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Seminar 3 - Cataract
Seminar 3 - Cataract
FARADIANA
ROIHAN
ARIF
TASNIM
2
Glaucoma
Cataract
Diabetic/hypertensive retinopathy
Mononeuritic multiplex
CRVO (central retina vein occlusion)/CRAO
Corneal injury
Retinal detachment
Uveitis
TIA
Trauma
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History of presenting illness
4
Past Med
-Newly diagnosed hypertension
Family hx
-Unremarkable
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Refractive error
Cataract
Glaucoma (primary open angle)
Retinal disease diabetic retinopathy
Age related macular degeneration
Tumours and inflammation: intraocular
tumor, tumor of optic nerve
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Allnormal
Right eye post operative
Red eye reflex not symmetrical both side
Reduced red reflex on left eye
Reduced diameter of red reflex on right eye
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Congenital cataract
Senile cataract
Complicated cataract (Diabetic cataract &
parathyroid tetany)
Cataract due to radiant / heat energy
Traumatic cataract
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Pathogenesis
Heredity (genetic mutation)
Maternal (malnutrition & infection)
Foetal ( oxygenation), metabolic disorder
(galactosaemia), trisomy 21
Idiopathic
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• Symptoms
– Visual impairment
– Nystagmus
• Signs
– White reflex (leucocoria)
– Ophthalmoscopic examination (black opacity
against red background)
– Systemic congenital heart disease
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Pathogenesis
History of “anticipation”
Sunlight exposure
Old age (“age related cataract”)
Diabetes
Atopic dermatitis
Myotonic dystrophy
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• Degeneration & opacification of lens
(hydration, denaturation & coagulation of
proteins)
• Formation of aberrant lens
• Fibrous metaplasia of lens fibres
• Abnormal product of metabolism, drugs or
metals
• Slow sclerosis of the central nucleus fibres
(senile nuclear cataract) – brown pigment
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Symptoms
Frequent changes of glasses
Diminished visual acuity
Glare
Coloured halos
Monocular diplopia / polyopia
“myopic shift” & Colour shift (senile nuclear
cataract)
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Signs
Slit lamp examination (yellow layer in the
posterior cortex, lost of fundus details)
Ophthalmoscopic examination (dark shadow)
Blackened pupillary reflex (senile nuclear
cataract)
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Pathogenesis
Disturbance of nutrients in the lens (inflammatory
/ degenerative disease)
Diabetic cataract
Excess glucose sorbitol (sugar alcohol) osmotic
imbalance at lens
Parathyroid tetany
Deficiency of parathyroid hormone
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• Symptoms
– Impaired vision
• Signs
– Anterior segment (opacification of cortex)
– Posterior segment ( posterior cortical cataract)
– Ophthlamoscopic examination (vaguely defined,
dark area seen in the posterior cortex)
– Slit lamp examination (irregular borders of
opacity, breadcrumb‟s appearance, rainbow
display, snow flakes, crystalline flakes)
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Pathogenesis
Heat (infrared)
Irradiation (X-ray)
Electric (passage of powerful current)
Ultrasonic radiation (heat & concussion)
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Pathogenesis
Concussion
Perforating corneal injuries
• Signs
- Rosette-shaped‟ cataract (posterior cortex / anterior
cortex)
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Early
Glare
Frequent changes of glasses
Black spot
Uniocular diplopia / polyopia
Coloured halo
Colour value changes
Late
Impaired central vision
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Cataracts may be classified according to
1. age of onset
2. morphology
3. grade
4. maturity of cataract
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CONGENITAL ACQUIRED
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Congenital Presenile Senile
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Classification of Cataract Morphology
Fibre-based Sutural Congenital sutural
Concussion
Storage disorder
Deposition
Non-sutural Lamellar
Nuclear
Cortical
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Type Picture Cause Properties
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Type Picture Cause Properties
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Type Picture Cause Properties
posterior
with abnormalities of capsule ± posterior
segment
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Grading system is designed to quantify the degree of
opacification.
These vary from simple assessment by direct ophtalmoscopy
to the Lens Opacities Classification System II [LOSCII], where
slit lamp examination is compared to a standard set of
photographs [separate set for nuclear, cortical, and posterior
subcapsular].
It involves grading 4 features of the cataract:
- nuclear color (NC)
- nuclear opalescence (N)
- cortical cataract (C)
- posterior subcapsular (P)
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A B
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Maturity Description
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Hypermature
cataract
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• improve visual function depends on degree of
impairment and visual needs of individual,
most patients with a vision of 6/18 or worse
in both eyes because of lens opacities
benefit from cataract surgery
• diabetic retinopathy
• cataract prevents adequate retinal
examination or laser treatment
• lens induced glaucoma
• uveitis
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• Choice of anaesthesia
• Incision: via cornea or anterior sclera
• Technique of cataract removal
• Correction of aphakia: by intraocular lens
implantation, contact lens or aphakic
spectacles
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Phacoemulsification method
A very small tunnel incision (about 3mm
wide) is made in the eye and a circular hole
(diameter about 5 mm) is made in the
anterior capsule of the lens.
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A fine ultrasonic probe is then used to liquefy
the hard lens nucleus (phacoemulsification)
through this hole.
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• A folded replacement lens is then inserted into the
empty lens capsular bag and allowed to unfold.
• A high viscosity gel substance (viscoelastic) often is
used to protect the delicate endothelial cells that
line the posterior surface of the cornea during the
operation.
• This is then washed out at the end of the
procedure.
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Sutures often are not required as the tunnel
incision is self sealing.
These advances in technique have considerably
improved the speed of recovery and visual
rehabilitation after cataract surgery.
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Break Up and Remove the Cataract Lens
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Extracapuslar cataract extraction (ECCE)method
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Intracapsular method
• In this method, the entire lens is
removed within its capsule, usually
with a cryoprobe, after the suspensory
ligaments of the lens have been
dissolved by the enzyme chymotrypsin.
• As there is no remaining lens capsule,
the vitreous gel in the eye can move
forward and block the flow of aqueous
through the pupil.
• A hole cut in the iris (iridectomy)
allows the aqueous to bypass the pupil.
This method is now usually used only in
special situations.
• The procedure has a relatively high
rate of complications due to the large
incision required and pressure placed
on the vitreous body
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80% achieve 6/12 vision or better following
surgery
Failure to improve usually due to pre-existing
disease
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Corneal edema Elevated IOP
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Wound leak Iris prolapse
• intra-ocular
bacterial infection which
occurs in 1/1000 cases, with
crippling visual complications
in more than 50% of the
cases, depending on the
etiologic organism
• These include Staph.
epidermidis, Staph. aureus,
Pseudomonas, and Proteus. The hallmark findings: posterior
• Ix: AC tap and vitreous biopsy and anterior chamber
inflammation and Hypopyon
• Treatment : topical, intra-
vitreal, peri-ocular, and
systemic antibiotics together
with steroid therapy when
indicated.
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1. Posterior
capsule
opacification
Late- 2. Cytoid
4. Retinal
macular
detachment complication edema
3. Corneal
decompesation
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Posterior capsule ossification Cystoid macular oedema
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Retinal detachment
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Steroid drops (to reduce inflammation)
Antibiotic drops (to prevent infection)
Non-pharmacology advice:
- to avoid very strenuous exertion and ocular
trauma ( eg: heavy lifting )
- wear dark glasses
- prevent your eyes from coming into contact
with water and soap
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