerabic
CATARACT - Opacification of lens and/or capsule
CONGENITAL AND DEVELOPMENTAL CATARACT
= presents since birth
+ MC Cataract®: Blue Dot cataract / Cataracta
Punctata Cerulea
= Stationary
~ Visually non significant
+ MC Visually significant cataract ~ Lamellar /
Zorular cataract®
= A zone of opacity in the fetal nucleus
~ Spoke like opacities called Riders
~ Seen in Hypercalcaemia , Vit D deficiency
+ Cataracta centralis pulverulenta
In Embryonic nucleus
Powdery opacities present
~ Visually insignificant
Stationary
+ Total / Membranous Cataract :
Congenital Rubella
Triad:
C = Cataract (eye has Salt & Pepper Retinopathy,
Congenital Glaucoma)
seen in
H- Heart diseases
D = Deafness (SNHL)
Surgery for Congerital Cataract: Lens Aspiration
with Primary Post Capsulorrhexis + Partial Anterior
Vitrectomy + PCIOLs
ACQUIRED CATARACT
+ Cortical Cataract
+ Nuclear Cataract
Cortical Cataract
1, Immature Senile Cataract
MC Type of Senile Cataract ~ Cuneiform Cortical
Cateract .
Hyper mature Cortical Cataract
Complications:
1, Phacomorphic Glaucoma?
+ Anterior chamber shallow
+ Narrowing of angle
DOC in MayKing &+ Angle closure glaucoma
2, Phacolytie Glaucoma
+ Cortex has undergone lysis
+ Leads to Hypersensitivity reaction
Hyper mature Nuclear Cataract
Complications:
+ Spontaneous Subluxation / dislocation of lens
ROSETTE CATARACT
+ Seen in Blunt Trauma
+ Flower shaped cataract either in the anterior
or posterior chamber
+ Vossius Ring - Iris pigment deposition on the
anterior capsule
COMPLICATED CATARACT?
Occurs as Complication of Intra ocular Disease
Tumour
I~ Inflammatory disease
6 - Glaucoma
E- Endophthalmitis
R- Retinal diseases eg, Retinitis Pigmentosa , Retinal
Ophthalmology
Detachment, High Myopia
Features
+ Posterior Subscapular location of cataract
+ Bread crump appearance?
+ Polychromatic Lustre?
+ Axial Spread
SNOW FLAKE/ SNOW STORM
CATARACT
+ Seen in pt. With Diabetic Mellitus (sorbitol
pathway)
SUNFLOWER CATARACT?
+ Wilson disease / Cu Metabolism
+ KF Ring / KAYSER-FLETSHER rings - Golden
brown discolouration at the Descemet
membrane,
MANAGEMENT OF CATARACT:
Surgical
Types of Anaesthesia -
1, General Anaesthesia Children / Mentally unstable
J adults
DOC in MayKing &Cerebellum Quick Revision Notes,
2. Local anaesthesia:
+ Retrobulbar block + Facial nerve block
Peribulbar block
Subtenon’s block
Topical anesthesia ~ Proparacaine eye drops
Types of Surgeries
+ ECCE ( Incision 10 - 12mm): sutures +
+ SICS (Incision 6 -8 mm ): suture +/-
Phacoemulsification surgery (incision- 3mm)
MICS Micro incision cataract surgery (incision-
2mm)
+ FLACS - Femtosecond laser assisted cataract
surgery. Laser used for-
~ Incision
~ Capsulorrhexis
~ Primary Fragmentation of Nucleus
~ Astigmatism Neutralising incision
INTRAOCULAR LENS
+ Non-foldable: PMMA
+ Foldable: Acrylic
~ Morofocal Lenses - Single focus
~ Multifocal Lenses - Multiple rings, Glare &
Halos
EDOF - Extended depth of focus
COMPLICATIONS OF CATARACT
SURGERY:
Expulsive choroidal Haemorrhage
+ Endophthalmitis (J vision, ? pain, 7 redness)?
‘Tit Intravitreal Antibiotics, Vitrectomy
‘Most imp. step in prevention - Perioperative Povidone
Iodine
+ Posterior
complication)
T/t: NAYAG laser (anterior capsulotomy) (1064 rim)
capsular Opacification (MC
* Spontaneous subluxation / dislocation of lers.
+ MC 2. Marfaris Syndrome - Up & out
+ Weil-Marchesani syndrome
+ Ehler Danlos
+ Homocystinuria- down and in
Vossius ring?
+ = Deposition of pigment in the anterior capsule
seen after blunt trauma,
CORNEA
j
toe =,
ae |
---—
= |
= eee |}
DOC in MayKing &1. Epithelium- stratified squamous non keratinised
epithelium, 5-6 layer thick
Bowman's Membrane- does rot regenerate
Stroma
Duc's layer- strongest layer
Descemet’s Membrane
Endothelium - does not regenerate
INVESTIGATIONS IN CORNEA
+ Pachymetry : assessment of the thickness of
‘the cornea
+ Keratometry : assessment of the curvature
of the cornea
+ Topography : assessment of the corneal
‘thickness, shape & surface.
+ Keratoscopy : assessment of the corneal
shape
+ Corneal Aesthesiometry : assessment of the
corneal sensations
+ Sodium Fluorescent dye: to stain the corneal
ulcers / defect
+ Rose Bengal stain : to stain Dead cells
s
+ Sodium Fluorescene dye
= Orange colour dye
~ Cobalt blue light used
Ophthalmology
Defect appears green
DISEASES OF CORNEA
BACTERIAL ULCERS
Pain, photophobia, watery eyes
Hypopyon : sterile, has Inflammatory cells
v
Pus in anterior chamber
MC Contact lens induced ulcer - Pseudomonas?
Hypopyon corneal ulcer / Ulcus serpens -
Pneumococcus®
Topical antibiotics - cone, Tobramycin /
Cefazolin / Gentamicin
‘Adjuvant therapy ~ Atropine (For pain relief)
FUNGAL ULCER
Filamentous furgi
DOC- Natamyein
Dry looking ulcer
Cheesy necrotic base
Satellite lesions?
Hypopyon ~ Non sterile
H/O injury with animal tailor leaf
Signs >> symptoms
Non filamentous furgi : DOC - Amphotericin B
VIRAL ULCER
HSV - Corneal lesions, Dendritic lesions —>
forms a geographic ulcer -> Stroma necrotic
ulcers -> Disciform keratitis
Loss of corneal sensation
HZV ~ Corneal lesion: Punctate keratitis»
pseudodendritic ulcer, Uveitis, Retinitis,
Oculomotor involvement. T/t- steroids given
under antiviral cover.
Hutchinsor's Rule -If Lesion on the tip of rose
+, 7 risk of corneal ulcer because both are
supplied by same Nasociliary branch
Dendritic Ulcer -
Fluorescence stain®
DOC in MayKing &Cerebellum Quick Revision Notes
ACANTHAMOEBA ULCER
+ Weak interlinkage in the corneal stroma
+ Myopic Shifts : Irregular myopic astigmatism
+ Retinoscopy: Scissor reflex / Yawning reflex
+ TOP Applanation :Pulsating mires
+ S/L: Vogt's Striae - vertical striae, stress
lines which disappear on counter pressure on
cornea,
+ Munson's Sign - Notching of lower lid on
looking down,
+ Fleischer Ring: iron deposition on epithelium
+ Rx: C3R- Corneal collagen cross linking with
Riboflavin
+ For Flattening - INTACS are used
+ Neurotrophic ulcer
+ Pain out of proportion
+ Pseudo dendrites
+ Ring uleer®
+ cultured on Non rutrient agar enriched with
[Link] ° DEGENERATIONS- DYSTROPHIES
+ Stained by Calcoflour white + Arcus Serilis (MC correal degeneration )
+ Lactophenol blue + Degenerations - acquired
+ DOC-PHMB (Poly Hexa Methylene Biguanide), + Dystrophy - Hereditary
Chlorhexidine
Q, Recurrent corneal erosion is a feature of:
+ H/O contact lens users using home made
contact lens saline, tap water , swimming with ‘A. Keratoglobus
conic lene 8. Keratoconus
CORNEAL ECTASIA C. Glaucoma
Keratoconus® D. Corneal dystrophy
+ Bulging of cornea
+ Epithelial dystrophy: Mop dot dystrophy /
Finger print dystrophy
DOC in MayKing &Stromal Dystrophy (MC dystrophy)
+ Macular
‘Mucopolysaccharidosis present
~ Aleain Blue stain
+ Granular dystrophy
~ Hyaline deposits
~ Masson Trichrome stain
+ Lattice dystrophy
~ Amyloid deposits
~ Congo red stain
(Marilyn Monroe always gets her man in L A city)
CORNEAL TRANSPLANT
"@ @©®
Ophthalmology
+ Full thickness transplant
+ Cadaveric donor
1, Lamellar Keratoplasty: Partial thickness
+ Deep Anterior Lamellar Keratoplasty (DALK)
+ Descemet's Stripping Automated Endothelial
Keratoplasty (DSAEK)
CONJUNCTIVA
27 Fomiceal
Bulbar
areal
Conjunctiva
Marginal
Conjunctiva
\3— Fomiceat
Conjunctiva
Papillae consist of hyperplastic conjunctival
tissue full of inflammatory cells, normally
seen in the palpebral conjunctiva,
Associated with bacterial and allergic
conjunctivities
Follicles consist of hyperplastic lymphoid
tissue & appear as elevated lesions encircled
by blood vessels. Typically seen in reaction
to topical agents, adenoviral & chlamydial
disease
DOC in MayKing &Cerebellum Quick Revision Notes
CONJUNCTIVITIS - inflammation of
conjunctiva
1. Bacterial Conjunctivitis
Adenoviral Conjunctivitis
Viral Conjunctivit
‘Membranous conjunctivitis- by C. diphtheria
(bleeds on peeling)
Pseudomembranous Conjunctivitis (does not
bleed on peeling)
~ Stophs
~ Strep
~ H. influenza
~ Neisseria gonorrhoea
‘Angular conjunctivitis?
~ Moraxella axenfeld, on inner canthus of eye
Picorra virus
Adeno virus
Coxsackie virus
Echo virus
Pharyngoconjunctival
Fever (PCF)
Follicular conjunctivitis
Epidemic
keratoconjunctivitis (EKC)
~-Mild, transient disease|
—No care sought
~~ Serotypes 3, 7
~~ Follicular conjiitis + fevet|-
+HA + Pharyngitis
~~ Looks like the flu
Chlamydial Conjunctivitis
+ Trachoma
+ Caused by Chlamydia trachomatis A, B, C2
+ D~Kcauses Inclusion conjunctivitis, swimming
pool conjunctivitis.
~~ serotypes 8, 19, 37
May be preceded by URTI
= + 2nd eye involved in 3-7 days
DOC in MayKing &WHO
2.5 Follicles on upper palpebral conjunctiva is
Pathognomic
Scarring ~ Arlt line
Pannus
Herbert's follicle
Herbert's Pits
‘Surgery for trichiasis,
Antibiotics
Facial cleanliness
Environment Hygiene
= DOC- Azithromycin 1g single dose stat
~ spread through fomites
~ Imp. cause of preventable blindness
NEONATAL CONJUNCTIVITIS - Ophthalmia
Neonatorum
Causes:
Chemical : 1% silver Nitrate solution used to
prevent gonococcal conjunctivitis
Bacterial - gonococcal
Viral: HSV-2
Chlamydial (most common)
boc
Ophthalmology
VERNAL KERATOCONJUNCTIVITIS
+ Spring Catarrh / VKC
+ Occurs in summer
+ Hypersensitivity reaction
+ Giant papillae on upper tarsal conjunctiva
(Paving stone appearance)
+ Moxwell lyon sign
+ Pseudogerontoxon
+ Shield Corneal ulcer
+ Rx: Steroids, Mast cell stabilizers (Sodium
cromoglycate)
PHLYCTENULAR CONJUNCTIVITIS
+ Type IV hypersensitivity reaction
+ TB Antigens
+ Staphylococcus antigen
+ Rx: Steroids
DEGENERATIVE CONDITIONS
+ Pinguecula - remains stationary / localized,
doesrit encroach cornea
+ Pterygium - forms a wing shaped fold,
encroaches over the cornea, elastotic
degeneration, has
+ 3parts-Head, Neck, Body, T/t: Surgical Excision
(conjunctival autograft), mitomycin C, 5-FU
MayKing &
85Cerebellum Quick Revision Notes
XEROPHTHALMIA
-d/t Vit A deficiency
+ XN- Night blindness
+ XF- fundal changes
+ XIA = Conjunctival Xerosis
+ XIB ~ Bitot’s spots
+ X2~ Corneal Xerosis
+ X3A- Keratomalacia «1/3rd
+ X38 Keratomalacia > 1/3rd
XS ~ Corneal Scarring
Rx: Vit A supplements
+ Child > ye ,> 8 kgs : 2 lakh ZU Orally - 0,1,
14 days
+ Child <1yr, «8 kgs: 1 lakh IU Orally /IM vit A
DOC in May
NEURO-OPHTHALMOLOGY
Papilledema
Pathophysiology of Papilledema (Hayreh's theory):
+ Disturbance in axoplasinic Flow causes stasis
and swelling of axors
+ Increased intracranial pressure is transmitted
‘along the subarachnoid space with optic nerve
sheath,
+ Increased ICT leads to increases optic nerve
tissue pressure which alters pressure gradient
H —choris
‘Shoe! Fostehor
cary artnos
High CSF Pressure
(Paoiiedera)
Axoplasmic Stass
Fat Tortuous Veins
AG
Normal ntraoeslar
Pressure
(18:20 mm Ha)
exams)
Etiology:
+ Tumours
+ Hemorrhage
+ Aneurysms
+ Infections
+ Orbital Causes
+ Intracranial Causes
ing ©‘Systemic conditions
‘Ocular causes - Retrograde axoplasmic flow
~ Trauma - Marked Ocular hypotony
= CRVO - Hemorrhages
~ AION
= Chronic Uveitis - Phthisis
Clinical Features:
Transient obscuration of vision- amaurosis
Fugax®
Normal Colour vision
Normal Pupillary reaction
Visual Fields- Enlargement of physiological
blind spot?
Features of Raised ICP
Focal neurological deficits with changes in
level of consciousness
Signs:
Normal Pupillary reaction
Fundus Picture
~ Obscuration of Disc Margin- Nasal margins
cre ist Sign
~ Hyperemia of Dise
~ Elevated Disc (champagne cork appearance/
cork screw appearance)
~ Swelling of surrounding retina producing
concentric retinal folds- Paton's lines
~ Dilated tortuous retinal veins
= Loss of Venous pulsations
~ Splinter hemorrhages in peripapillary region
Visual Fields - Normal
87
Ophthalmology
BENIGN INTRACRANIAL
HYPERTENSION
‘Also krown as Idiopathic intracranial
hypertension/ Pseudotumour cerebri
Tt isa diagnosis of exclusion
CT scan normal
CSF composition normal
+ CSF pressure
Commonly seen in fat, fertile female > 40 yrs
old
Drugs causing BIH?
F-00Ps
A-Vitamin A Toxicity, Amiodarone
Lithium
S- Long term Steroids or too rapid taper
E
T-Tetracycline, Doxycycline
Treatment:
Weight Loss
‘Medical Rx.
~ €.A Inhibitors- acetazolamide
~ Diuretics- Furosemide
Surgical Rx
~ Serial Lumbar Punctures
~ Shunt Placement- (L-P Shunt/ V-P Shunt)
DOC in MayKing &Cerebellum Quick Revision Notes
OPTIC NEURITIS
Popilitis Retrobulbar Neuritis
Neuroretinitis
2
Optic Nerve Head affected Optic Nerve offected behind the | Optic Nerve affected along with
eyeball Retira (maculer ares)
* Hyperemio ord edema of the Optic |+ Optic Nerve appears normel, |» Macular Star-° exudates that
nerve head + Typically described as ‘neither | form araurd the macula get
May be associated with per-popillary | the patient sees anything ror the | arranged in starlike manner
hemorrhages doctor sees anything”
> Mest frequent type nodults [+ Least common type
Most common type in Children + Frequently associated with + Mostly associated with Viral
Demyelinating disease- Multiple | diseases
Sclerosis + Rorely d/t demyelination
Etiology: Optic Neuritis
+ Tdiopethie
+ Demyelinating Disorder - Multiple sclerosis
Symptoms:
+ Sudden profound U/L vision loss ®
+ Dull Boring Pain in eye worsened with ocular
movements (on Upgaze)
+ Impaired dark adaptation
* Colour vision defect
+ Movement phosphenes & sound induced
phosphenes
+ Uhthof Phenomenon - worsening of symptoms
when there is raise in body temperature
Pulfrich Phenomenon - impaired depth
perception (swinging pendulum test)
+ Decreased Visual Acuity ©
+ Decreased Color Vision (red desaturation)
+ Decreased contrast/brightness sense
+ RAPD/ Marcus Gunn Pupil
boc
Disc Edema
‘Any Scotoma on Amsler Grid- most common is
Central scotoma
VEP shows reduced amplitude and delayed
trarsmission time
‘Treatment
High-dose intravenous steroids are the
treatment of choice for acute ON®
= Lgm IV steroid x 3 days
~ followed by 1 mg /Kg / day Oral steroids x
11 days
Oral steroids alone in conventional doses are
contraindicated,
ical trials
CHAMPS and CHAMPIONS
TOMS
Benefit
Precise.
CHAMPS - Controlled High-Risk AVONEX
Multiple Sclerosis Prevention Study
(Interferon beta 1a)
MayKing &+ CHAMPIONS STUDY- compared those who
had been receiving drug from start of CHAMPS
versus those who switched after receiving
placebo
+ ETOMS- Early Treatment of Multiple Sclerosis
‘Study-Interferon beta 1a
+ BENEFIT- Betaseron (Interferon beta 1b) in
Newly Emerging Multiple Sclerosis For Initial
‘Treatment Study
+ Precise Study - early Glatiramer Acetate
treatment in delaying Presenting with a
Clinically Tsolated Syndrome
RELATIVE AFFERENT PUPILLARY
DEFECT:
Marcus Gunn Pupil?
+ Afferent loop of the pupillary light reflex is
impaired (loss of sensory information)
+ Lesion- Optic nerve.
+ Main association: Optic neuritis due to multiple
sclerosis
+ Swinging Flashlight test for diagnosis
+ Dilation of the affected pupil in response to
light
Ophthalmology
HOLMES ADIE'S PUPIL
+ Regular and mildly dilated pupil (4-6mm):
+ Light-near dissociation:
+ Usually Unilateral:
+ Slow pupillary dilation in response to dark:
+ Slow redilation when re exposed to light:
+ Normal response to mydriatics
+ Pupil constricts with 0.125% pilocarpine
(cholinergic super sensitivity)
+ Lesion- ciliary ganglion
oe 6
fo oe
ARGYLL ROBERTSON PUPIL
+ Miotic, irregular pupils
+ Usually Bilateral
+ Pupils dilate very poorly with mydriaties
+ Caused by lesion in the pretectal area
+ Most commonly seen in tertiary neurosyphilis,
DOC in MayKing &Cerebellum Quick Revision Notes
WERNICKE'S HEMIANOPIC PUPIL
+ Optic tract lesion®
+ LIGHT REFLEX ABSENT on stimulating-
~ Affected side - temporal half of retina
~ Opposite side - nasal half of retina
HORNER’S SYNDROME? + LIGHT REFLEX PRESENT on stimulating-
+ Defect in the sympathetic Pathway ~ Affected side - nasal half of retina
= Opposite side - temporal half of retina
ee a
Accommodation Reflex Present
ARP
Pupillary Reflex Absent
HUTCHINSON'S PUPIL
+ Ptosis 1. Pupil on the side of Injury constricts
+ Miosis + Due to irritation of 3rd CN.
+ Anhidrosis + Pupil on other side-Normal
+ Apparent Enophthalmos 2, Pupil on the Injured side becomes DILATED
+ Dilatation lag + Due to paralysis of 3rd CN.
+ Heterochromia Tridis + Pupil on other side Constricts
3. Papils of Both sides are DILATED : No reaction to light
‘Masle Primary Secondary Teetary |
Medal ects Adduction
Loteral rectus Abduction
Inferior rectus Depression Exeyloterton Adetion
Siperior rectus Etotion Treyeotorsion adduction
Terr ebique Excyelotorson Elevation Abduction
Superior oblique Treyelotorsion Depression Abdvction
bocLata
6th
C.N. PALSY
Presentation:
Double vision
Esotropia in the primary position
Limitation of abduction on the side of the
lesion
Normal adduction
‘A compensatory face turn is towards the side
of the paralysed muscle in urilateral palsy.
Most common single EOM pelsy
Causes:
1, Ischaemia
2, Tumor (acoustic neuroma, meningioma)
3. Trouna
4, Elevated Intracranial pressure
boc
Ophthalmology
Congenital 6th N. palsies almost never occur in
isolation,
Leukemia & brainstem glioma are. important
considerations in children
3rd C.N. PALSY
Cculomotor nerve
Entirely motor in function
Supplies
~ All the Extraocular muscles except superior
oblique and lateral rectus
~ Levator palpebrae superioris
~ Intra ocular muscles- Sphincter pupillae and
ciliary muscle
Presentation:
Prosis
‘Abduction of globe-DOWN & OUT?
Intortion of the globe which increases on
‘attempted down gaze
Limitation of adduction
Limitation of elevation
Limitation of depression
Dilated pupil with defective accommodation
Causes
Idiopathic - about 25%
Vascular-Hypertersion & Diabetes (commonly
pupil sparing)
‘Areurysm-posterior communicating artery at
its junction with internal carotid artery
Trauma- subdural haematoma with uncal herni-
ction
MayKing &
312
Cerebellum Quick Revision Notes
4th C.N. PALSY- TROCHLEAR NERVE
+ Asymptomatic
+ Diplopia vertical
+ Head tilt position opposite to the side of the
lesion?
+ Hypertropia on the affected side.
+ Limitation of depression, most marked in
adduction
+ Extorsion, greatest in abduction.
+ Bilateral involvement should always be
excluded, particularly following head trauma.
+ Park's three-step test:2
~ Step one- In the primary position. In a
fourth nerve palsy, the involved eye is
higher
Step two- The eyes are examined in
right and left gaze to determine where
‘the hypertropia is greater. In superior
oblique weakness the deviation is worse
on opposite gaze — WOO6.
~ Step three- The Bielschowsky head till test
(BHT)
boc
ane
ou
=] [eneereeae]
Causes of 4th CN palsy
1. Idiopathic
+ Most are congenital
‘+ Symptoms may appear late in adult life
+ Old photograph will help (AHP)
2. Trauma
+ Frequently cause bilateral 4" nerve palsy
3. Microvascular
4, Aneurysms & Tumor
INTERNUCLEAR OPHTHALMOPLEGIA
MayKing &+ Lesion at the Medial Longitudinal Fasciculus
Mu
connection b/w 6th & 3rd CN
+ Impaired Adduction of ‘ipsilateral eye with
Nystogmus of the abducting eye
+ One and half syndrome- I/L MLF + PPRF Lesion
+ Eight and half syrdrome- T/L MLF + PPRF + 7th
rerve Lesion
col
Ophthalmology
MBINED C.N. PALSY
Orbital Apex Syndrome
Cavernous Sirus Thrombosis
Superior Orbital Fissure Syndrome
Tolosa Hunt Syndrome
Orbital Tumours
Fungal Infection in uncontrolled DM.
‘Mucormycosis, Aspergillosis
apart ote
(Kite poster
Lowertank ott caer ay cca)
Visual Field Defects
Laine) (6)
Meroe en as O @
©) Btongranonacpa © Oo
D, G, & H) Contralateral
chon
coat,
—
K) Contralateral
io
Prey
RETINA
RETINAL VASCULAR DISORDER
Prevalence IDD 40%, NIDD 20%
‘Microangiopathy - reduction in the number of
pericytes causing distension of capillary walls,
break down of the blood- retinal barrier -
leakage
The consequence of retinal nor-perfusion is
retinal ischaemia hypoxia,
Hypoxia- causes A-V_— shunts and
neovascularization.
Nonproliferative DR:
DOC in MayKing &
93Cerebellum Quick Revision Notes,
Intraretinal HE , hard exudates , oedema
Micro aneurysm?
Dot & Blot haemorrhage
~ Cotton wool spots
+ Proliferative DR
~ Neovascularisation®
~ T/t- laser photocoagulation
= Complication - Hge, tractional retinal
detachment
Nonproliferative DI Proliferative DR
Proliferative DR
Fluorescein Angiography
Retinal Photocoagulation
HYPERTENSIVE RETINOPATHY
+ Prolonged hypertension
+ Fundus picture
= Vasoconstriction - arteriolar narrowing
(AV2 1:3)
Leakage - abnormal vascular permeability ~
hemorrhages, exudates, retinal oedema
Arteriolosclerosis - thickening of the vessel
wall - changes at AV crossings- Salus sign,
Gunn sign, Bonnet sigh
CENTRAL RETINAL ARTERY
OCCLUSION
+ Cherry red spot
+ Causes:
Embolism-
1. From the heart
2. Carotid artery
fibrinoplatelet, caleific)
3, Vaso-obliteration- atherosclerosis, periarteritis -
associated with systemic vascular, haematological
disorders
disease (cholesterol,
Presentation
+ Acute loss of vision
+ Retinal ischemia time- 90 min.
DOC in MayKing &re
a ger
Signs
+ Retina white, foveo appears red
+ arterioles and verules- arrow
+ Central, branch
Treatment:
Ocular massage, TOPL
Causes of Cherry Red spot:
(GEE STING)
+ Berlin's cedema
+ Sialosis
+ Tay Sach’s disease
+ Ischaemia (CRAO)
+ Niemann Pick
+ Gangliosidosis type T
CENTRAL RETINAL VEIN
OCCLUSION
+ Splashed tomato fundus
+ Predisposing factors
1. Systemic age, systemic _ hypertension,
diabetes (veins compressed by the thicked
artery), blood hyperviseosity
2, Ocular - TEP, hypermetropia, congenital
abrormal.
* Central, branch
95
Ophthalmology
+ Presentation -Moderate loss of visual
acuity
* Signs:
© Tortuosity and dilatation of retinal
© Hemorrhages
© Cotton-wool spots
Optic dise oedema
+ Complication - CME neovascularization
Types:
+ Ischaemic type: 90 day Glaucoma/100 day
Glaucoma / Neovascular Glaucoma
+ Non Ischaemic : better prognosis
INFECTION
The Most Important Causes of Retinal Vasculitis
+ Idiopathic
+ Behcet's disease
+ Multiple sclerosis
+ Lupus erythematosus
+ Wegener's granulomatosis
+ Polyarteritis nodosa
+ Horton's arteritis
+ Sarcoidosis
DOC in MayKing &Cerebellum Quick Revision Notes
+ Tuberculosis
+ Borreliosis (Lyme disease)
Listeriosis
+ Brucellasis
+ Syphilis
+ Viruses
Eales Disease
+ MCC Vitreous haemorrhage in young males with
no h/o hypertension
no h/o trauma
+ Aetiology ; TB / Idiopathic
ACQUIRED MACULER DISORDERS
‘Age- Related Macular Degeneration ARMI
‘Types-
1. Atrophic- (non- exudative) - slowly progressive,
90%
2. Exudative -wet form -detachment of RPE,
choroidal neovascularization
Human retina es seen through an apthalmoscope,
Atrophic, Dry, Non exudative AMD
boc
+ The most common type, 90%
+ Slowly progressive atrophy of the RPE and
photoreceptors?
+ Presentation - gradual mild- to maderata
impairment of vision over several month or years.
+ Drusens deposited?
+ Deposition of abnormal material in Bruch
membrane®
+ Risk factor: UV rays / Smoking / lack of Anti
oxidation
Atrophic AMD
Early - drusen
Late - geographic atrophy
Exudative AMD
+ Exudative detachment of the RPE
+ Choroidal neovascularization grow from the
choriocopillaries through defects in Bruch
membrane into the sub- RPE space.
Choroidal Neovacularization
MayKing &7
Ophthalmology
Disciform Scar
‘about 1-15 um, which is 10 to 100 times better
‘than ultrasound or MRT
+ Anatomic layers within the retina can be
differentiated and retinal thickness can be
measured.
CYSTOID MACULAR EDEMA
Cystoid Macular Oedema
oo
Pseudophakic Non- Pseudophakic
4
Diabetic
Retinopathy
J
Retina Vein
Occlusions
J
Choroidal
Neovascular
‘Membrane
Amsler Grid
Fundus Fluorescein Angiography:
+ The Amsler grid is used to detect small
irregularities in the central 20 degrees of the
field of vision
+ Is.a quick and simple test that patients are
asked to use to monitor changes in their vision
ocT
+ Typical petaloid pattern in the central macula
secondary to dye leckage from perifoveal
capillaries
+ The dye accumulates in the cystic spaces in
‘the outer plexiform layer
+ Optical Coherence Tomography (OCT) is a new I Coherence T
imaging technique that provides high resolution OP tHCA! Coherence Tomography
and cross-sectional images of the eye :
Shows central cysts, loss of foveal depression
+ Analogous to ultrasound, but instead of using
of acoustic waves (as in ultrasound), it uses
light to achieve micrometer axial resolution.
+ The axial resolution of OCT in retinal tissue is
‘and macular thickening
Test of choice for diagnosis and follow up of
patients with CME
DOC in MayKing &Cerebellum Quick Revision Notes
Management
Medical Treatment
Rx: Steroids
Long standing - Intravitreal steroids
Intravitreal Anti VEGF
CENTRAL SEROUS RETINOPATHY
Tdiopethic, self-limited disease of young or
middle-aged adult
Usually unilateral, localized detachment of the
sensory retina,
Presentation
~ Sudden blurred vision in one eye, associated
with metamorphopsia
~FAG-breakdown of the blood- retinal barrier
which allows the passage of fluorescein into
subretinal space,
Prognosis
~ 80% spontaneous resolution normal vision
within 1-6 month
= 20% resolve within 12 month
Prolonged detachment or recurrent
attacks-permanent
~ Impairment of visual function
ocr
+ OCT can detect detachments that remained
undetected in FA,
+ It can also detect subretinal deposits like
fibrin and subretinal precipitates
4, Sub sensory fluid accumulation in CSC
b, Detected shallow SRD along with PED
HEREDITARY FUNDUS DYSTROPHY
Retinitis Pigmentosa
+ Triad : Vascular attenuation + Bony spicules
pigment + Optic Atrophy ( waxy)?
+ MC: Sporadic type
+ MC: AR (out of inherited)
+ AD: best prognosis
+ XLR: Worst prognosis
+ Group of hereditary disorders - progressive
loss of photoreceptors
+ Diffuse, usually bilateral, symmetrical
+ Cones, rods- predominant
+ Presentation-defective dark adaptation (right
blindness-nyctalopia)
DOC in MayKing &MYOPIC RETINOPATHY
+ Degenerative myopia
+ Progressive elongation of the globe is followed by
degenerative changes in the retina and choroid
+ Signs
~ Islands of chorioretinal atrophy
= Atrophy around the optic disc
Macule-brecks in bruch ——memb,,
Neovascularization haemorrhage
~ Posterior staphyloma, peripheral
degereration
RETINAL DETACHMENT
+ Separation of the sensory retina from the
Pigment epithelium
+ Rhegmatogenous- retinal break
+ Non-rhegmatagerous
Tractional
Exudative
Ophthalmology
Rhegmatogenous Retinal Detachment
:
+ Ttoccurs in patients with
History of previous trauma to the eye
~ Myopia
~ Peripheral retiral degenerations like lattice
degereration
+ Presentsas flashes and floaters, curtain falling
in front of the eye.
Peripheral Retinal Degenerations
Benign Predisposing
Cystoid degeneration
Lattice Degeneration
Equatorial Drusens ‘rail Track small holes
Reticular Pigmentary Degeneration
Traction Retinal Detachment100
Cerebellum Quick Revision Notes
Exudative Retinal Detachment
Definition: The retina is pulled into the vitreous
cavity by transvitreal traction
Etiology: Diabetic PvR, old
penetrating injuries
Clinicial features: The detached retina is
smooth, immobile, and concave toward the pupil.
No breaks are usually found on ophthalmoscopy.
Management: Vitrectomy, with release of
vitreous tractions is required
retinopathy,
Definition: The result of collection of fluid
beneath an intact sensory retina
Etiology: Choroidial neoplasm (e.g. melanoma),
chorioretinal inflammatory diseases,
malignant hypertension (as in toxcemia of
regnancy),hemorrhage from a sub retinal
rneo- vascular membrane (as in AMD), systemic
vascular and inflammatory diseases.
Clinical features: Smooth, transparent retinal
elevation, no retinal breaks nor pigment clumps
or red blood cells in the vitreous are identified
‘Management: Treat the underlying condition of
possible
Management
Each procedure requires location of the tear and
treating the retina around its edges by cryotherapy
or laser in order to create firm adhesions between
the sensory retina and the RPE layer and preventing
detachment,
Pneumatic retinopexy is best done for superior
breaks
‘The gas bubble will expand and being lighter
‘than the ocular fluids, will migrate upward to
‘tamporade superior breaks
Positioning-if the break is in the posterior
pole (close to the macula), the patient should
remain face down,
If the break was in the right temporal retina,
he should face on his left side.
Positioning should be applied for the first 2
weeks.
Scleral Buckle: Silicone explant-over the
sclera 360 degrees- in order to indent the
sclera and make it apposed to the underlying
detached retina
Pneumatic Retinopexy: -Intra-ocular injection
of gas (air or expandable gos) in order to
tamporade the retinal detachment and break
while the choroidal adhesions form
Vitrectomy with silicone oil
PPV (pars plana vitrectomy)
PPV was first introduced in 1972.
20-gauge 3 port PPV became the gold standard
Surgical Indications: Pars plana vitrectomy
is commonly recommended for the following
conditions:
= Macular hole.
‘Macular pucker
Vitreomacular traction
Refractory macular edema
~ Vitreous haemorrhage
DOC in MayKing &Tractional retinal detachment
Rhegmatogenous retinal detachment
~ Dislocated intraocular lens
~ Refractory wveitis
~ Retained lens material
~ Intraocular foreign bodies
- Floaters
X
ANATOMICAL CLASSIFICATION-
(US6) INTERNATIONAL
Uveitis Study Group
Anatomical:
+ Anterior uveitis
+ Intermediate uveitis
+ Posterior uveitis
+ Pan uveitis
ANTERIOR UVEITIS
‘Symptoms:
+ Pain
+ Photophobia
+ Redness
+ Lacrimation
+ Blurring of vision
Signs
boc
101
Ophthalmology
Keratin precipitates - aggregates on the
‘endothelium: Pathognomonic of uveitis
Cells: indicate Active uveitis
Flare: because of leaked proteins
Post Synechiae formation
Pupil : Miotic
Festooned Pupil
INTERMEDIATE UVEITIS
Intermediate uvei
inflammation of the ciliary
body (cyclitis, pars planatis).
L
=
ZZ *
Redness
Loss of vision
Floaters
Snow balls & snow banks
Anterior vitreous
Snowballs
‘Snow Banking102,
Cerebellum Quick Revision Notes
POSTERIOR UVEITIS
Signs:
+ Vitreous
+ Furdus lesions
Choroiditis
Retinitis
Old inactive lesion
~ Vasculitis
+ Poin
+ Redness
+ Loss of vision
PAN- UVEITIS
Inflammation of the entire uveal tract.
TREATMENT:
Aims
+ Relief pain & inflammation
+ Prevent ocular structural damage
+ Prevent visual loss & retinal or optic damage
Include:
+ Cycloplegia: Long acting cycloplegic agents
(Atropine, cyclopentolate, homatropine Jused
torrelief pain & photophobia by mydriasis
+ Corticosteroids
A. Local delivery of corticosteroids:
+ Topical corticosteroids
+ Periocular injections- in form of sub tenon
injections
+ Intravitreal injections and inserts
B. Systemic oral steroids (oral and intravenous)
+ Immunosuppressants
+ Biologics
+ Adjuvant therapy:
~ Cycloplegic
= Newer nonsteroidal anti-inflammatory
agents
~ Anti-vascular endothelial growth factor
(onti-VEGF) therapy: bevacizumab,
ranibizumab
UVEITIS AND SYSTEMIC
DISEASE
Cause of anterior uveitis:
HLA positive or seronegative group:
‘A-Ankylosing spondylitis,
B-Reiter's syndrome.
C-IBD" Inflamatory bowel disease’.
D-Psoriatic arthritis.
ANKYLOSING SPONDYLITIS
+ Young adults
+ Male are affected more with Arthritis
+ Axial skeleton
intervertebral joints
+ 90% positive HLA-B27
+ Acute, Recurrent, non-granulomatous Anterior
Uveitis
sacroiliac joint and
JUVENILE CHRONIC ARTHRITIS
1, Pauciarticular (<5)
2, Polyarticular (> 5 )
DOC in MayKing &3. Systemic
+ Bilateral, Chronic, non-granulomatous Ant.
Uveitis, painless.
+ Commoner in female patients, the young,
+ Pauciarticular disease <5 joints.
Complications:
+ Glaucoma (20%)
+ Cataract (40%)
+ Band Keratopathy (40%)
FUCHS HETOROCHROMIC
IRIDOCYCLITIS
+ Small stellate pan-corneal keratic precipitates
+ Star shaped KPs
+ Absence of posterior synechiae
+ Catareet
Posner - Schlossman Syndrome
+ Recurrent attacks of unilateral, acute mild
anterior uveitis with raised LOP
+ Rare, young adults
+ TOT few hours to several days
+ a/w HLA Bw54
+ Intervals between attack vary
+ Presentation-mild discomfort, haloes
+ Signs- corneal epithelial edema, few aqueous
cells, Fine preciprtates
+ T/t -topical steroids, antiglaucomatics
Ophthalmology
Pan Uveitis: Vogt Koyanagi Harada
(VKH)
\V- Visual symptoms ; serous retinal detachment
-Kutaneous symptom
H- Head
+ Multi-systemic auto-immune disorder affect
pigmented cells in the body.
+ Involves CNS, eyes, and skin
+ Neurological and auditory manifestations
+ Headache, Tinnitus
+ Integumentary findings, not preceding onset
of central nervous system or ocular disease,
such as alopecia, poliosis and vitiligo
Toxoplasmosis
+ MCC Congenital U/L Blindness
+ Headlight in fog appearance
+ Punched out lesions
+ Treatment: Antiprotozoal drugs- Clindamycin,
Sulphonamides, Steroids
Sarcoidosis
+ Eye lid
+ conjunctivitis , episcleritis, scleritis, and
sometime keratoconjuctivitis sicca
+ Anterior uveitis
+ Vitreous: diffuse vitritis, snowball opacities.
+ Fundus changes: periphlebitis (candle-wax
dripping), retinal granuloma, small and large
choroidal granuloma, optic nerve lesions,
BEHCET'S DISEASE
Ocular Features:
+ Bilateral, chronic with exacerbation and
remission, non- granulomatous pan-uveitis
DOC in MayKing &
103Cerebellum Quick Revision Notes,
+ Tridocyclitis - associated with transient
hypopyon
+ Vitritis
+ Retinitis
+ Vasculitis: venous occlusion, neovascularization,
Sympathetic Ophthalmitis
+ Bilateral granulomatous panuveitis
trauma ( penetrating trauma )
+ Onset :5 days to 66 years after trauma
+ Retina- Dalen fuch nodules present
after
+ Removal of injured eye after onset does not
help
+ Treatment: Aggressive _immunosuppressive
therapy
GLAUCOMA
10P> 24mm Ho
ow sion
TYplcaais changes Tyla el changes
Triad Of Abnormalities in: Die, Field And Intra~
Ocular Pressure (IOP) For The Diagnosis Of Glaucoma
‘Aqueous Formation:
+ Diffusion
+ Ultrafiltration
+ Secretion
Drainage
+ Trabecular mesh work
+ Uveoscleral outflow
Raised TOP > 21 mm Hg : Glaucoma
Top Measurement
+ Schiotz indentation tonometer
+ Applanation Tonometry - gold standard?
+ Perkins handheld Tonometry
+ Tonopen Tonometer
DOC in MayKing &Ophthalmology
+ Isopter contraction
+ Scotoma in Bjerrum's area
+ Seidel's Scotoma
+ Arcuate scotoma
+ Double arcuate scotoma
+ Ronne nasal step
+ Tunnel vision
Dise Signs
+ C:D ratio
+ Deep cup
+ Laminar dot sign
+ Asymmetry of C:0 of 0.2 between two eyes
Vascular signs
+ Bayoneting sign
+ Nasal shifting of vessels
Peripapillary signs
+ Flame shaped haemorrhage
+ Loss of nerve fibre layer
VISUAL FIELD CHANGES GONIOSCOPY
+ Perimetry: Humphrey visual perimeter To differentiate b/w Angle open type & Angle closure
type
Direct Gonioscopy
DOC in MayKing &106
Cerebellum Quick Revision Notes,
Some features of this technique are:
+ Patients must lie on their back
+ Gives adirect view of the anterior chamber angle
* Good magnification
+ Easy orientation for the observer
+ Possible simultaneous comparison of both eyes
Indirect Gonioscopy
Some features of this technique are:
+ Patient must be at the slit lamp
+ Indirect view of the anterior chamber angle
+ Faster than direct gonioscopy during routine
ophthalmological exam
+ Tt can be used to see the fundus (using the
central part of the lens) at the slit lamp
+ Inability tocompare the twoeyessimultaneously
CONGENITAL GLAUCOMA /
BUPHTHALMOS
Pathology: Hazy cornea - d/t Trabeculodysgenesis
(Trabecular meshwork not formed)
The Classical Triad of Signs/Symptoms
+ Epiphora/lacrimation
+ Photosensitivity
+ Blepharospasm
Cornea
+ Cloudiness secondary to edema
+ Haob’s Striae®
+ Horizontal Diameter »11.5 mm
GLAUCOMA IN ADULTS
Primary open angle glaucoma (POAG) - Raised IOP
(21 mm of Ha) associated with definite glaucomatous
optic disc cupping and visual field changes.
Ocular hypertension or glaucoma suspect - IOP
constantly more than 21 mm of Hg but no optic disc
or visual field changes
Normal tension glaucoma (NT6) or low-tension
glaucoma (LT6) - glaucomatous disc cupping with
or without visual field changes associated with TOP
constantly below 2imm of Hg
‘Angle Closure (narrow angle, acute congestive)
Glaucoma
+ Emergency situation occurring in person with
narrow Tridocorneal angle and shallow anterior
chamber.
+ TOP raised after it is being precipitated by
mydriasis
+ TOP rise rapidly to very high levels (40-60 mm
Hg)
+ Marked congestion
headache
of eyes and severe
+ Failure to lower TOP-» loss of sight
DOC in MayKing &+ Definite treatment ~ surgery
Closed angle glaucoma
Normat angle Angle closure
Trabecular meshwork iis
—
Sclora
Collecting venule
+ Be adrenergic blockers: Timolol , Betaxolol
and Levobunolol
+ adrenergic agonists: Dipivefrine, Apracloni-
dine and Brimonidine
+ PG analogues: Latanoprost, Travoprost, Bi-
‘matoprost, Tafluprost
+ Carbonic anhydrase int
Brinzolamide, Dorzolamide
itors: Acetazolamide
+ Mioties: Pilocorpine and Physostigmine
+ Rho Kinase Inhibitors : Netarsudil and
Ripasudil
B - adrenergic blocker in glaucoma -
MOA:
+ Topical p -adrenergic blockers have been ist
line of drugs ~ now P6 F2a
+ Lower TOP by reducing aqueous formation,
+ Advantages over mioties - produce less ocular
side effects, lipophilic and weak anesthetic
(Corneal hypoesthesia and damage)
+ Contrast to miotics ~ no effects on pupil size
tone of ciliary muscle and outflow facility
+ Ocular S/E : Ocular side effects: mild and
‘Ophthalmology
infrequent
~ Stinging, redness, dryness
~ Corneal hypoesthesia
~ Blepharoconjunctivitis
+ Systemic adverse effects: Major limitation of
use
~ Nasolacrimal duct obstruction
~ Life threatening bronchospasm - COPD and
asthma
~ Bradycardia, heart block and CHF - ADR
+ Will be not effective ino patient on systemic
+ Non selective ones are contraindicated in
newborns,
+ Effect has long term escape.
+ Inner canthus pressure - applied for 5 min
a - adrenergic agonists-MOA
+ al constrict ciliary BVs - reduced aqueous
secretion
+ a2 in ciliary epithelium reduce aqueous
secretion
+ Secondary role in enhancing drainage of
‘aqueous mainly through wveescleral outflow
and also trabecular outflow
+ {OP by 1 aqueous production (at +22),
Tuveoscleral outflow, 7 trabecular outflow
(62),
+ Dipivefrine (0.1%): Prodrug of adrenaline
“adr
+ Apraclonidine (0.5-1%}: Clonidine congener
+ Brimonidine (0.2%) : Newer clonidine congener,
more selective to a2
1. Brimonidine is contraindicated in infants: &
children aged up to 5 years,
2. Lesser effect during sleep
3, The most common antiglaucoma drug to couse
allergic reaction,
4. Cautious use in patients on Mono Amine Oxidase
Inhibitors or Tricyclic Antidepressants,
Prostaglandin analogues
Low concentration of PGF 2 a analogues | TOP by:
+ Increase uveoscleral outflow ( ciliary tissue
permeability and vascular permeability)?
DOC in MayKing &
107108
Cerebellum Quick Revision Notes,
+ Trabecular outflow less marked.
+ TOP in normal pressure glaucoma also
+ Topically TOT 425- 35%, well sustained
+ Ocular irritation ard pain
+ Good efficacy, once daily application and
absence of systemic complications - first
choice in open angle glaucoma
+ Other ADRs: iris pigmentation, thickening and
darkening of eye lashes etc.
1, Not effective in angle closure glaucoma and
corgenital glaucoma
2, Paradoxical rise in IOP if used more than once
daily
3. Prostaglandin Associated Orbitopathy may
occur with long term use (reversible).
+ Latanoprest(0,005% eye drop)
+ Travoprest (0.004%)
+ Bimatoprost(0,03% or 0.01%)
+ Tafluprost (0.015%)
Carbonic anhydrase inhibitors- MOA
+ Carbonic anhydrase present within ciliary
epithelial cells generates HCO3 ion secreted
into og. Humour
+ Inhibition of carbonic anhydrase - Limits
generation of bicarbonate ion-> reduction of
aqueous humour.
Acetazolamide:
+ Orally or /v
+ Used to supplement ocular hypotensive drugs
for short term indication like angle closure,
before & after surgery/laser therapy.
+ Long term use when IOP not controlled by
topical drugs.
+ Side effects: Systemic s/e - paresthesia,
anorexia, hypokalemia, acidosis, malaise,
depression (on long term use)
Dorzolamide: 2% eyedrop topical
Brinzolamide
1. Should be avoided inpatients with compromised
or failing corneal endothelium
2. Systemic CATs should be used with care in
patient on diuretics to avoid hypokalemia,
3. Cautious use in older patients, diabetics and
cko.
4, Contraindicated in patients with kidney stones
‘nd sulphate allergy
Miotics
+ 1n1970s- were standard antiglaucoma drugs.
+ Last option because of several drawbacks
myopia, diminution of vision, headache
Pilocarpine:
+ Causes miosis by contraction of iris sphincter
muscle -rremoves pupillary block and reverses
obliteration of iridocorneal angle.
+ Contraction of ciliary muscle -»pulls on scleral
spur ard improves trabecular patency.
+ Max of 10-20% IOP reduction - 0.5% to 4%
solution
TREATMENT OF ANGLE CLOSURE
GLAUCOMA
+ Hypertonic mannitol (20%) 15-2g/kg or
Glycerol (10%)
~ IV infusion -decongest eye by osmotic
action
= Glycerin 50% - retention enema
+ Acetazolamide (0.59) IV followed by oral 8D
started concurrently
+ Miotic: If above reduced the IOP - topical
Pilocarpine 1-4% every 10 mins initially & then
cat longer intervals
+ Topical B blocker: Timolol 0.5% 12 hourly in
addition
+ Latanoprost (0.005%) / Apraclonidine (1%)
may also be added.
+ Chronic rarrow angle: miotic/other drugs for
longer period
STRABISMUS
+ Strabismus: misaligrment of the visual axes
+ Orthophoria: perfect alignment of the visual
DOC in MayKing &Ophthalmology
‘axes. Most individuals have heterophoria with effort,
+ Heterophoria (latent squint) tendency of the + Heterotropia: (manifest squint) which is
eyes to deviate. Ocular alignment maintained present at all times
squint
hee
Apparent Latent squint
= (eterophoray
Mani
Comitah squint
alternating
| Convergent Divergent
Convergent Divergent
HETEROTROPIA + Non accommodative esotropia- it includes
congenital or infantile esotropia and acquired
Manifest Squint era
+ Dissociation of the eyes wherein the deviation
inall the direction of gaze NEAR TRIAD=accommodatioon+convergence: miosis]
* Types The left eye is turned inward-note that the light
~ Comitant/ non paralytic squint reflection in the eyes is rot symmetric
~ Tncomitant / paralytic squint
Comitant squint
+ It isa type of squint characterized by normal
extraocular movements and constant degree of
‘squint inall the direction of gaze
+ Types
~ Esotropia(convergent squint)
~ Exotropia (divergent squi
Exotropia (divergent squint) Essential/congenital ET
Clinical features:
+ Presents at 6 months of birth
~ Hypertropia or hypotropia (Vertical squint)
1, Esotropia
+ Convergent strabismus with eye deviated
rasally + Family history common
+ Accommodative esotropia- is due to the * Characteristic of ET
increased convergence associated with ee
accommodation reflex
DOC in MayKing &10
Cerebellum Quick Revision Notes
~ Large angle (> 30 prism D)
~ Angle at distance = near
+ Normal refractive error (therefore not
accommodative ET)
+ Alternating fixation in primary position but
cross fixation in side-gaze
+ Need to exclude VI CN palsy (cover one eye,
elicit Dolls reflex)
+ Latent nystagmus and asymmetrical OKN
response may be present
2. Exotropia
+ Divergent strabismus with eye deviated
outward temporally is called exotropia
+ Tteanbe infantile exotropia, primary exotropia,
and secondary exotropia
The right eye is turned outward-again, not the light
reflection in the eyes is not symmetrical
3. Hypertropia
+ This characterized by vertical misalignment of
eyes with upward deviation of the squinting eye
+ The common causes are.
~ Trochlear nerve palsy
~ Thyroid eye disease.
~ Brown's syndrome
The right eye is turned upward- light reflection not
symmetrical
4
4. Hypotropi
+ Tt is characterized by vertical misaligrment
of the eyes with downward deviation of the
squinting eye
The right eye is turned downward: light reflection in
eyes is not symmetric
Incomitant squint
+ It is characterized by limited or restricted
extraocular movements and varying degree of
squint in different directions of gaze types
+ Paralytic and restrictive squint
1. Paralytic squint
+ Tt is characterized by limited extraocular
movements in the direction of action of the
paralyzed muscle and varying degree of squint
indifferent directions of gaze
ci:
+ Diplopia,
+ Vertigo,
+ Nausea, and vomiting
+ False projection of the object
+ Limitation of the ocular movements in the
direction of action of the paralyzes muscles
+ Compensatory head posture to neutralize the
diplopia
Clinical Types
+ Oculomotor nerve palsy
+ Trochlear nerve palsy
+ Abducent nerve palsy
+ Total ophthalmoplegia
+ Interruclear ophthalmoplegia
DOC in MayKing &Ophthalmology
2. Restrictive Squint “What is the pathogenesis?" Pontine.
+ It is characterized by restriction of the Gysgerasia with 3rd CN
‘extraocular movements with small deviation in
the primary position of gaze innervating both MR and LR
Etiology: DIAGNOSIS OF SQUINT
* Usually caused by the fibrosis of the + Assessment of visual acuity and refractive
extraocular muscle or by restriction of the exer
movement of the extraocular muscle
+ Corneal reflex test
+ The common clinical syndromes associated
restrictive squint includes, + Cover test
+ Brown's syndrome. + Prism bar cover test
+ Strabismus fixus + Maddox rod test
+ Duane's retraction syndrome + Maddox wing test
Duane's Retraction Syndrome + Assessment of binocular vision
+ The main clinical feature is retraction of the
globe on attempted adduction TREAT AEN OF SGQUINT
Tec cist! ttn tye + Optical correction of the underlying refractive
error
Glossifieation + Orthoptic exercises
Type 1 + Surgical correction of the affected muscle
- on (resection of recession of the muscle)
~ Limitation in abduction eye reel
~ Can present as an ET ~ The stronger eye is patched to force
‘the brain to interpret images from the
Type 2 strabismic eye.
15% ~ Eye patches will not change the angle of the
Limitation in adduction ‘strabismus.
~ Gon present as an XT Typically, eye patching is used only if
amblyopia is present.
Type 3
~ 25%
~ Limitation in both adduction and abduction
Usually orthophoric
Clinical features:
+ Females more common
+ Left eye in 60%, bilateral in 20%
+ Retraction of globe on adduction (sine qua non)
~ Co-contraction of MR and LR
‘Associated with narrowing of palpebral
fissure
DOC in MayKing &
Mmm2
Cerebellum Quick Revision Notes
PRINCIPLES OF STRABISMUS
SURGERY :
Weakening procedures .
+ Recession
+ Margirel myotemy
+ Posterior Fixation suture
Strengthening procedures
+ Resection
+ Tucking
+ Advancement
Recession Surgery
Resection Surgery .
Frontal bone
Zygomatic bone
Maxillary bone
Ethmoid bone.
‘Sphenoid bone
Lacrimal bone
Palatine bone
Dimensions- Alignments of Orbit
Alignment of the orbits
medial walls are saan
parallel bf 5
lateral walls are peas
perpendicular
a
C7 cn soo
eyeballs make an
angle of 22.5 with the
orbital axes.
‘Medial Walls are parallel
Lateral Walls are perpendicular
Walls of Orbit
For esotropia
+ Recession of MR & resection of LR of squinting
eye
+ Recession of medial rectus of both the eyes
For exotropia
+ Recession of LR and resection of MR of
squinting eye
+ Recession of lateral rectus of both the eyes
The
ORBIT :
Anatomy of Orbit
Quadrangular truncated pyramidal in shape.
‘Seven bones make up the bony orbit:
boc
May
bony orbit has four walls
‘Medial wall
Lateral wall
Roof
Floor
Clinical Application :
Medial Orbital Wall
ing ©