LENS & CATARACT

Gusti Zidni Fahmi

Tegar Chandra B.R.
LENS & CATARACT (PATHOLOGY)
 Age related cataract (Senile Cataract)
 Very common cause of visual impairment in older adults
 50-70% between ages 60-75yrs
 Pathogenesis:
 Multifactorial and not completely understood.
 As lens ages its mass 
 Thickness 
 Accommodative power 
 Lens Nucleus compressed and hardened (Nuclear
Sclerosis) as new layers of cortical fibers as formed
concentrically
 Lens proteins (Crystallines) – chemically modified and
aggregate -> protein dg BM 
The resulting proteins aggregates cause:
 Abrupt fluctuations in refractive index
 Scatter light rays
 Reduce transparency
 Chemical modification of nuclear lens proteins also
produce pigmentation (yellow/brownish with
advancing ages)
 Perubahan tsb berhubungan dg:  concentration of
glutathione and K+, conc. of Na+ and Ca++,  Hydration
 There are 3 main types of age-related cataracts:

1. Nuclear

2. Cortical
3. Posterior Subcapsular
Nuclear Cataract
In adults past middles ages
some degree of nuclear
sclerosis and yellowing is
considered physiologically
normal. This condition interferes
minimally with visual function.
Nuclear
 Excessive sclerosis and
yellowing (nuclear
sclerosis) cause central
opacity.
 Degree of scleroses,
yellowing and
opacifications
evaluated with Slit-lamp
bio-microscope with off-
axis illumination through
a dilated pupil.
Nuclear Cataract
 Progression slow
 Belateral, (± asymmetric)
 Visual impairment greater of
distance vision than of near vision
  refractive index and thus myopic
shift in refraction (Lenticular
myopia). This myopic shift
transiently enables presbyopic
individulas to read without
spectacles (second sight)

 Progressive yellowing of the lens causes poor hue discrimination

especialy at the blue end of the visible light-spectrum
 In very advanced cases the nucleus becomes opaque and
brown (brunescent nuclear cataract)
Cortical Cataract
 Early changes:
 Changes in ionic composition + hydration + cortical

opacification
 Bilateral, often asymmetrical
 A common symptom : glare from intense focal light
sources, such as car headlights. Monocular diplopia may
also result
 First visible signs of cortical cataract formation (SL bio-
microscope) are vacuoles & water clefts in ant. & post.
cortex
 Cuneiform opacities (cortical spokes): wedge shaped,
form near the periphery the lens, with pointed ends
oriented toward the center
Cortical Cataract
The cortical spokes appear white when viewed with SL bio-microscope
and dark shadows when viewed by retroillumination

 Karena lensa terus menerus menyerap air, lensa

dapat membengkak dan menjadi katarak kortikal
intumescent.
 Ketika seluruh korteks dari kapsul sampai nukleus
menjadi putih dan opak, katarak dikatakan telah
matur.
Katarak Hipermatur :
Material korteks
yang berdegenerasi
keluar melalui kapsul
lensa, sehingga
kapsul menjadi
berkerut dan
mengecil.
Morgagnian Cataract :
with further liquefaction
of the cortex allows free
movements of the
nucleus within the
capsular bag
Posterior Subcapsular
(Cupuliform) Cataract (PSC)

1. PSCs often seen in  First indication: subtle

iridescent sheen in the
patients younger than
posterior cortical layers
those presenting with (SLB exam)
nuclear/cortical  Later stages:
cataracts  Granular
opacities and
2. PSC located in the  A plaque like
posterior cortical layer opacities of
posterior
and is axial in location
subcapsular
cortex appear
Posterior Subcapsular
(Cupuliform) Cataract
(PSC)
Patient complains of :
 glare and
  vision
 PSC obscures more of the
pupillary area when miosis
is induced by:
 Bright light
 Accommodation
 Miotics
 Near VA tends to be
decreased more than
distance VA
 Some patients experience
monocular diplopia
 Other causes of PSC:
 Age related – main type
 Trauma
 Corticosteroids
 Inflammations
 Ionizing radiations
DRUG INDUCED CATARACTS

1. Corticosteroids

2. Phenothiazines

3. Miotics

4. Amiodarone

5. Tamoxifen
DRUG INDUCED CATARACTS

1. Corticosteroids  Cataract Formation: orally,

 Long term use of steroids topically, or by inhalation
cause PSCs
 The use of high-dose intraocular
steroids to treat retinal
 Occurrence related to: neovascularization and
 Dose inflammation also results in the
 Duration of development of PSCs and ocular
treatment hypertension.
 Histopathology:
 Susceptibility to
 Similar to senescent PSC
steroids (vary) changes
 Some steroid-induced PSCs in
children may be reversible with
cessation of the drug
DRUG INDUCED CATARACTS

2. Phenothiazines
 Chloropromazine, Thioridazine
 Phenotiazines, a major group of
Psycho-tropic medications, can
cause pigmented deposits in the
anterior lens epithelium in an
axial configuration
 Deposits appear to be affected
by dose and duration
 Visual changes associated with
phenothiazine are usually
insignificant
DRUG INDUCED CATARACTS

3. Miotics

 Anticholinesterases (Ecothiophate, demacrium) pilocarpine,

phospholine lodide
 These can cause cataracts
 Cataract dose and duration related
 Cataract may progress to posterior cortical and nuclear
 First appears as small vacuoles within and posterior to the anterior lens
capsule and epithelium (Best appreciated by retroillumiunation)
 Visually significant cataracts common in elderly patients (Topical
anticholinesterase)
 Progressive cataract not reported in children (Echothiophate for
accommodative esotropia)
DRUG INDUCED CATARACTS
4. Amiodarone
 Antiarrythmia medication has been
reported to cause stellate anterior
axial pigment deposition (Visually
insignificant)
5. Statin
 3-hydroxy-3-methylglutaryl coenzyme A
(HMG-CoA) reductase inhibitors 
associated with cataract when taken in
excessive doses.
 Concominant use of simvastatin and
erythromycin, which increases circulating
statin levels  associated with
approximately a twofold-increased risk of
cataract.
6. Tamoxifen
 Cataract development and
tamoxifen use were once thought to
be linked; this suggested association
has not been substantiated.
 Crystalline maculopathy has been
reported in patients receiving high-
dose tamoxifen therapy.
 Cataract development and
tamoxifen use were once thought to
be linked
 Crystalline maculopathy has been
reported in patients receiving high-
dose tamoxifen therapy
TRAUMA
1. Contusion
1.1 Vossius ring
 Blunt injury to the eye can cause a
ring of pigment (known as a Vossius
ring) from the pupillary ruff to be
imprinted on the anterior surface of
the lens
 Vossius ring is visually insignificant and
gradually resolves with time, its
presence indicates prior blunt trauma
TRAUMA
1.2 Traumatic Cataract
 Non-perforating injury may cause
lens opacification either as an
acute event or as a late sequela
 The initial manifestation of a
contusion cataract is a stellate or
rosette-shaped opacification
(rosette cataract), usually axial in
location, that involves the posterior
lens capsule
1.3 Dislocation and Subluxation
 During a blunt injury to the eye,
rapid expansion of the globe in an
equatorial plane immediately
follows compression
 Symptoms and signs of traumatic
lens subluxation include fluctuation
of vision,impaired accommodation,
monocular diplopia, and high
astigmatism
TRAUMA
2. Perforating or Penetrating
Injury
 A perforating or penetrating
injury of the lens often causes
opacification of the Complete
cortical opacification after
perforating injury, with
disruption of the lens capsule
cortex at the site of the
rupture, usually progressing
rapidly to complete
opacification
TRAUMA
3. Intraocular Procedures
 Intraocular procedure may be associated with cataract formation,
either soon after surgery or following a longer period of healing.
 Examples : posvitrectomy, Intravitreal injections, Trabeculectomy,
keratoplasty

4. Intralenticular Foreign Bodies

 Small foreign body can perforate the cornea and the anterior lens
capsule and become lodged within the lens
 Intralenticular foreign bodies may cause cataract formation in some
cases but do not always lead to lens opacification
TRAUMA
5. Radiation
5.1 Ionizing radiation
 lens is extremely sensitive to ionizing radiation

 The first clinical signs of radiation-induced cataract are often punctate

opacities within the posterior capsule and feathery anterior subcapsular
opacities that radiate toward the equator of the lens
5.2 Infrared radiation
 Exposure of the eye to infrared (IR) radiation and intense heat over time can
cause the outer layers of the anterior lens capsule to peel off as a single layer
 Cortical cataract may be associated with this condition, in which case it is
known as glassblower’s cataract
5.3 Ultraviolet radiation
 lens is susceptible to damage from ultraviolet (UV) radiation long-term exposure
to sunlight is associated with an increased risk of cortical cataracts
TRAUMA
6. Metallosis
6.1 Siderosis bulbi
 Intraocular iron-containing foreign bodies
can cause siderosis bulbi, a condition
characterized by deposition of iron
molecules in the trabecular meshwork, lens
epithelium, iris, and retina
 Later manifestations of siderosis bulbi are
complete cortical cataract formation and
retinal dysfunction
6.2 Chalcosis
 intraocular foreign body deposits copper
in the Descemet membrane, anterior lens
capsule, or other intraocular basement
membranes
TRAUMA
7. Electrical Injury
 Electrical shock can cause
protein coagulation and
cataract formation

8. Chemical Injuries
 Alkali injuries to the ocular
surface often result in cataract,
in addition to damaging the
cornea, conjunctiva, and iris.
 Cortical cataract formation may
occur acutely or as a delayed
effect of chemical injury.
METABOLIC CATARACT
1. Diabetes Mellitus
 Diabetes mellitus can affect lens
clarity as well as the refractive
index and accommodative
amplitude of the lens
 Cataract is a common cause of
visual impairment in patients with
diabetes mellitus
 Acute diabetic cataract, or
“snowflake” cataract, refers to
bilateral, widespread subcapsular
lens changes of abrupt onset and
typically occurs in young
individuals with uncontrolled
diabetes mellitus
METABOLIC CATARACT
2. Galactosemia
 Galactosemia is an inherited autosomal recessive inability to convert
galactose to glucose
 Typically, the nucleus and deep cortex become increasingly opacified,
causing an “oil droplet” appearance on retroillumination .
 The cataracts can progress to total opacification

 In posterior lenticonus, a bulge in the posterior capsule causes the oil

droplet appearance on red reflex examination.
METABOLIC CATARACT

3. Hypocalcemia
 Cataracts may develop in association with any condition that
results in hypocalcemia

4. Wilson Disease
 inherited autosomal recessive disorder of copper metabolism

 ocular manifestation of Wilson disease is the Kayser-Fleischer ring,

a golden-brown discoloration of the Descemet membrane around
the periphery of the cornea
METABOLIC CATARACT

5. Myotonic Dystrophy
 inherited autosomal dominant
condition characterized by
delayed relaxation of contracted
muscles, ptosis, weakness of the
facial musculature, cardiac
conduction defects, and
prominent frontal balding in
affected male patients
EFFECTS OF NUTRITION, ALCOHOL, AND SMOKING
 Some studies have suggested that taking multivitamin
supplements, vitamin A, vitamin C, vitamin E, niacin, thiamine,
riboflavin, or beta carotene or increasing protein intake may
protect against cataract development
 Several studies have suggested that the antioxidants lutein and
zeaxanthin provide some protection against nuclear and
cortical cataracts
 Smoking, the use of smokeless tobacco products, and
excessive alcohol consumption are significant, avoidable risk
factors for cataract
CATARACT ASSOCIATED WITH UVEITIS
 Lens changes often occur as a
result of chronic uveitis or
associated corticosteroid
therapy
 The formation of posterior
synechiae is common in uveitis
 Lens changes in cataract
secondary to uveitis may
progress to a mature cataract
 Cortical cataract formation
occurs in up to 70% of cases of
Fuchs heterochromic uveitis
LENS CHANGES WITH HYPERBARIC OXYGEN THERAPY
 The lens may also undergo changes after hyperbaric oxygen
(HBO) therapy
 Several reports have documented subsequent development of
nuclear cataract
PSEUDOEXFOLIATION SYNDROME
 Pseudoexfoliation syndrome is a systemic
disease in which a matrix of fibrotic material (a
basement-membrane-like fibrillogranular white
material) is deposited in many bodily organs
(cornea, iris, lens, anterior hyaloid face, ciliary
processes, zonular fibers, and trabecular
meshwork)
 These deposits believed to comprise elastic
microfibrils, appear as grayish-white flecks
(pupillary margin and lens capsule)
 Associated with: atrophy of the iris at the
pupillary margin, deposition of pigment on the
anterior surface of the iris, poorly dilating pupil,
increased pigmentation of the trabecular
meshwork, capsular fragility, zonular
weakness, and open-angle glaucoma.
CATARACT AND ATOPIC DERMATITIS

 Atopic dermatitis is a chronic, erythematous dermatitis, accompanied

by itching and often seen in conjunction with increased levels of
immunoglobulin E (IgE) and a history of multiple allergies or asthma
 Cataracts are usually bilateral, and onset occurs in the second to third
decade of life
 These cataracts are anterior subcapsular opacities in the pupillary area
that resemble shieldlike plaques
PHACOANTIGENIC UVEITIS
 An immune-mediated granulomatous inflammatory initiated by lens
protein released through a rupture lens capsule that trigger a severe
inflammatory reaction.
 Usually occurs with following traumatic rupture of the lens capsule or
following cataract surgery when cortical material is retained within the
eye. Onset accurs days to weeks after the injury.
 Characterized with: a red, painful eye with injection, chemosis, and
anterior chamber inflammation with the cells, flare, and keratic
precipitates. Occasionally, glaucoma develops due to obstruction of
the trabecular meshwork and formation of synechiae.
 Histologic examination: a zonal granulomatous inflammation
surrounding a breach of lens capsule.
 Lens extraction is the definitive therapy for this condition.
LENS-INDUCED GLAUCOMA

1. Phacolytic Glaucoma

 Phacolytic glaucoma is a complication of a mature or

hypermature cataract
 The usual clinical presentation of phacolytic glaucoma consists
of abrupt onset of pain and redness in a cataractous eye that
has had poor vision for some time
 Cornea may be edematous, and significant flare reaction
occurs in the anterior chamber
 Initial treatment of phacolytic glaucoma consists of controlling
the IOP with ocular hypotensive medications and managing the
inflammation with topical corticosteroids
 Surgical removal of the lens is the definitive treatment
LENS-INDUCED GLAUCOMA

2. Lens Particle Glaucoma

 Glaucoma occurs within weeks of the initial surgery or

trauma,but it may occur months or years later
 Medical therapy to lower IOP and to reduce intraocular
inflammation is indicated.
 If the IOP and inflammation do not respond quickly to this
treatment, surgical removal of the retained lens material may
be required
LENS-INDUCED GLAUCOMA
3. Phacomorphic Glaucoma
 Lens grows in the anterior–posterior
dimension it can cause pupillary
block and induce secondary angle-
closure glaucoma
 The patient presents with a red,
painful eye and a history of vision
changes as a result of cataract
formation prior to the acute event
 The cornea may be edematous, and
gonioscopy reveals a closed anterior
chamber angle
 The condition responds to laser
iridotomy, but definitive treatment
consists of cataract extraction
LENS-INDUCED GLAUCOMA

4. Glaukomflecken

 Gray-white epithelial and anterior cortical lens opacities that occur

following an episode of markedly elevated IOP
 Acute angle-closure glaucoma

ISCHEMIA
 Ischemic ocular conditions,
such as pulseless disease
(Takayasu arteritis),
thromboangiitis obliterans
(Buerger disease), and
anterior segment necrosis,
can cause PSC
 The cataract may progress
rapidly to total opacification
of the lens.
CATARACTS ASSOCIATED
WITH DEGENERATIVE OCULAR
DISORDERS
 Cataracts can occur in association
with many degenerative ocular
disorders, such as retinitis
pigmentosa, essential iris atrophy,
and chronic hypotony
 These secondary cataracts usually
begin as PSCs and may progress to
total lens opacification
BIBLIOGRAPHY

 American Academy of Ophthalmology, The Eye M.D. Association.

Pathology, Lens and Cataract, BCSC. San Fransisco: American
Academy of Ophtalmology, 2016 – 2017. 73 - 105p.
 TERIMA KASIH
Mohon Saran dan Bimbingan.