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Cataract
- 2. Definition: Any opacity in the lens or its capsule whether developmental or acquired is called a cataract. Usually developmental opacities are stationary and partial Acquired opacities progress till entire lens is involved Damage to the lens by trauma, toxins, hydration or UV rays affect lens transparency.
- 3. Cataract is due to degeneration and opacification of formed lens fibres, formation of aberrant lens fibres or deposition of other materials in their space. This is due to Hydration Denaturation of lens proteins Sclerosis
- 4. • Heredity • Age • UV radiation • Dietary deficiencies of Vitamins A,C,E • Severe diarrhoea • Diabetes • Smoking • Corticosteroids
- 5. Classification: by cause: congenital, senile(age-related), complicated, metabolitic, drug-induced, toxic, traumatic, secondary by age:congenital, acquired by location: cortical, nuclear, subcapsular by shape: dot-like, coronary, lamellar by degree: immature, intumescent, mature, hypermature
- 6. Symptoms: decreased vision: most obvious and important because of reduced transparency of lens decreased contrast sensitivty refractive error like myopia due to change in RI of nucleus and hence frequent change of glasses monocular diplopia and coloured halos due to irregular refraction by different parts of lens Glare due to scattered light rays Change in color values ie red is accentuated
- 7. Grade’s standards of nuclear hardness: Ⅰ transparent,no nucleus,soft Ⅱ yellow-white or yellow,soft Ⅲ dark yellow,moderate hard Ⅳ brown or amber, hard Ⅴ brown or black,extremely hard
- 9. The Lens Opacity Classification System II (LOCS II) photographic grading standards. N = Nuclear photographs. Stage 0 = normal; I–III = various stages of nuclear cataract. For nuclear opalescence, the average opalescence across the entire nuclear region is used. An opalescence that is less than or equal to Photographic Standard 0 = grade 0; if the opalescence is less than or equal to Standard I, the grade is 1, and so on. For Color Grading of the nucleus, only the N2 standard is used. (<N2 for color=0, equal to N2 in color=1, and N2 for color = 2) C = Cortical photographs. 0-Trace (Tr) = normal; I–IV = various steps of cortical cataract (roughly CII ¼, CIII ½, CIV ¾. CV > ¾). P = Posterior subcapsular photographs. 0 = normal; I–III = various stages of posterior subcapsular cataracts
- 10. Most common type Most patients are beyond their 50’s. Occurs equally in men and women Earlier in tropical countries Considerable genetic influences
- 11. The most common type Etiopathogenesis : Hydration followed by coagulation of proteins in the cortex. Stages: (1) Lamellar seperation (2) Incipient cataract (3) Immature stage (4) Mature stage (5) Hypermature stage
- 12. Demarcation of cortical fibres owing to their separation by fluid. Demonstrated by Slit-lamp examination only. Characteristic grey appearance of pupil due to scattering of light Changes are reversible.
- 13. Wedge shaped opacities with clear areas in between( Lens striae). Most common in periphery and lower nasal quadrant. Only seen in dilated pupil Irregularities in refraction, visual deterioration and polyopia.
- 15. Opacification becomes more diffuse and irregular. Lens is swollen. Iris shadow still visible. Anterior chamber becomes shallow.
- 17. Complete opacification Whole cortex is involved Lens appears pearly white in colour Also known as ripe cataract No iris shadow
- 19. Cortex is disintegrated and transformed into pultaceous material. Usually occurs in two forms:- 1. Morgagnian hyper–mature cataract 2. Sclerotic hyper–mature cataract
- 20. MORGAGNIAN CATARACT Complete cortex is liquefied and appears milky white in colour. Nucleus settles at the bottom. Calcium deposits may also be seen on the lens capsule. SCLEROTIC HYPER–MATURE CATARACT Disintegrated cortex. Shrunken lens sometimes appears yellow Wrinkled anterior capsule . Dense white capsular cataract in pupillary area. Deep Anterior-Chamber. Tremulous Iris .
- 22. Etio-pathogenesis:- Intensification of age related degenerative changes associated with dehydration and compaction of nucleus ie nucleur sclerosis Features: start earlier, generally on 40’s Hard cataract is formed. Significant increase in water insoluble protein. Lens becomes in-elastic and looses power of accommodation. Changes begin centrally and slowly spread to periphery. Cortex is clear
- 23. slowly progressive, not likely to be mature. Deposition of tryptophan derived pigments that gives characteristic colour to nucleus cataracta brunescens- brown cataracta nigra- black Cataracta rubra- dusky red Vision: no vision damage early, myopia due to increase in RI of nucleus .
- 25. Features: start earlier Subcapsular opacities extending towards equator posterior subcapsular cataract: cause obvious vision defect early because near the nodal point Best seen on retroillumination
- 27. Congenital cataract (present at birth) Developmental cataract (develops soon after birth) Developmental opacity are usually partial & stationary Etiology: (1) Maternal and infantile malnutrition (2) maternal infection (3) defective oxygenation
- 28. Punctate (blue dot) cataract Anterior Capsular cataract Anterior cortical cataract Pyramidal Reduplicated Posterior polar cataract Embryonal (nuclear) cataract Coronary cataract Fusiform cataract Zonular (Lamellar) cataract Total cataract
- 30. Punctate (blue dot/ cataracta coerulea) cataract: Most common type Appears as multiple, tiny blue dots scattered all over the lens, especially in the cortex. Bluish color is due to the effects of dispersion of light. When near sutures- sutural cataract Visual acuity is not affected
- 31. Anterior Polar Cataract It is sharply demarcated opacity at the anterior lens capsule. Due to delayed formation of the anterior chamber, during development due to contact of capsule and cornea It may project forwards into the anterior chamber like a pyramid (pyramidal cataract); Or underlying cortex becomes opaque (anterior cortical cataract) When both are present ther is a clear zone of subcapsular epithelium in between (reduplicated cataract) These opacities are stationary and rarely interfere with vision.
- 32. Associated with persistent hyaloid remnants(mittendorf dots),posterior lenticonus & persistent anterior fetal vasculature Common in minimal degree & visually insignificant With persistent hyaloid artery , lens deeply invaded by fibrous tissue leading to total cataract Posterior Capsular ( Polar) Cataract
- 33. Zonular (Lamellar) Cataract Accounts for 50% of visually significant cataract Zone around embryonic nucleus (usually in area of fetal nucleus) become opacified, area around opacity is clear Linear opacities like spokes of a wheel (called riders) may run outwards Usually bilateral,formed just before/shortly after birth and affect vision Often hereditary (autosomal dominant) Associated with hypovitaminosis D or hypocalcemia &maternal malnutrition
- 34. Coronary Cataract Around puberty Situated in deeper layers of cortex &superficial layers of adolescent nucleus Corona or club shaped opacities near periphery of lens ,usually hidden by iris while rest areas are free Non progressive & does not interfere with vision
- 35. Nuclear Cataract Associated with rubella Incidence more if infection contracted in 2nd month Development of lens inhibited at very early stage Embyonal nuclear cataract Progressive ,becomes total cataract Associated microphthalmos, salt and pepper retinopathy, deafness, heart defects
- 36. Fusiform Cataract Anteroposterior spindle shaped opacities sometimes with offshoots Resemble coral hence called coralliform or spindle shaped cataracts Genetically determined Discoid cataract- disc like opacity behind nucleus in posterior cortex
- 37. Cataract that develops secondary to a primary ocular disease. Characterstic feature is polychromatic lustre and bread crumb appearance Chronic anterior uveitis: most common Polychromatic lustre at posterior pole If persists anterior and posterior opacities develop
- 38. Acute congestive angle closure: focal infarcts of lens epithelium – small grey-white anterior subcapsular, or capsular opacities- glaukomfecken Pathological myopia: posterior subcapsular opacities and early onset nucleur sclerosis that increase myopia Heridity fundus dystrophies: Lebers: total cataract Stickler syndrome: cortical cataract
- 39. Diabetic cataract: Mech: hyperglycemia excess glucose to metabolize into sorbitol in lens osmotic overhydration Is of 2 types 1) classic diabetic cataract : rare, fluid vacuoles in capsule then dense white subcapsular opacities in cortex : snowflake cataract 2) age-related cataract of diabetic patients: earlier and rapid progression of senile cataract
- 40. Myotonic dystrophy: fine dust like opacities with tiny iridescent spots in cortex- christmas tree cataract May progress to stellate opacity at posterior pole Atopic dermatitis: shield like dense anterior subcapsular plaque
- 41. Galactosemia: anterior and posterior subcapsular lamellar opacities- oil drop cataract Wilsons disease: sunflower cataract Parathyroid tetany: Children : lamellar opacities Adults: anterior/ posterior punctate opacity
- 42. Snowflake cataract Christmas tree cataract Oil droplet cataract Sunflower cataract
- 43. Corticosteroid cataract : posterior subcapsular cataract Chlorpromazine cataract Miotic cataract : Anterior subcapsular cataract Trinitrotoluence cataract Other drugs like busulfan, chloroquine, amiodarone Metals like iron, gold, copper
- 44. Causes: Concussion– Rosette cataract Penetrating trauma Heat cataract: seen in glassworkers and ironworkers, small posterior cortex opacity with zonular exfoliation Radiation cataract: posterior subcapsular opacities near posterior pole Electric cataract : anterior / posterior iridescent opacities with stellate pattern