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DISEASES OF LENS

DR D.JEYA LATHA MS,DO.


ANATOMY
 TRANSPARENT
 BICONVEX, CRYSTALLINE STRUCTURE
 PLACED BETWEEN IRIS & VITREOUS IN A
SAUCER SHAPED DEPRESSION PATELLAR
FOSSA
 POSTERIOR CAPSULE OF THE LENS IS
ATTACHED WITH VITREOUS BY
LIGAMENTUM HYALOIDEO CAPSULARE
(WIEGER’S LIGAMENT)
BERGER’S SPACE IS BETWEEN HYALOID
FACE & LENS CAPSULE
 WEIGHT – 255 mg

 RADIUS OF CURVATURE

>ANT SURFACE -10 mm


>POST SURFACE – 6 mm
REFRACTIVE INDEX -1.39mm
REFRACTIVE POWER -16 – 17 D
STRUCTURE OF LENS
 LENS CAPSULE
>Thickest basement membrane of the
body
> Thicker anteriorly than posteriorly
> Stain positively with PAS
> Highly elastic but not contain any
elastic tissue
ANTERIOR LENS EPITHELIUM
 SINGLE LAYER OF CUBOIDAL NUCLEATED
EPITHELIUM
 METABOLIC, SYNTHETIC & TRANSPORT
IN FUNCTION
 EQUATORIAL REGION IS COLUMNAR
WHICH FORMS NEW LENS FIBRES
 NO POSTERIOR EPITHELIUM WHICH IS
USED UP IN FILLING CENTRAL CAVITY OF
LENS VESICLE
LENS FIBRES
 FIRST FORMED FROM POSTERIOR
EPITHELIUM & LATER FROM EQUATORIAL
REGION
 HEXAGONAL IN CROSS SECTION
 BOUND TOGETHER BY GROUND
SUBSTANCES
 ARRANGED IN THE FORM OF Y SHAPED
SUTURES
 NUCLEUS
> CENTRAL PART WITH OLDEST
FIBRES
CORTEX
> PHERIPHERAL PART WITH
YOUNGEST LENS FIBRES
CILIARY ZONULE
 RUN FROM CILIARY BODY
 FUSE WITH OUTER LAYER OF LENS
CAPSULE AROUND EQUATOR
 HOLD THE LENS IN POSITION
 ENABLE THE CILIARY MUSCLE TO ACT ON
IT
PHYSIOLOGY
 TRANSPARENCY OF THE LENS IS DUE TO
> SPARSITY OF CELLS
> SINGLE LAYER OF EPITHELIAL
CELLS
> CLOSE ALIGNMENT OF CELLS
> SEMIPERMEABLE LENS CAPSULE
> AVASCULARITY / SAME REFRCTIVE
INDEX
> PUMP MECHANISM OF LENS FIBRES
> HIGH CONCENTRATION OF REDUCED
GLUTATHIONE
BIOCHEMICAL COMPOSITION
 WATER – 65%
 PROTEIN – 34% ( Insoluble – Albuminoid)
 (Soluble – Crystallines)
 AMINO ACIDS – No tryptophane,cystine,
 Hydroxy proline
 CARBOHYDRATES – Glucose, Fructose,
 LIPIDS – Lecithin
 ELECTROLYTES – Potassium inside the lens
 ASCORBIC ACID
METABOLISM
 LENS EPITHELIUM GENERATES ENERGY
FROM CARBOHYDRATE METABOLISM
 ANAEROBIC METABOLISM – 85% (EM
Pathway)
 HMP SHUNT
 KREB’S CYCLE
 SORBITAL PATHWAY
 LENSEPITHELIUM
MAINTAINS LOW
CONCENTRATION OF
Na/water WITHIN THE
LENS BY Na-K –ATPase
PUMP
CATARACTOGENISIS
 RISK FACTORS
> INCREASING AGE
> U V RADIATION
> DIETARY FACTORS – VIT A, C ,E Defi
> SEVERE DIARRHOEA
> DIABETES / HYPERTENSION / SMOKING
> RENAL FAILURE
> MYOPIA / GLAUCOMA
> STEROIDS
> GENETIC
PATHOGENISIS OF CATARACT
 ANY OPACITY IN THE LENS OR ITS
CAPSULE IS CALLED CATARACT
 THREE BASIC MECHANISMS
> Damage to lens capsule
> Changes in lens fibre protein
synthesis
> Increased lens hydration
CORTICAL CATARACT
AGING
|
LENS CAPSULE MORE PERMEABLE
|
ACCUMULATION OF Na ions& H2O
|
INCREASED HYDRATION
DISRUPTION OF LENS FIBRE MEMBRANE
|
VACUOLES FORMATION
|
INCREASED RATIO OF INSOLUBLE TO
SOLUBLE PROTEIN
|
OPACIFICATION
NUCLEAR CATARACT
U – V RADIATION
|
PHOTO OXIDATION OF AROMATIC
AMINO ACIDS
|
BROWN PIGMENTATION
|
DEPOSITION OF ABNORMAL LIPOPROTEIN
DECREASED REDUCED GLUTATHIONE
|
INCREASED INSOLUBLE PROTEIN
|
NUCLEAR CATARACT
CLASSIFICATION
CONGENITAL OR DEVELOPMENTAL
TRAUMATIC
> MECHANICAL
> IRRADIATION
> ELECTRIC SHOCK
COMPLICATED
SECONDARY
TOXIC
 COMPLICATED CATARACT
> ANTERIOR UVEITIS
> HIGH MYOPIA
> RETINAL DETACHMENT
> RETINITIS PIGMENTOSA
> GLAUKOM FLECKENS
 SECONDARY CATARACT
> DIABETES
> HYPOCALCAEMIA
> MYOTONIC DYSTROPHY
> ATOPIC DERMATITIS
 TOXIC CATARACT
> CORTICOSTEROIDS
> MIOTICS
> CHLORPROMAZINE
> GOLD
 SYNDROMES
> DOWNE’S
> LOWE’S
> WILSON’S DISEASE
> FABRY’S DISEASE
> TREACHER COLLINS
SENILE CATARACT
 AFTER THE AGE OF 50
 BILATERAL – But develops earlier in one
eye
 EQUAL IN MEN & WOMEN
 PRE SENILE CATARACT – Less than 50 yrs
TYPES
 CORTICAL OR SOFT CATARACT (75-80%)
 NUCLEAR CATARACT OR HARD
CATARACT (20 -25%)
CORTICAL CATARACT
 HYDRATION FOLLOWED BY COAGULATION OF
PROTEINS
 TWO TYPES
1) CUNEIFORM – Wedge shaped opacity
at periphery
2) CUPLIFORM ( Posterior cortical cat )
Saucer shaped opacity at posterior
cortex
CUNEIFORM CATARACT
 SYMPTOMS
> Painless progressive loss of vision
> Uniocular diplopia or polyopia
> Coloured halos
> Black spots
> Glare
> Progressive decrease in peripheral
field
> White opacity inside the black of the eye
STAGES
 STAGE OF LAMELLAR SEPARATION
 STAGE OF INCIPIENT CATARACT
 IMMATURE STAGE
 MATURE STAGE
 HYPERMATURE STAGE
LAMELLAR SEPARATION
 Demarcation of cortical fibres by fluid
 Seen with S\L
 Invisible ophthalmoscopically
 Greyish in colour due to increase in
reflection & scattering of light
INCIPIENT CATARACT
 Wedge shaped spokes of opacities in periphery
of the lens ( cuneiform opacities) commonly in
lower nasal quadrant
 Sectorial alterations in the refractive indices of
the lens fibres
 Irregular refraction & polyopia
 Greyish colour with oblique illumination
 Black against the red back ground with
ophthalmoscope
IMMATURE STAGE
 Diffuse opacification & irregular so that
deeper layers of cortex become opaque &
cloudy
 Progressive hydration of cortical layers
 Greyish or Greyish white colour
 Iris shadow present
 Fundal glow is faint
 4th purkinje image distorted not absent
 IRIS SHADOW
As long as any clear lens substance
between pupilary margin of iris & the
opacity as in IMC the iris throws a shadow
upon the grey opacity when the light is
cast upon the eye from one side
 INTUMESCENT CATARACT
Progressive hydration of the cortical
layers may cause swelling of the lens
making anterior chamber shallow causing
phacomorphic glaucoma
MATURE STAGE
 White or pearly white
 No iris shadow
 Absent fundal glow
 Vn is HM or PL
 4th purkinje image absent
HYPERMATURE STAGE
 Cortex becomes disintegrated & is
transformed into a pultaceous mass
 Lens becomes shrunken
 Anterior capsule becomes thickened
 Iris becomes tremulous
 AC becomes deep
 Degeneration of zonule leading to luxation
of lens
 TWO TYPES
A) MORGAGNIAN CATARACT
B) SCLEROSIS ( shrunken cataract )
 MORGAGNIAN CATARACT
> Cortex becomes fluid
> Nucleus sink to the bottom of the
lens
> liquefied cortex is milky
> Nucleus is as a brown mass limited
above by a semicircular line
COMPLICATIONS
 SUBLUXATION OR DISLOCATION OF LENS
 LENS INDUCED GLAUCOMA
 LENS INDUCED UVEITIS
 ABSOLUTE GLAUCOMA ( No PL )
CUPLIFORM CATARACT
 Dense aggregations of opacities like a
plaque just beneath the capsule
 Usually in the posterior cortex
 Cataract progresses towards the equator
not axially towards the nucleus
 Seen as a yellow layer in S\L
 Markedly diminishes the vn
 Vn better in darkness
NUCLEAR CATARACT
 Occur earlier than cortical cat (After 40)
 Blurs distant vn more than NV
 Tinted dark brown, dusky red, or even
brown
 Colour is due to melanin deposition &
photo oxidation of aromatic amino acids
 Progressive myopia due to increased RI
 Progression is very slow
 Hypermaturity never occurs
SYMPTOMS
 Defective vn for distance
 Induced myopia
 Myopia neutralises plus power of
presbyopia ( second sight )
 Finally loss of vn
SIGNS
 Vn is reduced to HM
 Yellow, brown, or black in colour
 Iris shadow is present
 Fundal glow is blackened
GRADING
 GRADE 1 - Grey or Greenish yellow
 GRADE 2 - Yellow nucleus
 GRADE 3 - Amber
 GRADE 4 - Brown to black
DIFF BET CORT & NUCL CAT
CORTICAL CATARACT NUCLEAR CATARACT
1) Start at late 50 Earlier than cortical type
2) Uniocular diplopia, No such symptoms
poyopia, halos
3)Index hypermetropia Index myopia
4)Greyish white to milky Yellow, brown or black
white
5)Gradually progressive Slowly progressive
Hypermaturity never
ocurs
COMPLICATED CATARACT
 Disturbances in nutrition of lens due to
inflammation or degeneration
 CAUSES
1) IRIDOCYCLITIS
2) DEGEN MYOPIA
3) RETINITIS PIGMENTOSA
4) RETINAL DETACHMENT
5) ANTERIOR SEGMENT ISCHAEMIA
FEATURES
 Opacification occurs in posterior cortex
 Ophthalmoscopically seen as dark area
 S/L – greyish white with irregular borders
called as BREAD CRUMBS appearences
 Polychromatic lusture
 Remain stationary for long time
 VN much impaired as the opacity is in
nodal point of the eye
TREATMENT
 Control inflammation with local & systemic
steroids
 IOL implantation
DIABETIC CATARACT
 TWO TYPES
1 ) EARLY ONSET SENILE CATARACT
2 ) TRUE DIABETIC CATARACT
FEATURES
 BILATERAL
 PROGRESS MORE RAPIDLY
 DEPEND ON DURATION OF DM
 INCREASED OXIDATIVE DAMAGE
 ANT OR POST SUB CAPSULAR REGION
 SNOW FLAKE CAT ( White dots )
mechanism
 Excessive glucose in lens
|
Metabolizes to sorbital
|
Increases osmolarity
|
Imbibition of H20 in to the lens form vacuoles
|
opacification
GALACTOSAEMIA
 Autosomal Recessive
 Inherited congenital disease
 Inborn inability to metabolise galactose
 Classical – GPUT Deficiency
 Milder disorder – Galacto kinase deficiency
 Bilateral cataract , MR , Hepato
spleenomegaly , failure to thrive in
classical type
MECHANISM
 Failure of conversion of Galactose to
Glucose leads to increase in Galactose
levels in blood & accumulation of Galactilol
with in the lens
 Osmotic swelling of lens fibres
FEATURES
 Bilateral cataract in early life
 Anterior & posterior sub capsular lamellar
opacity first
 Later becomes total
 Regression occurs if milk & milk products
are eliminated from the diet
DIAGNOSIS
 REDUCING SUGAR IN URINE
 RBC ENZYME ASSAY
TRAUMATIC CATARACT
 Due to penetrating injury
 Star shaped opacity in posterior cortex
called Rosette
HEAT CATARACT
 Prolonged exposure to IR rays
 Disc shaped opacity in posterior cortex
 True exfoliation of lens capsule
 IR rays absorbed by pigment of iris & CB
 Glass blowers cataract
POSTERIOR CAPSULAR
OPACIFICATION
 AFTER CATARACT OR SECONDARY
CATARACT
 OPACITY WHICH FOLLOWS ECCE
MECHANISM
 In IMC soft clear cortex sticks to the capsule
 Shut off by adhesion of the remains of
anterior capsule to the posterior capsule
 Cuboidal cells that line the anterior
capsule fullfil their function of forming
new lens fibres
 Fibres are abortive & opaque as they are
formed in abnormal conditions
 TYPES
> CAPSULAR
> CAPSULO LENTICULAR
> PIGMENTARY or Hgic
ELSCHNIG PEARLS
 Sub capsular cells proliferate & instead of
forming lens fibres develops into large
balloon like cells which fills the pupilary
aperture
SOMMERRING
 RING ENCLOSED BETWEEN TWO LAYERS
OF LENS CAPSULE
 CAUSE TROUBLE BY BECOMING
DISLOCATED INTO AC
TREATMENT
 DISCISSION OR NEEDLING USING
ZEIGLER’S KNIFE
 CAPSULECTOMY WITH FINE SCISSORS
 YAG LASER CAPSULOTOMY
SUBLUXATION OF LENS
 Portion of zonule absent
 Lens is displaced sideways
 Remains behind the pupil
DISLOCATION OF LENS
 Lens loses all zonular supports
 Lens moves either forwards in to AC or
backwards into vitreous
AETIOLOGY
 CONGENITAL
 ACQUIRED
1) Spontaneous – due to stretching
> Buphthalmos
> High myopia
2) Degenerative
> Hypermature cataract
3) Trauma
ECTOPIA LENTIS
 DEFINITION
Congenital bilateral subluxation or
dislocation of the lens usually upwards &
bilateral
CAUSES
 FAMILIAL
 SYSTEMIC DISEASES
> Marfan’s syndrome
> Homocystinuria
 SECONDARY TO EYE D
> Uveitis
> Hypermature cataract
> Pseudo exfoliation
TRAUMA
SYMPTOMS
 In subluxation – lens becomes spherical
producing myopic astigmatism
 In dislocation – Eye becomes
hypermetropic with loss of accomodation
 Dislocated into AC or vitreous causes
secondary glaucoma
 Uniocular diplopia & Glare
SIGNS
 Irregular deep AC with tremulousness of
iris & lens
 Dislocated lens appears in pupilary area as
a dark cresent in oblique illumination
 Posterior dislocation into vitreous causes
lens induced uveitis
TREATMENT
 Anterior dislocation – Lens removal after
controlling IOP
 Subluxation - Best possible correction
with glasses through aphakic portion
 Posterior dislocation with uveitis – lens
removal. With out uveitis no trt
MANAGEMENT OF CATARACT
 MEDICAL TRT – NOT USEFUL
 SURGICAL TRT
INDICATIONS OF SURGERY
 OPTICAL REASONS – No longer to carry
out his day to day activities with best
visual correction
 Medical reasons
> phacolytic glaucoma
> Secondary angle closure G due to
intumescent cataract
> Vitreoretinal diseases
INVESTIGATION
 To detect underlying local or systemic
pathology
 To prevent intra operative or post
operative complications
 To calculate IOL power
 To predict the visual outcome after
surgery
HISTORY
 Any trauma or inflammation of the eye
 Any posterior segment disease like
macular lesions, venous thrombosis,
vitreous hge.
 Nature of glasses, using in the past
 DM, HT, Cardiac problems, bronchial
asthma, dental & aural problems, etc.
 Drug allergy.
LOCAL INVESTIGATIONS
 OCULAR EXAMINATION
> Vn & Refraction of the eye to be
operated
> Perception of light ( PL )
> projection of rays ( PR )
> Pupilary reactions
> S\L examination
> IOP
> Patency of lacrimal passages
> Fundus examination
IMPORTANCE OF PL &PR
 No PL – Visual improvement after surgery
is nil
 Accurate PR – Excludes RD
 In accurate PR – In RD, Chorioretinal
atrophy , Advanced stage of glaucoma
SLIT LAMP EXAMINATION
 To evaluate the type & extent of cataract
 To evaluate the health of cornea
 To find out the evidences old iridocyclitis
 To find out any pathology of anterior
segment of the other eye
 Conjunctival swab for culture & sensitivity
 Calculation of IOL Power
 Macular function tests
 B – scan
 Systemic investigations
IOL POWER CALCULATION
1) Based on basic refraction
> P = 19D +[R X 1.25 ]
2) Using S R K regression formula
> keratometry
> USG – A scan
MACULAR FUNCTION TESTS
 Two point discrimation test
 Maddox rod test
 Colour vision test
 Pupillary light reflex
 Purkinje’s entoptic view of retina
 Blue field entoptoscopy
 Amsler’s Grid test
 Photo-stress test
 Laser interferometry & PAM
 Foveal ERG
 VER
 USG –B Scan
 Specular microscopy
SYSTEMIC INVESTIGATION
 Blood pressure
 Blood sugar (pp)
 Dental check up
 ENT check up
 Urine examination
 X-ray chest, ECG,
 Cardiological evaluation
SURGICAL TECNIQUES
 ICCE
 ECCE WITH IOL
 PHACO EMULSIFICATION WITH IOL
 GLAUCOMA SURGERY WITH CATARACT
SURGERY
 KERATOPLASTY WITH CATARACT
SURGERY ( Triple procedure )
ECCE
 Excision of central part of anterior capsule
 Expression of nucleus
 Cortical cleaning
 Posterior capsule, equatorial region &
peripheral part of anterior capsule are
intact
MERITS
 Chances of vitreous loss is minimal
 Vitreous related ant segment complication
are negligible
 Less chance of CME due to intact capsule
 Intact PC guards against infection for
prolonged period
DEMERITS
 Difficult microsurgical procedure
 Costly & takes time to master
 PCO is common
 Can’t be done in dislocated lens & is
difficult in subluxated lens
ICCE
 Whole crystalline lens including the
capsule is removed leaving a clear
pupillary area
MERITS
 Simple, quick, cheap, & suitable for camp
surgery
 No chance of after cataract
 No possibility of developing uveitis &
secondary glaucoma
 Cosmetically looks better
DEMERITS
 Not safe below 35 yrs
 IOL implantation impossible
 Vitreous related AC problem is higher
 Incidence of CME is higher
 Incidence of aphakic RD is high
 Corneal astigmatism is more as limbal
section is larger
PHACO EMULSIFICATION
 Basically ECCE with phacoemulsifier which
is sophisticated instrument
 Lens nucleus & cortical matter are
emulsified by ultrasonic vibration (1mm
titanium needle vibrating 40,000 times/sec
 Removed by simultaneous controlled
irrigation & aspiration
 Whole pc & part of AC are left intact
MERITS
 Sutureless cataract surgery
 More rapid wound healing
 Shorter convalescence
 Early stabilisation of refraction with
minimum or no astigmatism
DEMERITS
 The equipment is expensive
 More difficult technique
 High incidence of complications by the
beginers
 Difficult to perform in white mature
cataract & Grade 4 nuclear cataract
COMPLICATIONS
 LOCAL ANAESTHESIA
> RBH
> PERFORATION OF GLOBE
> OCULOCARDIAC REFLEX
> INTRACRANIAL SPREAD OF DRUGS
OPTICAL REHABILITATION
 SPECTACLE
 CONTACT LENS
 IOL
DURING SURGERY
 Injury to cornea – DM detachment
 Damage to endothelium
 Vitreous loss
 PC rent
 Nucleus drop
 Expulsive hge
EARLY PO COMPLICATION
( First 3 wks )
 Iris prolapse
 Flat or shallow AC (wound leak or
choroidal detachment)
 Pupilary block glaucoma
 Residual lens matter
 Secondary glaucoma
 Po iridocyclitis
 Endophthalmitis
LATE COMPLICATIONS
 CME
 PCO
 RD
 ENDOTHELIAL DECOMPENSATION
 SUN SET SYNDROME ( Inferior
subluxation )
 SUN RISE SYN ( Sup subluxation )
 WIND SHIELD WIPER SYNDROME
IOL - MATERIALS
 IDEAL MATERIAL SHOULD BE
> High optical quality
> Light wt
> Resistant to bio degradation
> Lack of inflammatory reaction
> Lack of antigenicity
> Lack of carcinogenicity
PARTS OF IOL
 OPTIC – Non foldable – PMMA
Foldable – Silicone & Hydrogel
 HAPTICS – poly propylene
PC IOL – 10 degree anterior angulation
of haptics
AC IOL - Posterior angulation of haptics
SHAPE – ROUND OR OVAL
EDGE – SQUARE OR ROUNDED
TYPES OF IOL
 Three piece lens
Optic & the haptic made of different or
same material
One piece lens
Optic & the haptic made of the same
material
SIZE OF OPTIC
5 – 6mm in diameter
TOTAL DIAMETER
13.5 – 14 mm