Presented during lens session in NMCTH, Birgunj, Nepal

1. AGE RELATED CHANGES OF
LENS AND GRADING OF
CATARACT
BIPIN BISTA
RESIDENT
OPHTHALMOLOGY

2. INTRODUCTION
• LENS SHOWS AGE RELATED CHANGES IN STRUCTURE, LIGHT TRANSMISSION,
METABOLIC CAPACITY & ENZYME ACTIVITY.
• LIGHT TRANSMISSION IS DECREASED D/T INCREASED BRUNESCENCE OF LENS
• LESS ELASTIC – DECREASE IN ACCOMMODATION – PRESBYOPIA
• METABOLIC ACTIVITY IS DECREASED
• DECREASE IN ANTI-OXIDANTS
• CHANGES IN CRYSTALLINS – AGGREGATION, DEGRADATION AND INCREASED
INSOLUBILITY.

3. MORPHOLOGY
• AFTER 2ND DECADE OF LIFE, THERE IS INCREASE IN MASS AND DIMENSION D/T
PROLIFERATION OF LENS EPITHELIAL CELLS AND DIFFERENTIATION INTO LENS
FIBER.
• WITH THE CONTINUOUS GROWTH OF EPITHELIAL CELLS AGE OF CELLS DECREASE
TOWARDS OUTER UNITS OF THIS REGION AS THE NEWEST ONE IS FOUND IN
PROGERMINATIVE ZONE AND OLDEST FIBERS ARE FOUND IN CENTER OF
NUCLEUS.
• EACH GROWTH SHELL REPRESENT A FIBER THAT ARE YOUNGER THAN PRECEDING
SHELL.
• WITH AGE, EPITHELIAL CELLS GETS FLATTEN WITH INCREASING BASAL SURFACE
AREA , THUS CELL COVERAGE FOR ANTERIOR CAPSULE LESSENS WHICH LEADS

4. MORPHOLOGY
• LENS FIBER SHOWS A TOTAL LOSS OR PARTIAL DEGENERATION OF NUMBER OF
PLASMA MEMBRANE AND CYTOSKELETAL PROTEINS WITH AGEING.
• SIGNIFICANT DEGRADATION IN MAJOR INTRINSIC PROTEIN -26, SPECTRIN,
VIMENTIN AND ACTIN
• CHOLESTEROL TO PHOSPHOLIPID RATIO IS DECREASED, WHICH LEADS TO
DECREASE IN MEMBRANE FLUIDITY AND PARTIALLY RESPONSIBLE FOR NUCLEAR
SCLEROSIS
• CHANGE IN PLASMA MEMBRANE AND CYTOSKELETAL MEMBRANE LEADS INCREASE
IN NUMBER OF FURROWED MEMBRANE AND MICROVILLI
• DEEPER CORTICAL FIBERS AND NUCLEUS AREN’T PRONE TO RUPTURES D/T
INCREASED CHOLESTEROL CONTENT.

5. MORPHOLOGY-ULTRASTRUCTURAL CHANGE
• LOSS IN LAMINATION AND INCREASE IN NUMBER OF LINEAR DENSITIES.

6. PHYSIOLOGICAL CHANGES
• CHANGE IN CELLULAR JUNCTION AND ALTERATION IN CATION PERMEABILITY.
• MAJOR GAP JXN PROTEIN MIP26 LOSES IT’S A.A TO NEW VARIANTS.
• MEMBRANE POTENTIAL OF ISOLATED, PERFUSED LENS AT 20 YEARS IS -50MV BUT
AT 80 YEARS IT DECREASES TO -20MV.
• NA+ CONTENT INCREASES WITH AGE FROM 25 TO 40 MEQ/L, THUS, NA+ / K+
PERMEABILITY RATIO INCREASES APPROXIMATELY 6 TIMES WHICH WOULD LEAD
TO INCREASED OPTICAL DENSITY.
• IONIC CHANGE LEADS TO DECREASED MEMBRANE FLUIDITY ALSO RESULTS FROM
INHIBITION OF CA+ - ATPASE THUS LESSER CALCIUM ION IS PUMPED OUT.

7. BIOPHYSICAL CHANGES
• ABSORPTION OF BOTH UV RAYS AND VISIBLE LIGHT INCREASES WITH AGE.
• FREE AND BOUND AA ( TRYPTOPHAN, TYROSINE & PHENYL ALANINE),
FLUOROPHORES, YELLOW PIGMENTS AND SOME ENDOGENOUS COMPOUNDS
(RIBOFLAVIN) ARE RESPONSIBLE FOR ABSORPTION OF LENS.
• TRYPTOPHAN IS CLEAVED IN PRESENCE OF SUNLIGHT AND AIR TO FORM N-
FORMYL KYNURENINE AND METABOLIC PRODUCTS 3-HYDROXYL KYNURENINE
GLUCOSIDE (3-HKG)
• UV-A (315-400NM) AND 3-HKG ABSORBS BETWEEN (295-445 NM) AND
TRYPTOPHAN ABSORBS BETWEEN 295- 340 NM

8. BIOPHYSICAL CHANGES
• INCREASED CAPACITY OF LENS TO ABSORB LIGHT WITH INCREASED
SCATTERING PROPERTY OF LENS LEADS TO DECREASED TRANSPARENCY.
• NON ENZYMATIC GLYCATION OF PROTEIN BY MAILLARD REACTION LEADS TO
INCREASED FORMATION OF ADVANCED GLYCATION END PRODUCTS WHICH
INCREASES YELLOWING OF LENS.
• THIS REACTION IS INITIATED BY THE ATTACHMENT OF A SUGAR MOLECULE
(E.G., GLUCOSE) TO AN AMINO ACID, NORMALLY VALINE OR LYSINE. IN YOUNG
LENSES, 1.3% OF LYSINE RESIDUES OF HUMAN CRYSTALLINS (BOTH SOLUBLE
AND INSOLUBLE) ARE GLYCATED, BUT BY THE AGE OF 50 YEARS THIS
INCREASES TO 2.7% AND TO APPROXIMATELY 4.2% IN OLDER LENSES.

9. BIOCHEMICAL CHANGES
• OVERALL METABOLIC ACTIVITY DECREASES WITH AGE .
• LOSS OF PROTEIN FORMATION
• DECREASED GLUCOSE METABOLISM ( DECREASE IN GLYCERALDEHYDE-3-
PHOSPHATE DEHYDROGENASE, GLUCOSE-6-PHOSPHATE
DEHYDROGENASE,ALDOLASE,ENOLASE, PHOSPHOGLYCERYL KINASE &
PHOSPHOGLYCERATE MUTASE)
• DECREASE IN CATALASE AND SUPEROXIDE DISMUTASE , ACSCORBATE AND
GLUTATHIONE ( DECREASE IN GLUTATHIONE SYNTHEASE AND GAMMA GLUTAMYL
CYSTEINE SYNTHETHASE – DECREASE UPTAKE OF L-CYSTEINE)
• GLUTATHIONE PEROXIDES RESPONSIBLE FOR LIPID PEROXIDES AND HYDROGEN
PEROXIDE BREAKDOWN DECREASES ( REDUCED FORM >> OXIDISED FORM).

10. CRYSTALLINS
• ACCUMULATION OF HIGH–MOLECULAR-WEIGHT (HMW) AGGREGATES
• PARTIAL DEGRADATION OF POLYPEPTIDES
• INCREASED INSOLUBILITY
• PHOTO-OXIDATION OF TRYPTOPHAN AND THE PRODUCTION OF
PHOTOSENSITIZERS
• LOSS OF SULFHYDRYL GROUPS
• NONENZYMATIC GLYCATION
• DEAMIDATION OF GLUTAMINE AND ASPARAGINE RESIDUES
• RACEMIZATION OF ASPARTIC ACID RESIDUES
These changes
can alter the
short-range
spatial order of
the crystallins
and therefore
decrease
transparency

11. CRYSTALLINS
• POST-TRANSLATIONAL MODIFICATION : INTRAMOLECULAR DISULPHIDE BOND
WITHIN ALPHA A-CRYSTALLINS, GLYCATION OF LYSINE RESIDUES, CROSS –
LINKING ,DEAMIDATION OF A ALPHA CRYSTALLINE AND GAMMA S CRYSTALLINE
AND LOSS OF C-TERMINAL END OF A ALPHA CRYSTALLINE LEADS TO
DECREASE ACTIVITY OF CHAPERONE PROTEIN.
• DECREASE SOLUBILITY D/T OXIDATION OF SULFHYDRYL GROUP : LEADS TO
DISULPHIDE FORMATION
• INCREASE IN GLYCATION OF CRYSTALLINS IN PRESENCE OF GLUCOSE OR
ASCORBIC ACID RESULTS IN CROSS-LINKING AND FORMATION OF HMW.

12. CRYSTALLINS
• DEAMIDATION OF ASPARAGINASE RESIDUES CAN ALTER THE STRUCTURE ;
DISTABILISE THE PROTEIN AND INCREASE ITS SUSCEPTIBILITY TO
PROTEOLYTIC DEGRADATION.
• RACEMISATION OF ASPARTYL RESIDUE : CONVERSION OF THE L-ISOMER
(NORMAL FORM) INTO THE D-ISOMER

13. AGE RELATED CATARACTS
• NUCLEAR
• CORTICAL
• POSTERIOR SUBCAPSULAR

14. NUCLEAR CATARACT
• CAUSES CENTRAL OPACITY
• GREATER AMOUNT OF SCATTERING OF LIGHT AND
YELLOWING
• BILATERAL, ASSYMMETRIC
• POOR COLOR DISCRIMINATION
• MONOCULAR DIPLOPIA
• SLOWLY PROGRESSIVE
• GREATER VISUAL IMPAIRMENT (DISTANT>NEAR)
• LENTICULAR MYOPIA D/T INCREASED R.I
• SECOND SIGHT : IN PATIENTS WITH MYOPIC SHIFT, THEY
WILL BE ABLE TO READ WITHOUT GLASSES
• BRUNESCENT CATARACT

16. CORTICAL CATARACT
• ASSOCIATED WITH LOCAL DISRUPTION OF
MATURE LENS FIBER STRUCTURE.
• WITH THE LOSS OF ESSENTIAL
METABOLITES, EXCESSIVE PROTEIN
OXIDATION AND PRECIPITATION
• PROGRESSION VARIES
• C/O GLARE
• HISTOLOGICALLY – LOCAL SWELLING &
DISRUPTION OF LENS FIBERS CELLS &
GLOBULES OF EOSINOPHIL – MORGAGNIAN
GLOBULES.

17. CORTICAL CATARACT
• VACUOLES AND WATER CLEFT
• SEPARATION OF LAMELLAE BY THE CLEFTS
• WEDGE SHAPED OPACITY AT THE
PERIPHERY AND CENTRAL SHARP POINTED
OPACITY IN CENTER – CUNEIFORM /
CORTICAL SPOKES.
• WHITE OPACITY ON SLIT-LAMP AND DARK
SHADOWS ON RETROILLUMINATION
• WEDGE SHAPED OPACITY SPREADS ALONG
THE ADJACENT FIBERS
• INTUMESCENT CATARACT

18. HYPERMATURE CORTICAL CATARACT
• DEGENERATED CORTICAL MATTER
LEAKS AND CAUSES SHRUNKEN
CAPSULE.

19. MORGAGNIAN CATARACT
• FURTHER LIQUEFACTION OF THE
CORTEX, ALLOWS FREE MOVEMENT
OF NUCLEUS IN CAPSULAR BAG.

20. POSTERIOR SUBCAPSULAR CATARACT
• SEEN IN YOUNGER AGE THAN NUCLEAR
AND CORTICAL CATARACT
• PRESENT IN POSTERIOR CAPSULE
• LOCATED AXIALLY
• INCREASED DIMINUTION OF VISION
(NEAR>FAR) OBSCURES MORE LIGHT IN
PUPILLARY APERTURE
• GLARE
• ALSO OCCURS AS A RESULT OF
CORTICOSTEROID, ALCOHOL USE, TRAUMA
TO IONIZING RADIATION.

21. POSTERIOR SUBCAPSULAR CATARACT
• HISTOLOGICALLY, OCCURS BY POSTERIOR MIGRATION EPITHELIAL CELL
MATTER, LEADING TO SWELLING AT POSTERIOR AXIS WHICH ARE CALLED
WEDL OR BLADDER CELLS.

22. DRUG INDUCED LENS CHANGES
• CORTICOSTEROIDS : LONG TERM USE MAY CAUSE PSC. RELATED TO DOSE
AND DURATION
• INTRA-OCULAR USE FOR RETINAL NEOVASCULARISATION AND INFLAMMATION
HAS HIGHEST INCIDENCE OF PSC AND STEROID INDUCED OCULAR
HYPERTENSION

23. PHENOTHIAZINES
• PIGMENTARY DEPOSIT IN THE ANTERIOR LENS EPITHELIUM IN AN AXIAL
CONFIGURATION
• CHLORPROMAZINE AND THIORIDAZINE

24. MIOTICS
• ECHOTHIOPHATE IODIDE >> PILOCARPINE
• SEEN IN PATIENTS WITH LONGER THERAPY
• SMALL VACULOES
• PROGRESSION TO POSTERIOR CORTICAL AND NUCLEAR REGION

25. AMIODARONE
• STELLATE PIGMENT DEPOSITION IN ANTERIOR CORTICAL AXIS
• ALSO DEPOSITED IN CORNEAL EPITHELIUM AND CAUSES OPTIC
NEUROPATHIES

26. STATINS
• 3-HYDROXY-3-METHYLGLUTARYL COENZYME A (HMG-COA) REDUCTASE
INHIBITORS : INCREASED USE IS ASSOCIATED WITH NUCLEAR CATARACT.

27. TRAUMA
• CONTUSION
 VOSSIUS RING : RING OF PIGMENT FROM THE PUPILLARY RUFF TO BE IMPRINTED ON ANTERIOR
SURFACE
 TRAUMATIC CATARACT : INVOLVE ONLY A PORTION OR ENTIRE LENS, INITIALLY THERE IS STELLATE
OR ROSETTE SHAPED CATARACT USUALLY AXIAL IN LOCATION
 DISLOCATION AND SUBLUXATION : EQUATORIAL EXPANSION FOLLOWING COMPRESSION WHICH
DISRUPT ZONULAR FIBERS . COULD BE ANTERIOR OR POSTERIOR. PHACO/IRIDO DONESIS, HIGH
ASTIGMATISM, MONOCULAR DIPLOPIA.
• PERFORATING AND PENETRATING INJURY : OPACIFICATION OF CORTEX AT THE SITE
• IOFB
• RADIATION

31. RADIATION INDUCED CATARACT
• IONISING RADIATION : EXTREMELY SENSITIVE, MORE THAN 20 YEARS,
YOUNGER ARE MORE SUSCEPTIBLE , PUNCTATE OPACITY WITHIN THE
CAPSULE, FEATHERY ANTERIOR SUBCAPSULAR OPACITY THAT RADIATE TO
EQUATOR. X-RAY -0.001 TO 10 NM WAVELENGTH
• INFRARED RADIATION : GLASS BLOWER CATARACT , PEELING OFF OF THE
ANTERIOR CAPSULAR LAYER, ASSOCIATED WITH CORTICAL CATARACT
• UV RADIATION : CORTICAL CATARACT IN EXPOSURE TO SUNLIGHT.
• MICROWAVE RADIATION : LESS LIKELY IN HUMANS, ANTERIOR/POSTERIOR
SUBCAPSULAR CATARACT.

32. CHEMICAL INJURY
• ALKALI IS POTENT TO CAUSE CATARACT IN ADDITION TO DAMAGE TO CORNEA
AND CONJUNCTIVA
• INCREASES PH AND DECREASES AQUEOUS GLUCOSE AND ASCORBATE
• ACID ARE LESS LIKELY TO CAUSE CATARACT.

33. METALLOSIS
• SIDEROSIS BULBI : IRON IOFB,
EPITHELIUM AND CORTICAL FIBER :
YELLOWISH TINGE INTO RUSTY
BROWN DISCOLORATION
• CHALCOSIS : COPPER CONTAINING FB
DEPOSITS IN DM, ANTERIOR LENS
CAPSULE OR OTHER BM, RESULTING
IN SUNFLOWER CATARACT – PETAL
SHAPED DEPOSITION OF WELLOW OR
BROWN PIGMENT IN LENS CAPSULE
THAT RADIATES FROM ANTERIOR POLE
TO THE EQUATOR.

34. ELECTRICAL INJURY
• PROTEIN COAGULATION AND
CATARACT FORMATION
• MORE LIKELY IF THERE IS HEAD
TRANSMISSION
• INITIALLY, LENS VACUOLES ARE SEEN
IN ANTERIOR MID PERIPHERY AND
LATER ON LINEAR SUBCAPSULAR
OPACITIES
• MAY REGRESS, REMAIN STATIONARY
OR MAY LEAD TO COMPLETE
CATARACT.

35. METABOLIC CATARACT: DIABETES MELLITUS
• AFFECTS LENS CLARITY AS WELL AS R.I AND ACCOMMODATIVE AMPLITUDE OF LENS.
• ACUTE MYOPIC SHIFTS
• BILATERAL WIDESPREAD SUBCAPSULAR LENS
• MULTIPLE GREY WHITE OPACITIES THAT HAVE A SNOWFLAKE APPEARANCE : SUPERFICIAL
ANTERIOR AND POSTERIOR CORTEX.
• CLEFTS AND VACUOLES ARE FORMED
• UNEASY TO DIFFERENTIATE
• ACCUMULATION OF SORBITOL AND ACCOMPANYING CHANGES IN HYDRATION, INCREASED
NON-ENZYMATIC GLYCATION OF LENS PROTEIN AND INCREASED OXIDATIVE STRESS

36. SNOW FLAKE CATARACT

37. GALACTOSEMIA
• INHERITED AR DISORDER
• INABILITY TO CONVERT GALACTOSE TO GLUCOSE
• INCREASED CONVERSION INTO GALACTITOL
• DEFECT IN 1 OF 3 ENZYMES : GALACTOSE-1-PHOSPHATE URIDYLTRANSFERASE,
GALACTOKINASE, UDPGALACTOSE-4 EPIMERASE
• CLASSIC GALACTOSEMIA : GAL-1-PUT
• SYMPTOMS : MALNUTRITION, JAUNDICE, HEPATOMEGALY MENTAL DEFICIENCY (1ST WEEK OF
LIFE)
• FATAL IF UNTREATED
• “OIL DROPLET APPEARANCE ON RETROILLUMINATION

38. HYPOCALCEMIA
• IDIOPATHIC, D/T UNINTENDED DESTRUCTION OF PARATHYROID GLAND DURING
THYROID SURGERY
• PUNCTATE IRIDESCENT OPACITY IN ANTERIOR AND POSTERIOR CORTEX
• MAY BE STABLE OR PRODUCE SERIOUS COMPLICATION

39. WILSON DISEASE
• HEPATOLENTICULAR DEGENERATION
• SUNFLOWER CATARACT : REDDISH BROWN PIGMENT ON THE ANTERIOR
CAPSULE, SUBCAPSULAR CORTEX IN A STELLATE SHAPE.

40. MYOTONIC DYSTROPHY
• AD
• DELAYED RELAXATION OF CONTRACTED MUSCLES, PTOSIS, WEAKNESS OF
FACIAL STRUCTURE, CARDIAC CONDUCTION DEFECTS, PROMINENT FRONTAL
BALDING
• POLYCHROMATIC IRIDESCENT CRYSTAL MADE UP OF WHORLS OF
PLASMALEMMA FROM THE LENS FIBER.
• THESE CRYSTALS ARE SEEN IN CASES OF CHOLERSTEROL CRYSTAL
DEPOSITION AS WELL.

41. EFFECTS OF NUTRITION, ALCOHOL AND
SMOKING
• SEVERAL EPISODE OF DIARRHOEA
• ASSOCIATION OF VITAMIN A,C & E
• SMOKERS WITH HIGH LEVEL OF BETA CAROTENE HAVE INCREASED RISK OF
LUNG CANCER
• LUTEIN (SPINACH, KALE AND BROCCOLI) AND ZEAXANTHINE : CAROTENOIDS
FOUND IN LENS
• SMOKER AND ALCOHOLIC HAVE INCREASE RISK OF NUCLEAR OPACITY AND
MACULAR DEGENERATION.

42. POSTVITRECTOMY CATARACT
• TREATMENT INDUCED CATARACT
• USUALLY RESOLVES
• DEVELOPS CATARACT WITHIN TWO YEARS POST-OPERATIVELY
• ASSOCIATED WITH INCREASED OXYGEN TENSION

43. CATARACT AND HYPERBARIC OXYGEN
THERAPY
• FRANK NUCLEAR CATARACT
• RESOLVES AFTER CESSATION OF THERAPY

44. CATARACT AND ATOPIC DERMATITIS
• OCCURS IN 2ND TO 3RD DECADE
• UPTO 25% CASES
• USUALLY BILATERAL
• ANTERIOR SUBCAPSULAR OPACITY : SHIELDLIKE OPACITY

45. ISCHAEMIA
• TAKAYASU ARTERITIS
• BUERGER DISEASE
• ANTERIOR SEGMENT NECROSIS
• USUALLY CAUSE PSC

46. DEGENERATIVE OCULAR DISORDERS
• RETINITIS PIGMENTOSA
• IRIS ATROPHY
• CHRONIC HYPOTONY
• ABSOLUTE GLAUCOMA

47. • OPHTHALMOLOGY : YANOFF AND DUKER : 4TH EDITION
.AMERICAN ACADEMY OF OPHTHALMOLOGY : SECTION 11 : 2014-2015
•THANK YOU