Download Cataract : A detailed note and more Study notes Ophthalmology in PDF only on Docsity!
Cataract
CATARACT 101 — WITH PATHOLOGY OF
EACH TYPE
A cataract is an opacity of the crystalline lens caused by biochemical degeneration of lens fibers, protein aggregation, hydration changes, and oxidative damage.
1. AGE-RELATED (SENILE) CATARACT —
TYPES & PATHOLOGY
Senile cataract occurs due to oxidative stress, UV exposure, decreased glutathione, membrane lipid peroxidation, and aggregation of crystallins.
We divide them into 3 major types:
A. Nuclear Cataract (Nuclear Sclerosis)
Pathology
Progressive sclerosis of the lens nucleus → fibers become compacted and dehydrated Increased insoluble proteins Yellow to brown pigment deposition (urochrome accumulation) Oxidation → cross-linking of crystallins Refractive index rises → myopic shift (“second sightˮ)
Clinical Clues
Central opacity Yellow → amber → brown (“brunescent cataractˮ) Distance vision worse; reading may temporarily improve
B. Cortical Cataract
Pathology
Begins in the lens cortex (outer layers) Caused by disruption of electrolyte balance → accumulation of water → formation of lamellar clefts and vacuoles These clefts coalesce into radial, wedge-shaped “spoke-likeˮ opacities Leads to swelling (intumescent cataract possible)
Clinical Clues
Radial spokes seen on oblique illumination Glare prominent Vision worse in bright light (pupil constriction exposes opacities)
C. Posterior Subcapsular Cataract (PSC)
Pathology
PSC forms at the posterior pole just in front of the posterior capsule.
Migration of epithelial cells from equator → posterior pole Abnormal cells undergo balloon-like swelling Wedl cells) Accumulation of granular globules and dysplastic fibers Affects the zone of highest visual significance (nodal point)
Clinical Clues
Early, disproportionately severe visual symptoms Severe glare, near vision affected early Seen as granular plaque-like opacity at posterior capsule
2. MATURE, HYPERMATURE &
MORGAGNIAN CATARACTS
A. Blunt Trauma — Rosette Cataract
Pathology
Shock waves through lens → disruption of posterior cortex fibers Flower-shaped (rosette) opacity around posterior pole
B. Penetrating Trauma
Pathology
Violation of capsule → hydration of lens fibers → sudden opacification May lead to membranous cataract (scarred capsule remnants)
C. Electric Shock / Radiation
Pathology
DNA damage to lens epithelial cells Opacities begin centrally or posterior subcapsular
4. DEVELOPMENTAL / CONGENITAL
CATARACTS — TYPES & PATHOLOGY
A. Zonular Lamellar) Cataract Most Common
Pathology
Defect in a specific layer of the developing lens Opacity limited to one lamella Etiology: hypocalcemia, maternal infection, hereditary
B. Nuclear Cataract Congenital Rubella)
Pathology
Intrauterine infection → damage to lens fibers → central, dense opacity
Often associated with deafness, heart disease
C. Anterior Polar Cataract
Pathology
Small, central subcapsular opacity Defective closure of fetal fissure / incomplete resorption Non-progressive
D. Posterior Polar Cataract
Pathology
Defect at posterior capsule due to persistence of hyaloid artery remnant Adherent to posterior capsule High risk of posterior capsular rupture during surgery
E. Blue Dot Cerulean) Cataract
Pathology
Tiny bluish opacities in cortex Non-progressive, hereditary Normal vision until adulthood
F. Total Congenital Cataract
Pathology
Global involvement of fibers Often due to metabolic disorders (galactosemia → oil droplet cataract)
5. SECONDARY CATARACTS — TYPES &
PATHOLOGY
A. Diabetic Cataract
Pathology
6. PATHOLOGY OF LENS IN GENERAL
(Important Theory Point)
Loss of transparency occurs due to: Protein denaturation Crystallin aggregation Increased lens permeability Reduced Na/KATPase activity Oxidative stress & free radicals Hydration changes (cortical clefts) Abnormal epithelial cell migration PSC
No vascular or nerve supply, so damage accumulates.
Comparison Table: Nuclear vs Cortical vs
Posterior Subcapsular Cataract
Feature Nuclear Cataract Cortical Cataract
Posterior Subcapsular Cataract PSC
Location Central nucleus Peripheral lens cortex Just in front ofposterior capsule
Pathology
Fiber sclerosis, pigment deposition (urochrome), ↑ insoluble proteins
Hydration, electrolyte imbalance → cortical clefts & vacuoles → radial spokes
Migration of epithelial cells Wedl cells, granular plaque at posterior pole
Appearance Yellow → amber → brown (brunescent)
Radial spoke-like opacities
Granular, plaque-like opacity at posterior pole
Onset Slow, age-related Gradual Early, disproportionatevisual symptoms
Symptoms
Distance vision poor; myopic shift (“second sightˮ)
Glare; fluctuating vision; worse in bright light
Severe glare; near vision affected early
Effect on Vision Central vision slowly↓
Peripheral → central involvement; glare significant
Early ↓ near vision; marked glare disability
Night vs Day Vision Better in dim light^ Worse in bright light^
Vision poor in bright light & dim light (glare)
Glare Mild–moderate Prominent Very prominent (mostsevere)
Refractive Change
Myopic shift (increased refractive index)
Minimal early; may cause hypermetropic shift if cortical swelling
Minimal; sometimes slight hypermetropia
Risk Factors Aging, smoking UV exposure, osmotic changes
Steroids, diabetes, uveitis, radiation
Slit Lamp Findings
Dense central opacity, brunescence
Wedge-shaped white spokes starting periphery
Fine granular opacities at posterior pole
Impact on Driving/Night Vision
Moderate High glare → difficultydriving^ Max glare → earlydifficulty
Progression Very slow Slow–moderate Fast progression Common Associations
High myopes, smokers Diabetics, dehydration^
Steroids, uveitis, radiation
Surgical Difficulty
Hard nucleus → phaco more difficult Moderate
Easier nucleus but high glare symptoms indicate early surgery
Visual Rehabilitation Good^ Good
Good but may need earlier surgery for quality of life
Clinical Features
Symptoms
Posterior subcapsular P Graded 0.16/8 depending on severity.
Complications of Cataract
Phacomorphic glaucoma (swollen lens → angle closure) Phacolytic glaucoma (leaky proteins → macrophage blockage) Subluxation/dislocation Lens-induced uveitis Mature → hypermature Morgagnian cataract
Indications for Surgery
“VISAˮ
Visual acuity poor or affecting ADL Intraocular pressure complications Suspected lens-induced pathology Aesthetic/diagnostic needs (retina evaluation)
Preoperative Assessment
Vision testing Slit lamp grading Tonometry Fundus exam (if view unclear B-scan) Biometry IOL power calculation) Keratometry Axial length Formulas: SRKII, SRK/T, Hoffer Q, Holladay 1
Management
A. Medical
NONE reverses cataract Temporary improvement with refractive correction
B. Surgical Options
1. Phacoemulsification Gold standard)
Small incision 2.23 mm) Ultrasound emulsification Foldable posterior chamber IOL Fast recovery, minimal astigmatism
2. MSICS Manual Small Incision Cataract Surgery)
Sutureless scleral tunnel Preferred for dense cataracts Low-cost, excellent outcomes
3. ECCE Extracapsular Cataract Extraction)
Large incision 10 12 mm) Rigid IOL Rare now
4. ICCE Intracapsular)
Lens + capsule removed Aphakia → anterior chamber IOL Obsolete, except hypermature subluxated cases
IOL Types (Intraocular Lenses)
Zonular dialysis Descemetʼs membrane detachment Suprachoroidal hemorrhage (rare, dangerous)
Early Post-op
Corneal edema Raised IOP Hyphema Infection (endophthalmitis) Wound leak
Late Post-op
Cystoid macular edema Irvine–Gass) Posterior capsular opacification (“after-cataractˮ) Treated by Nd:YAG capsulotomy
IOL decentration/dislocation Chronic uveitis Special Cataracts
Diabetic Cataract
“Snowflake cataractˮ in young diabetics Earlier PSC in adults
Steroid-Induced Cataract
Classically PSC
Traumatic Cataract
Rosette-shaped after blunt trauma Membranous in penetrating injury
Congenital Cataracts
Lamellar, nuclear, blue dot, rosette, polar (anterior/posterior) Indications for early surgery: visual axis obstruction → risk of amblyopia
1. Nuclear Cataract — Diagram +
Explanation
_________
/ \
| NUCLEUS | Central yellow/brown opacity
| Dense) |
_________/
| |
Cortex) (Cortex)
Diagram Interpretation
The central nucleus becomes sclerotic, compact, and yellow-brown. Pigment deposition (urochrome) makes it brunescent. Increasing refractive index → myopic shift (“second sightˮ).
Pathology
Nuclear fiber dehydration Protein denaturation Cross-linking of crystallins Oxidative stress from aging & smoking
2. Cortical Cataract — Diagram +
Explanation
____________________
Pathology
Abnormal migration of epithelial cells to posterior pole Swollen dysplastic cells Wedl cells) Granular deposits due to steroid/diabetes/uveitis damage
4. Mature Cataract
____________________
| Entire Lens → |
| Completely | Homogeneously white/opaque lens
| Opaque |
____________________/
Diagram Interpretation
Whole lens becomes pearly white. No red reflex.
Pathology
Total cortical opacification Loss of transparency in all layers
5. Hypermature Cataract (Morgagnian)
________
/ \
| ( ) | Floating brown nucleus
| | Liquefied cortex (“milkyˮ)
________/
Diagram Interpretation
Cortex liquefies (white milk-like fluid).
Dense nucleus sinks to bottom. Capsule becomes wrinkled.
Pathology
Liquefaction of cortex Leakage of lens proteins → phacolytic glaucoma Capsular fibrosis/shrinkage
6. Traumatic Rosette Cataract
_________
/ * * \
| * * * | Star / flower-shaped (rosette) opacity
\ * * * * /
Diagram Interpretation
Posterior cortex exhibits flower-shaped opacities. Occurs after blunt trauma.
Pathology
Shock-wave disruption of posterior lens fibers
7. Congenital Lamellar (Zonular) Cataract
_________
/ _____ \
| | | | Opacity confined to one “ringˮ (lamella)
_______/
Diagram Interpretation
One ring (lamella) affected: central clear, outer clear. Classically symmetric.
Sorbitol accumulation → osmotic swelling → cortical vacuoles
