lens for undergraduate final 1-2012

8/3/2019 Lens for Undergraduate Final 1-2012

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Dr. Abdelmonem Hamed

Fellow of Baylor of College of Medicine, USA

Professor of ophthalmology, Benha University, ARE

LENS

11


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Lens

It is a transparent, spheroidstructure

It alter the refractive index of the

light entering in the eye, RI = 1.39.

It does not have nerve, bloodvessels or connective tissue.

Biconvex shape results from theanterior surface (r=10mm) beingless convex than posterior surface(r=6mm).

Prof . Dr. Abdelmonem Hamed 22


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Anatomical Considerations

Diameter varies from 9to 10 mm

Lens grow in size

continuouslythroughout life. Itsweight is about 65milligrams at the birth

and up-to 258 mg by80 years of age.

Antero-posteriorthickness changes with

accommodation. 33Prof . Dr. Abdelmonem Hamed


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Lens

Lens issuspended ineye by

Zonules ofZinn which areinserted onanterior

surface andequatorial lenscapsule and

attached tociliar bod .44

Prof . Dr. Abdelmonem Hamed


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Lens-Anatomy

Histologically lens is

consisted of :

1. Capsule which is

a thick collagenese basement membrane, transparent, elastic acellular envelop,

thick at ant. pre-equatorial region (21micron),

Anterior pole is approximately 14 micron thick.

thinnest at the posterior pole (4 micron).

It contains the epithelial cells and allows a passageof small molecules both into and out of lens

55Prof . Dr. Abdelmonem Hamed


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Lens-Anatomy

2. Lens Epithelium :

It is a single layer of cells lining the anteriorcapsule and extends to the equator.

Zones of epithelial cells:a. Central cells do not actively divide, they divideunder pathological conditions only.

b. Pre-equatorial : cells rarely divide.

c. Equatorial germinal zone: constitute of stem cell.



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Lens - Anatomy

The anterior cuboidal cells

gradually become columnar andelongated (lens fibres) towards theequator.

The lens epithelium:secretes the lens capsule and

also regulate the transport of metabolite,

nutrients and electrolytes to the lens 77Prof . Dr. Abdelmonem Hamed


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Lens - Anatomy

3. Lens substance: It constitute themain mass of the lens. It is divide into-

a. Nucleusb. Cortex



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Lens - Anatomy

The Nucleus: consistsof

(i) Embryonic nucleus(it contains primary lens

fibers that are formed inlens vesicle)

(ii) Fetal nucleus: itcontains embryonic

nucleus and all fibersadded to the lens beforebirth

(iii) Infantile nucleus:

From birth to puberty. 99

i

iiiiiiv

cortex



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Lens Cortex

It is located peripherally and is composedof fibers formed continuously after sexualmaturation. It is further divided into:

Deep cortex

Intermediate cortex

Superficial cortex



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Lens - Crystalline

Lens fibres contain high concentrations ofcrystalline.

Crystalline represent the major protein of the

lens (constitute 90% of total protein content oflens).

Crystalline has the following constituents:

Alpha

Beta and,

Gamma



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Lens - Functions

The lens serves two major functions:

Focusing of visible light rays on the fovea through:

Its refractive power

accommodation

Preventing ultra-violet radiation from reaching theretina



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Lens - Sutures

Are found both at anteriorand posterior poles of thenucleus.

Anterior and posterior Y shaped suture lines areformed at the junction of

lens fibres.They are formed by

overlap of ends ofsecondary fibers in each

growth shell. 1313Prof . Dr. Abdelmonem Hamed


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Lens Physiology

Metabolic needs of theadult lens is met by

the aqueous andvitreous.

There is continuous

transport of ions intoand out of the lens.



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Lens - Physiology

Lens function :metabolism of glucoseto produce energy , and

protein synthesis

Glutathione is found

in high concentration(antioxidant).



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Lens -

Physiology

Accommodation occurs by ciliary musclecontraction, increasing the curvature of

anterior surface , thereby changing refractiveindex of lensincrease lens power.

Light transmission and elasticity of lensdecreases with age.



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Age changes in the Lens

Overall light transmission decreaseswith age, lens becomes less elastic,

reducing its ability to accommodatewhich leads to presbyopia.



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Cataract

Any opacity in the lens or its capsule,whether developmental or acquired iscalled cataract.

Developmental opacities are usuallypartial and stationary, whereas

acquired opacities are progressive.They progress until the entire lens isinvolved.



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Classification of Cataract

1919

evelopmental Acquired1. Age related (senile)2. Cataract associated with

ocular diseases3. Cataract associated with

systemic diseases (pre-senile)4. Traumatic Cataract5. Drug induced cataract

1. Anterior polar2. Posterior polar3. Coronary4. Cortical spoke-like

5. Lamellar6. Central pulverulent7. Sutural8. Focal dots



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Risk Factors for Cataract

Senility

Sunlight (specially UV)

Severe Diarrheal dehydrationVitamin A,C, E deficiency

Diabetes

Smoking

Corticosteroids



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Etiology of Cataract

Aging: Senile cataract

Systemic Diseases Diabetes,

Hypoglycaemia, Hypoparathyroidism,Myotonic Dystrophy, Galactosaemia,Alport Synd., Lowe Synd., SticklerSynd., Down Synd.

Skin Diseases Atopic Dermatitis,Ichthyosis



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Physical Factors Trauma (Blunt /Perforating) , Electric Shock, Radiation

Toxic Agents Corticosteroids,

Anticholinesterases, Chlorpromazine,Busulfan, Choroquine, Amiodrone, Cigrettesmoker, Copper, Iron, Gold, naphthalene,lactose, Galactose, selenite, thallium,

Dinitrophenol, ParadichlorobenzeneDeficiency of amino-acids or Riboflavin (B2)



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Pathogenesis of Cataract

1. Caused by:

degeneration and opacification ofexisting lens fibers, or

formation of aberrant fibers or

1. Factors causing disturbance ofcritical intra and extra-cellularequilibrium of water andelectrolyte lead to opacification.

Prof . Dr. Abdelmonem Hamed 2323


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Pathogenesis of Cataract

3. Fibrous metaplasia of fibres (incomplicated cataract)

4. Epithelial cell necrosis(Glaucomflecken)

5. Deposition of abnormal products ofmetabolism, drugs or metals.



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Etiopathogenesis of Cataract

Three biochemical factors areevident in cataract formation:

1. Hydration: seen particularly inrapidly developing forms. Actualfluid droplets collect under thecapsule forming lacunae between

fibres, the entire tissue may swell(intumescent) and becomes opaque.



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Etiopathogenesis of Cataract

2. Denaturation of lens proteins - Ifthe proteins are denatured with anincrease in insoluble protein, a dense

opacity is produced. (soft cataract).

3. Sclerosis: There is sclerosis of thenucleus due to long term effect of the

ultraviolet irradiation. (photo oxidation of aromatic amino A acids).(hard cataract).



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Symptoms of Cataract

1. Painless, progressivegradual diminution ofvision due to reduction intransparency of the lens

2. Frequent change ofglasses due to rapidchange in refractiveindex of the lens



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3. Loss or markeddiminution of visionin bright sunlight.

4. Monocular diplopia inpresence of corticalspoke opacities

5.

Glare in due toincreased scatteringof light



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6. Colored haloes around the light asseen in cortical cataract due toirregular refractive index indifferent parts of the lens.

7. Color shift , reds are accentuated



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Differential Diagnosis of

painless gradual diminution ofvisionChronic open angle glaucoma

Macular degenerationOptic atrophy

Corneal dystrophy

Retinopathy associated with systemicdisorders (hypertension or diabetes)



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Etiological Theories

1. Biological

a. An expression of senility

b. Genetic

2. Immunological

3. Functional, due to excessiveaccommodation.



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Etiology of Cataract contd

4. Local disturbancesa. of nutritional supply

b. of the chemistry of lens due to disturbancesof permeability

c. damage due to sunlight

5. General metabolic disturbances

a. changes in blood chemistry

b. toxic statesc. endocrine disturbances



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Classification of Age-related CataraAccording to Morphology

1. Subcapsular Anterior Posterior

2. Nuclear

3. Cortical

4. Christmas tree


S b l t t


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Subcapsular cataract

Anterior Posterior

34

CUPULIFORM CATARACT



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Nuclear cataract

Exaggeration of normal nuclearageing change

Causes increasing myopia

Increasing nuclear opacification

Initially yellow then brown

Progression


Cortical cataract


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Cortical cataract

Initially vacuoles and clefts Progressive radial spoke-like opacitie

Progression



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Christmas tree cataract

Polychromatic, needle-like opacitiesMay co-exist with other opacities


Classification according to maturity


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Classification according to maturity

Immature Mature

Hypermature Morgagnian38



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How to differentiate Immatureand Mature Cataract

IMMATURE CATARACT

1. Visual acuity isdiminished up tocounting finger.

2. Lens is opaque (Graywhite opacity) (not fullyopaque)

3.There is presence of irisshadow

4. Fundus details may bevisible.

MATURE CATARACT

1. Visual acuity reduced to PLor HM

2. Lens is uniformly opaque upto anterior capsule (usually

milky white)

3. No iris shadow

4. No fundus details



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Mature Cataract

Click to edit Master text styles

Second level Third level

Fourth level Fifth level

Click to edit Master text styles

Second level Third level

Fourth level Fifth level


Immature Cataract


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Investigations

Before taking patient for surgery:1. Macular function test with

1. two pin hole test. Patient looks throughan opaque disc perforated in the centre

with two pinholes close together. If thecentral area of retina is good, the patientappreciates the two lights.

2. Maddox rod test: Patient looks at a distantlight through the Maddox rod. The

macular function is good if the red line isstraight and unbroken.



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Investigations

2.

Projection of light rays: The test is done in a dark roomwith one eye covered. Patient is asked to look straightahead. Light is thrown from various directions and thepatient points the correct direction.

3. Entoptic view of fundus: The eyes are closed andglobe is firmly massaged through the lower lid with a

bare lighted bulb of a torch. The patient sees thevascular tree of the retina on an orange background.Any blanks or scotomas are noted.



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Investigations

2. Recording of IOP with tonometer3. Fundus examination of eye to be treated and of

fellow eye, if possible.

4. Photo stress test: The eye is exposed to brightlight for 15 seconds and recovery time is noted.

In macular disease, recovery time is prolonged(> 2 mintues). Normally it is less than 1 minute.

5. Ultrasonic investigation by B-scan, and ERG


Other causes of cataract - diabetes


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Other causes of cataract -diabetesJuvenile

White punctate or snowflakeposterior or anterior opacities

May mature within few days

Adult

Cortical and subcapsularopacities

May progress more quickly thanin non-diabetics


r causes of cataract - myotonic dystr


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r causes of cataract myotonic dystr

Myotonic facies Frontal balding

90% of patients after age 20 years

Stellate posterior subcapsular opacit

No visual problem until age 40 years45Prof . Dr. Abdelmonem Hamed

her causes of cataract - atopic derma


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her causes of cataract atopic derma

Cataract develops in 10%of cases between 15-30 years

Bilateral in 70%

Anterior subcapsular plaque(shield cataract)

Wrinkles in anterior capsule


is an inflammatory, chronicallyrelapsing, non-contagious andpruritic skin disorder

Causes of traumatic cataract
http://en.wikipedia.org/wiki/Inflammationhttp://en.wikipedia.org/wiki/Inflammation


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Causes of traumatic cataract

Penetration

Concussion

Vossius ring fromimprinting of iris pigment

Flower-shaped

Ionizing radiation

Electric shock

Lightning

Other causes


Drugs


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DrugsChlorpromazine

Long-acting miotics

Other drugs

Amiodarone

- initially posterior subcapsular

Systemic or topical steroids

- central, anterior capsulargranules


Secondary (complicated) cataract


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Secondary (complicated) cataract

Chronic anterior uveitis

High myopia

Posterior subcapsular

Hereditary fundus dystrophies Central, anterior subcapsular

opacities

Glaukomflecken

Follows acute angle-closure

glaucoma



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Treatment of cataract

No medicaltreatment iseffective once

the lensopacity hasdeveloped.



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PREOPERATIVE

PREPARATIONSProphylactic antibiotics: Local and systemic.The pupil is dilated with phenylephrine,tropicamide .

Anaesthesia and akinesia:Topical: 4% xylocaine, 0.5% proparacaine, etc.

Block: 2% xylocaine with adrenaline (epinephrine),0.5% bupivacaine and hyaluronidase

Prof . Dr. Abdelmonem Hamed 5151Prof . Dr. Abdelmonem Hamed


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Facial nerve block:

1. Van Lints method: Local anaesthetic is injected near theouter canthus of the eye.

4. O'Briens' method: 5 cc of anaesthetic is injected on theneck of the mandible just below the condyle.



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Ciliary block by retrobulbar

injection

1-2 cc of anaesthetic is injected into theneighbourhood of ciliary ganglionbehind the eyeball.



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Peribulbar anaesthesia

It is a much saferalternative method. Thepatient looks up straightat the ceiling and 5 ml of

local anaesthetic isinjected from the lateralpart of the lower lid. A 23G needle measuring 2.5

cm is directed almoststraight into the deepertissues and not in themuscle cone.



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Indication for surgery:

1. when routine work becomes difficultdue to reduced vision

2. Subluxated or dislocated lens

3. Lens induced complications likephacolytic uveitis / glaucoma,phacoanaphylactic endophthalmitis,phacomorphic glaucoma.



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Surgical Treatment:

Options

I. Intracapsular lens extraction(ICCE): Method of intracapsularcataract extraction (ICCE), nowbecoming obsolete, by which the entire

lens including the capsule is removedby rupturing zonular ligaments.



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II. Extracapsular Cataract Extraction(ECCE):

Methods :

1. Conventional ECCE

2. ECCE by small incision cataract surgery(SICS)

3. Lensectomy

4. Phacoemulsification



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Steps of ECCE

1. Anaesthesia

a. General Anaesthesia : In children,psychiatric patients, senile dementia

b. Local anaesthesia: Retrobulbarblock, peribulbar block, along with orwithout facial block , topical

anaesthesia



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Steps of ECCE

2. Cleaning of lids with 5% betadinesolution and instillation of betadinesolution in conjunctival sac

3. Draping

4. Superior Rectus suture in case ofconventional ECCE and SICS

5. Conjunctival flap in case of SICS



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Steps of ECCE

6. Scleral tunnel incision or Corneo-scleral section or corneal or cornealtunnel incision

7. Anterior chamber entry

8. Injection of ocular viscosurgicaldevice (OVD) in anterior chamber (HPMCor Sodium Hyaluronate)

9. Capsulotomy ( can opener orcontinuous curvilinear capsulorrhexis,CCC)



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Steps of ECCE

10. Hydrodissection andHydrodelineation

11. Nucleus delivery (in conventionalECCE and SICS) / Phacoemulsificationof nucleus (in phacoemulsification,machine , through titanium needleprovides energy for emulsification of

nucleus, needle vibrates at an speed of20,000 Hz and pulverizes the nucleus)



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Steps of ECCE

12. Cortical clean up by aspiration andirrigation (BSS or Ringer lactate is usedas irrigating fluid)

13. Filling of lens capsule (capsularbag) with OVD

14. Insertion of posterior chamber IOL

(in the bag, OR in the ciliary sulcus)



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Steps of ECCE

15. Removal of OVD from anteriorchamber

16. Closure of wound of entry(corneoscleral wound requires sutures10-0 silk or nylon), phaco and SICSincisions are self sealing.


Extracapsular cataract extraction


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p

1. Anteriorcapsulotomy

2. Completion ofincision

3. Expression ofnucleus

4. Cortical cleanup

6. Polishing of posteriocapsule, if appropria

5. Care not to aspirateposterior capsuleaccidentally

64Prof . Dr. Abdelmonem HamedProf . Dr. Abdelmonem Hamed

Extracapsular cataract extraction ( con


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8. Grasping of IOL andcoating with viscoel

substance

p

7. Injectionofviscoelasticsubstance

9. Insertion of inferiorhaptic and optic

11. Placement of hapticsinto capsular bag

10. Insertion of superihaptic

12. Dialling of IOL intohorizontal position

and not into ciliarysulcus


Phacoemulsification


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1. Capsulorrhexis 2. Hydrodissection

3. Sculpting of nucleus 4. Cracking of nucleus

5. Emulsification ofeach quadrant

6. Cortical cleanup aninsertion of IOL



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Advantages of ECCE over ICCE:

1. ECCE can be performed at all ages. Whereas ICCE cannot be performedbelow 40 years of age as the zonules are tight and there are greaterchances of vitreous loss.

2. Posterior chamber IOL can be implanted only after

ECCE. It cannot be implanted after ICCE.

3. Postoperative vitreous related problems (herniation inanterior chamber, papillary block and vitreous touch

syndrome) associated with ICCE are not seen after

ECCE.

4. Incidence of postoperative complications such as

endophthalmitis, cystoid macular oedema and retinal

detachment are much les after ECCE as compared to

that after ICCE.


CONGENITAL CATARACT


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CONGENITAL CATARACT

In healthy neonates In unwell neonates

2. Classification

3. Causes

1. Important facts


Important facts


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Important facts

33% - idiopathic - may be unilateral or bilateral 33% - inherited - usually bilateral 33% - associated with systemic disease - usually bilateral Other ocular anomalies present in 50%


Classification of congenital catara


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Classification of congenital catara

Anterior polar Posterior polar CoronaryCortical spoke-like

Lamellar Central pulverulent Sutural Focal dots


Anterior polar cataract


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pMay be dominant inheritance

Capsular Pyramid

With persistent pupillarymembrane

With Peters anomaly


Posterior polar cataract


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Posterior polar cataract

Ocular associations Persistent hyaloid remnants Posterior lenticonus Persistent hyperplastic primary vitreous


Coronary (supranuclear) catarac


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y

Round opacities in deep cortex Surround nucleus like a crown

Usually sporadic


Cortical spoke-like cataract


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Systemic associations Fabry disease Mannosidosis

74Prof . Dr Abdelmonem Hamed

Lamellar cataractUsually dominant inheritance


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Systemic associations Galactosaemia Hypoglycaemia Hypocalcaemia

Round central shell-like opacitysurrounding clear nucleus

May have riders

Usually dominant inheritance


Central pulverulent cataracti i h i


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Spheroidal opacity within nucleus Relatively clear centre Non-progressive

Dominant inheritance


Sutural cataract


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Opacity follows shape of Y suture

Usually X-linked inheritance


Focal dot opacities


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Blue dot cortical opacities Common and innocuous May co-exist with other opacities


auses of cataract in healthy neon


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auses of cataract in healthy neon

Hereditary(usually dominant)

Idiopathic

With ocular anomalies. PHPV

Aniridia

Coloboma

Microphthalmos Buphthalmos


Causes of cataract in unwell neon


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Intrauterine infections

Rubella Toxoplasmosis

Cytomegalovirus

Varicella

Metabolic disorders

Galactosaemia

Hypoglycaemia

Hypocalcaemia

Lowe syndrome


M t f


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Management ofDevelopmental CataractI. Investigations:

1. Detailed history

2. Detailed clinical examination-visual status, intra-ocular tension,fundus examination, B scanultrasonography to exclude posterior

segment abnormality like growth/retinoblastoma, A scan to determineaxial length of the eye, retinoscopyand cover test to exclude squint.


M t f


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Management ofDevelopmental Cataract

3. Laboratory investigations:

A. Blood Test

Blood glucose, calcium and phosphorus

RBC transferase and Galactokinase levels

TORCH test

Hepatitis B virus


M t f


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B. Urine analysis:

for galactosaemia (glycosuriaand galactosuria)


M t f


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B. Treatment

1. Timing of surgery

a. Bilateral Dense cataract by 6weeks

b. Bilateral partial if vision is not

significantly affected, surgery may bedelayed up to the age of 2 years or upto puberty


M t f


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c. Uniocular dense cataract-urgent surgery within days

d. Partial Uniocular cataract- ifvision is not significantly affected,surgery may be delayed up to the ageof 2 years or up to puberty


M t f


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2. Treatment options

* No treatment if vision is not affectedsignificantly

* Mydriatics- if opacity is central and visionimproves with mydriatics

* In cases in Rubella Cataract operationmay be delayed till 1-2 years of age. But early

surgery may be indicated if cataract is total,squint and nystagmus is developing.


M t f


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* Uniocular cataract if vision isaffected then early surgery, preferablywithin first six weeks of birth withimmediate fitting of contact lens.

* Fixation develops between 2-4 monthsof age, therefore any cataract interferingwith vision should be dealt before this age,and the earliest possible time is preferred

* Medical/ Paediatric fitness foranaesthesia should be obtained.


M t f


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3. Operative procedure

a. Aspiration and irrigation (ECCE)

b. Lensectomy (Pars plana oranterior route)

c. Aspiration and irrigation (ECCE)

with primary posterior capsulotomywith partial anterior vitrectomy


Management of


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4. Post-operative visual rehabilitation:

a. Posterior Chamber IOL (PMMA oracrylic polymer foldable lens) in patients

who are more than two years in age,Uniocular cataract where contact lensfitting is not possible/ practical.

b. Contact lens after surgery foruniocular cataract at very young age.


Management of


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c. Aphakic Spect- In bilateralcataract operated cases below the ageof two years. These cases are

implanted posterior chamber IOL assecondary procedure at later age.

d. Occlusion therapy for treatment

of amblyopia / prevention ofamblyopia.


OMPLICATIONS OF CATARACT SURGEROperative complications


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Vitreous loss

. Operative complications

Posterior loss of lens fragments Suprachoroidal haemorrhage

Iris prolapse

Striate keratopathy Acute bacterial endophthalmitis

Early postoperative complications

Late postoperative complications Capsular opacification Implant displacement Corneal decompensation Retinal detachment

Chronic bacterial endophthalmitis 91Prof . Dr. Abdelmonem HamedProf . Dr. Abdelmonem Hamed

Operative complications of vitreous loM t


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Sponge or automated anterior vitrectomy

Management

nsertion of PC-IOL if adequate casular support present


Insertion of AC-IOLIf adequate capsular support absent


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If adequate capsular support absent

. Peripheraliridectomy

Glide insertion

4. Coating of IOwith viscoelsubstance

. Insertion of IOL 6. Suturing ofincision

Constriction of pupil


anagement of posterior loss of lens fragmenagments consisting of 25% or more of lens should be removed


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agments consisting of 25% or more of lens should be removed

Pars plana vitrectomy and removal of fragment


Management of suprachoroidal( l i ) h h


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(expulsive) haemorrhageClose incision and administer hyperosmotic agent

Drain blood

Pars plana vitrectomy

Air-fluid exchange

Subsequent treatment after 7-14 days


Early postoperative complicationsIris prolapse


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Cause

Usually inadequatesuturing of incision

Most frequently followsinappropriate management

of vitreous loss

Excise prolapsed iris tissue

Resuture incision

Treatment

Iris prolapse


Striate keratopathyCorneal oedema and folds in Descemet membra


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Corneal oedema and folds in Descemet membra

Cause

Damage toendothelium

during surgery

Treatment

Most cases resolvewithin a few days

Occasionally persistencases may requirepenetratingkeratoplasty


Acute bacterial endophthalmitis


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Common causativeorganisms

Staph. epidermidis

Staph. aureus

Pseudomonas sp.

Incidence - about 1:1,000

Patients own externalbacterial flora is mostfrequent culprit

Source of infection

Contaminated solutionsand instruments

Environmental flora includithat of surgeon andoperating room personnel


Preoperative prophylaxis


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Staphylococcal blepharitisChronic conjunctivitis

Chronic dacryocystitis Infected socket

Treatment of pre-existing infections


Peroperative prophylaxis


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Instillation of povidone-iodinePostoperative injection ofantibiotics

Meticulous prepping and draping



Signs of severe endophthalmitis


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Signs of severe endophthalmitis

Pain and marked visual loss Absent or poor red reflex

Corneal haze, fibrinous exudate andhypopyon

Inability to visualize fundus withindirect ophthalmoscope


Signs of mild endophthalmitis


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Mild pain and visual loss

Anterior chamber cells

Small hypopyon

Fundus visible with indirectophthalmoscope


ifferential diagnosis of endophthalmit


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No pain or hypopyon

Uveitis associated withretained lens material

No pain and few if any anterior cells

Sterile fibrinous reaction

Posterior synechiae may develop


Management of Acute Endophthalmiti


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g p

. Preparation of intravitreal injections

. Identification of causative organisms Aqueous samples

Vitreous samples

3. Intravitreal injections ofantibiotics

4. Vitrectomy - only if VA is PL

5. Subsequent treatment


reparation for sampling and injection


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reparation for sampling and injection

Antibiotics Mini vitrector


Sampling and injections (1)


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Make partial-thickness sclerotomy3 mm behind limbus

Insert mini vitrector


Sampling and injections ( 2 )


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Aspirate 0.3 ml with vitrector

Give first injection of antibiotics

Disconnect syringe from needle

Give second injection

Remove vitrector and needle

Inject subconjunctival antibiotics

Insert needle attachedto syringe

containing antibiotics


Subsequent Treatment


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1. Periocular injections

Vancomycin 25 mg with ceftazidime100 mgor gentamicin 20 mg with cefuroxime

125 mg Betamethasone 4 mg (1 ml)

2. Topical therapyified gentamicin 15 mg/ml and vancomycin 50 mg/ml drop

Dexamethasone 0.1%

3. Systemic therapy Antibiotics are not beneficial

Steroids only in very severe cases


Types of capsular opacificationElschnig pearls Fibrosis


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Elschnig pearls

Proliferation of lens epithelium

Occurs after 3-5 years

Usually occurs within 2-6months May involve remnants ofanterior

capsule and cause phimosis

Fibrosis


Treatment of capsular opacification


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Nd:YAG laser capsulotomy

Accurate focusing is vital Apply series of punctures

in cruciate pattern (a-c)

3 mm opening is adequate (d)

Damage to implant

Potential complications

Cystoid macular oedema- uncommon

Retinal detachment- rare except in high myopes


Implant displacementDecentration Opti

c


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Decentration

May occur if one haptic is insertedinto sulcus and other into bag

Reposition may be necessary

Remove and replace if severe

Opticcapture


Corneal decompensationTP di i i


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Anterior chamber implant

Fuchs endothelial dystrophy

Penetrating keratoplasty in severe c

Guarded visual prognosis becauseof frequently associated CMO

TreatmentPredispositions


Retinal detachment risk factors


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Disruption of posterior capsule

Intraoperative vitreous loss

Laser capsulotomy, particularlyin high myopia

Treat prophylactically before orsoon after surgery

Lattice degeneration


Chronic bacterial endophthalmitis

Signs


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Low virulence organisms trappedin capsular bag

Late onset, persistent, low-gradeuveitis - may be granulomatous

White plaque on posterior capsule Commonly caused by P. acnes or Staph.

epidermidis

Signs


Treatment of chronic endophthalmiti


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Initially good response to topicalsteroids

Recurrence after cessation of treatm Inject intravitreal vancomycin Remove IOL and capsular bag if

unresponsive


ABNORMALITIES OF LENS SHAPE


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2. Lenticonus

1. Coloboma

3. Small lens


Coloboma


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Coloboma of irisColoboma of choroidGiant retinal tear

Ocular associations


LenticonusPosterior Anterior


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Posterior axial bulge Unilateral - usually sporadic

Bilateral - familial or in Lowesyndrome

Anterior axial bulge

Associated with Alport syndrome


Small lensMicrophakia Microspheroph


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Small diameter Small diameter and spherical

May be familial (dominant)

akia

Systemic association- Lowe syndrome

Systemic association- Weill-Marchesani syndrome


ECTOPIA LENTIS


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1. Acquired

2. Isolated familial ectopia lentis

3. Associated with systemic syndromes

Marfan syndrome Weill-Marchesani syndrome

Homocystinuria

4. Treatment options


Acquired ectopia lentisTrauma Stretched zonules


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Buphthalmos Megalocornea

Anterior uveal tumoursDegenerate eye



Isolated familial ectopia lentisAutosomal recessive


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Pupil may be normal Pupil may be displaced in oppositedirection (ectopia lentis et pupillae)


Autosomal dominantSystemic features of Marfan syndrome


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Limb-trunk disproportion Arachnodactyly

Pectus excavatum

High-arched palate

Aortic dilatation, dissectionand regurgitation

Mitral valve prolapse


cu ar ea ures o ar an syn romeLens Retinal detachment


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Upward subluxation Zonule usually intact

Axial myopia

Blue scleraCornea planaAngle anomaly andglaucoma

Lattice degeneration


Autosomal recessiveWeill-Marchesani syndrome


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Systemic features

Short stature

Ocular features

Short stubby fingers (brachydactyly)

Mental handicap

Microspherophakia

Angle anomaly and glaucoma

Usually anterior lens subluxation


Homocystinuria Autosomal recessive

Defect in cystathio beta synthase


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Defect in cystathio beta-synthase

Systemic features

Malar flush and fine, fair hair Marfanoid habaitus

Increased platelet stickiness Mental handicap

Ocular features

Downward lens subluxation

Disintegration of zonule


Treatment Options for Ectopia Lenti


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For induced astigmatism

1. Spectacle correction

For aphakic portion

Associated cataract

3. Surgical removal

Lens-induced glaucoma

YAG laser zonulysis to displace lens out of visual

Endothelial touch

When other methods are inappropriate



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Thank you

lens for undergraduate final 1-2012

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