Lens Disorder Cataract and Displacement Lecture PDF

Lens Disorder Cataract and Displacement LECTURE BY ‫د سليمان يونس جعي‬ 1 Lens anatomy: 1-Gross anatomy 1-Transparent ,biconvex elastic structure. 2-Avascular( derives its nutrition from aqueous humor) and not innervated. 3-Lies behind the iris and in...

Lens Disorder Cataract and Displacement LECTURE BY ‫د سليمان يونس جعي‬ 1 Lens anatomy: 1-Gross anatomy 1-Transparent ,biconvex elastic structure. 2-Avascular( derives its nutrition from aqueous humor) and not innervated. 3-Lies behind the iris and infront of vitreous-Suspended from ciliary body by a ring of zonular fibres (suspensory ligaments/zonules of Zinn)which insert in the equatorial region. 4-In unaccommodated state: i-Equatorial diameter=10mm. ii-Thickness(anterioposterior)=4mm. iii-Anterior surface. -Radius=10mm (less convex). -Center called anterior pole. iii-Posterior surface. -Radius =6mm (more convex). -Center called posterior pole. -Nodal point lie at posterior pole of lens.-Rays entering eye through it undergo no refraction. -Dioptric power =+18D (30% of refractive power of the eye). 2 2-Lens structures 1- Capsule → i-Elastic membrane ii-Thickest in the equator zone iii-Thinnest at posterior pole iv-Responsible for moulding of lens substance during Accommodation 3 2-Subcapsular epithelium→ i-Single layer under anterior and equatorial capsule but not under posterior capsule ii-Cells at equator have mitotic activity→ new lens fibers formed throughout life. →The lens grows in both anterioposterior and equatorial dimensions throughout life 3-Lens substance→ I-Cortex –New soft lens fibers which surrounding adult nucleus II-Nucleus-Older hard lens fibers 4 nucleus→-Embryonic(the innermost fibers) -Fetal-Infantile and Adult nucleus III-Lens sutures→ Meeting of the ends of lens fibers -Anterior Y shaped suture is erect -Posterior Y shaped suture is inverted Zonules : (suspensory ligaments/zonules of Zinn) -Comprise sheets of suspensory fires (fibrilin) -Arise at ciliary body and attach to the lens pre-equatorial,equatorial, post-equatorial area 4 Lens transparency: As the cells elongate transparency attained by→ -Loss of organelles(including nucleus, mitochondria and ribosomes)→so light passing through the lens no longer absorbed or scattered by these structures -Tight regular arrangement of cell fibres (minimizing light scatter) -80% of crystallin composition -Absence of blood vessels Function of the lens: 1-To refract light (refractive power =+18D) 2-To provide accommodation 3-To absorption UVR so protect the retina 4-To maintain its own clarity As the lens ages, it increases in weight and thickness and decreases in accommodative power CATARACT Latin=waterfall/floodgate →Opacification of the lens (Any congenital or acquired opacity in the lens capsule or substance irrespective of the effect on the vision is a cataract). 5 Symptoms of cataract: → Gradual painless decrease of vision. May be C/O:Monocular diplopia,ghosting,change in refraction(myopic shift in nuclear sclerosis 6 SENILE CATARACT Lens opacity affecting old people -Is the most common type of cataract -Age-related cataract is a very common cause of visual impairment in older adult(Above 50 years) -Sex –equal male and female -Bilateral progressive lens opacification but usually one eye affected before other -Pathogenesis of cataract: unclear but may be due to: -Age changes in the permeability of lens capsule -degenerative aging process lead to lens protein lysis -UVR? -Protein denaturation by overproduction of oxidants? -The lens undergo →Hydration of lens fibres in cortex→ Opacification of cortex 7 -As new layers of cortical fibers are formed concentrically , the lens nucleus undergoes compression and hardening →Pathological nuclear sclerosis(hardness) Morphological classifications→ A-Cortical senile cataract B-Nuclear senile cataract C-Subcapsular senile cataract Types of senile cataract : According to maturity of cataract A-Cortical senile catatact: Subdivided into stages: 1-Immature stage :The lens is partially opaque Red reflex i-Opacity start as peripheral clefts and vacuoles between lens fibres in cortex (due to hydration of lens fibres)→typical cuneiform(wedge shaped) or radial spoke-like opacities(Incipient stage)→ slowly extend to center of lens and affect vision ii-Appear as dark shadow on red reflex back ground iii-Symptoms: -Vision drop to counting fingers (CF) -Glare (light scattering)from focal light sources such as car headlights -Difficulty of vision at night(night blindness) -Uniocular diplopia in incipient stage 2-Mature stage:The lens is completely opaque 8 i-The entire cortex from the capsule to the nucleus becomes white and opaque. ii-Vision drop to hand movement (HM) iii- Absent of red reflex Intumescent (swollen)cataract : In advanced immature (or mature )stage→ rapid break down of lens proteins → as the lens continue to take up water(aqueous)it becomes swollen(Intumescent) with stretched capsule → lead to shallow anterior chamber→ Phacomorphic glaucoma Shallow A/C in intumescent cat. 3-Hypermature stage: i-Typical hypermature cataract(Shrunken totally opaque lens) Cataract has shrunken and wrinkled anterior capsule due to lysis of cortex and leakage of water out of the lens →Shrunken lens substance→ I-The capsule wrinkled II-Deep anterior chamber III-Tremulous iris iv-Red reflex absent Complications 9 I-Subluxation or posterior dislocation of lens II- Leakage of irritant lens proteins into A/C lead to -Phacolytic glaucoma -Phacotoxic uveitis ii-Morgagnian cataract -The lens does not shrink -Liquefaction of cortex allows the harder nucleus to drop inferiorly, but still within the capsule B-Senile nuclear cataract: a-Do not follow cortical stages (Intumescent and hypermaturity do not occur) b-Progressive index myopia occur(presbyope may start to read without reading glasses) c-Opacity progress very slow d-Day blindness may occur due to pupil constriction e-Red reflex appears as a ring around the nuclear opacity f-Lens might acquire a color- -black cataract or cataracta nigra -brown cataract(Brunescent) 10 Characteristic of nuclear cataract: i-Do not follow cortical cataract stages (Intumescent and hypermaturity do not occur) ii-Opacity progress very slow iii-Day blindness may occur due to pupil constriction ,not effect near vision iv-Red reflex appears as a ring around the nuclear opacity v-Lens nucleus might acquire a color due to chemical modifications of lens proteins -Black cataract or cataracta nigra ---deposition of melanin -Brown cataract(Brunescent)—deposition of Urochrome pigments C-Subcapsular cataract: 1-Posterior subcapsular cat.(PSC) -Lies just in front of posterior capsule -The opacity start in central (axial) of the lens beneath the posterior lens capsule and extends peripherally -PSC manifest as vacuolated ,granular or plaque-like appearance -It has a more profound effect on vision than comparable cortical or nuclear cataract ,due to its location at nodal point of the eye Patients C/O glare and poor vision under conditions of miosis→ -Headlights of oncoming cars -Bright sunlight 11 -Near vision impaired more than distance vision (accommodation cause miosis and nodal point effected) PSC also seen in : Trauma-systemic diseases—inflammations-corticosteroids- radiations 2-Anterior subcapsular cat TRAUMATIC CATARACT Trauma is the most common cause of unilateral cataract in young. Causes: 1-Blunt trauma(contusions) – Concussion cat---- →Early –immediate after trauma →Late –after 1-2 year A concussion cataract(with intact lens capsule)initial manifestation is a stellate or rosette-shaped cat(flower-shaped cat),usually axial in location, that involve posterior cortex of the lens. Concussion injury may lead to development of Vossius ring-imprinting of iris pigment on the anterior lens capsule Vossius ring 2-Penetrating trauma With rupture of anterior capsule causing localized or total cataract 12 Complications→ Phaco-anaphylactic uveitis(phacogenic )=Iridocyclitis - It is an inflammatory reaction to lens proteins, due to rupture of anterior capsule →Secondary glaucoma due to blockage of trabecular meshwork COMPLICATED(SECONDARY)CATARACT As result of some primary ocular disease→ 1-Chronic iridocyclitis (most common) Start as polychromatic lustre at posterior pole→progress to maturity as inflammation persists 2-Retinitis pigmentosa →Posterior subcapsular opacity 3-High myopia →Posterior subcapsular and early onset nuclear sclerosis 4-Post acute congestive glauoma →anterior subcapsular or capsular opacities within pupillary area(glaucomoflecken/epithlium infarct) DRUG INDUCED CAT. 1-Steroid 13 -Both systemic and local are cataractogenic, initially posterior subcapsular then progress -Long term and high dose related to cataract formation 2-Chlorpromazine(treatment of schezophrenia)-→yellowish-brown deposit under anterior lens capsule 3-Busulphan—(treatment of leukaemia)- 4-Amiodarone—(for cardiac arrhythmias)-→anterior subcapsular opacity 5-Gold (for treatment of RA) 6-Miotics-long acting cholinsterase inhibitors →anterior subcapsular opacity 7-Allopurinol-intreatment of Gout DIABETIC CATARACT Effect of DM on the lens: Increase blood suger→increase glucose in aquoese→glucose entre lens by diffusion→increase glucose in lens in which some converted to Sorbitol→increase osmotic pressure that cause influx of water into lens which lead to swelling of lens fibres that lead to: i-Cataract ii-Transient increase in refractive index due to lenticular hydration→acute myopia iii-Decrease accommodative amplitude→early presbyopia Types of diabetic cataract: 1-Classical diabetic cataract -Due to osmotic overhydration -Appear as bilateral white punctate or snowflake cortical opacities in young with uncontrolled diabetes -Abrupt onset and rapid progression( may be resolve spontaneously or progress in few days) So a rapidly maturing bilateral cortical cataract in a child or young adult should alert the possibility of DM 2-Age-related cataract ----sorbitol accumulation →lens hydration -Occurs early in diabetics(Presenile cataract) -Nuclear opacity →progress Other cataracts with associate systemic diseases includes 1-Myotnica dystrophy-(Presenile cataract)→ stellate PSC +ptosis 14 2-Atopic dermatitis:Presenile cataract-Shield-like anterior subcapsular plaque or PSC 3-Neurofibromatosis type 2-presenile cataract (common)-PSC 4-hypoparathyroidism(hypocalcaemia)-PSC 5-Wilson disease(anterior or posterior subcapsular green ‘sunflower' cataract+corneal Kayser-Fleischer ring) RADITION CATARACT -Infrared radiation --as in Glass-blowers →exfoliation of the anterior lens capsule -UVR-UV-B range of 290-320 nm -Ionizing radiation –In treatment of ocular tumor 2-Determine the cause of cataract: by history and examination: ---- i-Age—Senile (age above 50y)or congenital (or developmental) cataract ii-History→e.g a-H/O trauma----→traumatic cataract b-Drugs history ---drug induced cataract (e.g. Steroid) 15 c-Systemic disease like DM→-Diabetic cat.(metabolic cat) iii-Proper ocular exam → anterior segment and posterior segment of BE If fundus cannot be seen due to mature cataract fundus of the other eye may be useful in bilateral disease as RP.high myopia.DR a-Looking for any signs of ---Complicated(secondary)cataract:- Chronic iridocyclitis-PS/Kps Retinitis pigmentosa-fundus examination of BE High myopia-using spectacles/refraction/fundus myopic changes Post acute congestive glaucoma (glaucomoflecken)-other signs of post ACG b-For visual prognosis :Assessment of → i -Pupillary reaction →Optic nerve function ii-Function of the retina: in case of mature cataract -Test PR (projection rays) for retinal periphery function if vision is less than 30cm -Ultrasound to detect any retinal disease like RD,introcular tumor,vitreous hg. iii-guarded visual prognosis- -Amblyopia -Corneal opacity -Macular or optic nerve disease c-Chick IOP-to detect glaucoma d-To avoid risk of sight threatening complications: Any source of infection like blepharitis, trichiasis, conjunctivitis or dacryocystitis →Should be treated first to prevent post operative endophthalmitis 3- IOL (Intraocular lens)calculation→ Biometry → Axial length by USA-scan keratometry → K1/k2 reading measures the anterior corneal surface power and axis of the least (K1-horizontal) and highest (K2-verical)meridians 16 Then for IOL power calculation: -Use formula(P=A-2.5L-0.9K) or use IOL master Types of IOL: Rigid IOLs –made of PMMA(polymethylmethacrylate) Foldable IOLs—made of silicone—Acrylic….. B-General health assessment: For diabetes, hypertension ,heart disease any drugs…. Routine investigations CATARACT SURGERY Indications of cataract surgery 1-Visual 2-Medical i -lens induced glaucoma ii -laser therapy as in DR 17 Anaesthesia Anesthesia: 1-Retrobulbar block: Aim to block the ciliary ganglion(anasthesia of iris and ciliary body)and paralysis of EOM Complications: retrobulbar hg,globe perforation 2-Akinesia: Temporary paralysis of the orbicularis muscle by facial nerve block 2-General anaesthesia-for children and psychoneurotic patients 1-Extracapsular cataract extraction(ECCE): Relatively large circumferential limbal incision(8-10mm)through which the nucleus is extracted and the cortical matter aspirated leaving behind an intact posterior capsule and IOL inserted 18 2-Phacoemulsification: Phaco is a sophesticated technique of ECCE Consists of breakdown of cataractous lens by application of ultrasounic vibration What advantage of phaco? Advantage of phaco over ECCE:→Small incision—→ I-During surgery =no eye decompression so:- -less suprachoroidal Hg. -less shallow AC -less vitreous loss(less rupture posterior capsule) II-Post-op wound problem such as iris prolapse eliminated. III-Advantage of sutureless incision → -Rapid wound healing -Post-op- less astigmatism -Early stabilization of refraction-3 weeks 3-Intracapsular cataract extraction(ICCE) 19 -The cataract is removed with its capsule -Lost popularity with introduction of modern extracapsular techniques -Its indicated in certain cases such as lens dislocation 4-I/A(Irrigation/Aspiration) Simcoe I/A cannula Phaco probe For cataract in young—(soft nucleus) By → -Automated removal-- using phaco tip or vitrector machine -Double-way cannula(Simcoe cannula) Surgical complications 1-Intraoperative complications : →Rupture of posterior capsule→Vitreous loss Complications of vitreous loss: Early→ i-iris prolapse ii-Uveitis iii-Secondary glaucoma(pupillary block glaucoma) Late→ i-Updrwan pupil 20  ii-Vitreous touch syndrome iii-Retinal detachment iv-Cystoid macular edema Management of vitreous loss → Anterior vitrectomy -clear the wound and AC of vitreous with manual (sponge /scissors)and/or automated vitrectomy +PI(Peripheral iridectomy)+A/C IOL PI A/C IOL Complications of A/CIOL→ i-Glaucoma ii-Bullous keratopathy(decompensated keratopathy) iii-UGH syndrome(uveitis/glaucoma/hyphaema) 2-Early post operative complications → Acute postop. endophthalmitis Most cases become evident within first 24-48 hr post op. Organism-staph. epidermidis,staph. aureus,pseudomonas sp. 21 Clinical pictures-→ i-Pain with marked visual loss ii-Swelling of the lids iii-Congested eye,chemosis iv-Corneal edema v-Fibrinous exudates +/- hypopyon in A/C vi- Vitritis,and an absent or diminished red reflex. Management→ 1-Antibiotic-(drops,subconj,intravitreal,systemic) 2-Steroid(drops,subconj.,or systemic in severe cases) 3-Cyclogel eye drops 4- PPV(Parsplana vitrectomy) if vision=PL and not respond to medical treatment 3-Late postoperative complications →Posterior capsular Opacification(PCO) 3 types of PCO I-Elschnig’s pearls-→ -Due to proliferation of lens epithelium onto the posterior capsule at site of opposition between the remnants of the anterior capsule with the posterior capsule. -Most frequent type 22 -Common in children-3wk-5 months of surgery -Adult-50% of cases after 3-5 years II-Primary –residual subcapsular plaque III-Capsular fibrosis Indication of treatment---DV, impaired fundus exam, monocular diplopia or sever glare Treatment---YAG laser capsulotomy What is complication of cataract if left untreated? →Lens induced glaucoma: Clinical features: I-Phacomorphic glaucoma It is an acute secondary angle closure glaucoma due to intumescent cataractous lens Clinical feature: i-Painful red eye ii-High IOP iii-Shallow AC(closed angle) due to swollen cataractous lens that cause pupillary block iv-Dilated fixed pupil v-Lens opacity 23 II-Phacolytic glaucoma(Lens protein glaucoma) It is a secondary open-angle glaucoma in association with hypermature cataract) Due to shrunken hypermature cataractous lens with leakage of lens protein in A/C (and macrophage ) causing blockage of trabecular meshwork i-Painful red eye ii-High IOP iii-Deep A/C (open angle ) with lens material floating iv-Hypermature cataract Management of lens induced glaucoma→decrease IOP medically and Then → cataract surgery Other types of cataract surgery 1-SICS-small incision cataract surgery(type of ECCE) 2-FLACS---femtosecond laser-assisted cataract surgery Do; Capsulotomy Lens fragmentation Corneal incision Congenital (developmental)cataract i-It may be at birth (congenital) or developmental in early life ii-Occur in 3:10,000 live births iii-2/3 are bilateral CLASSIFICATIONS OF CONGENITAL CATARACT 24 Clinical picture of congenital cataract Usually noticed by parents Depend on size and position of opacity→ a-Large and central opacity →marked defect of vision b-Leukocoria(white pupillary area)-if opacity is large and dense c-Squint and nystagmus Clinical types of congenital cataract Opacity usually affect a particular zone and stationary 1-Zonular(Lamellar)cat-opacity 25  Strongly hereditary and are bilateral -Affect zone or lamella of lens fibers(Opacified fetal nucleus with clear center) -Clinically → the cataract is visible as an opacified layer that surrounds a clearer center and is itself surrounded by a layer of clear cortex. Viewed from the front, the lamellar cataract has a disk shaped. Often, additional arcuate opacities called riders. 2-Anterior polar cat -Frequently hereditary - Anterior polar cataracts are sometimes seen in association with other ocular abnormalities, including microphthalmos, persistent pupillary membrane. They do not require treatment but often cause anisometropia D/D opacity due to perforated small central corneal ulcer 3-Posterior polar cat -Cause marked defect of vision as the opacity near nodal point 4-Coronory cat 26 -Club-shaped opacities in the cortex that are arranged around the equator of the lens like a crown, or corona 5-Puncate (blue-dot)cat - Are small bluish opacities located in the lens cortex -Usually not affect vision 6-Sutural cat -Opacity affect Y-shaped sutures of foetal nucleus -Usually no affect vision 7-Nuclear cat -Opacities of the embryonic nucleus alone or of both embryonic and fetal nuclei They are usually bilateral and non-progressiv 27 8-Total cat -Common with rubella infection → virus cannot cross the lens capsule after the gestational age of 6 wks so the lens is immune. But able to stay in lens for up to 3 years after birth. So cataract removal may be complicated by excessive post-opertive inflammation caused by release of these live virus particles. Congenital rubella syndrome: Triad of 1-hearing loss 2-congenital cardiac defects 3-Ocular manifestation -Congenital cataract -Micro-ophthalmia -Retinopathy Metabolic association cataract: 1-Galactosaemia(impairment of galactose utilization-defeciency of enzyme GPUT) Oil droplet lens opacity which develops within the first few days or weeks of life 2-Galactokinase deficiency Lamellar cat 3-Lowe syndrome(oculocerebrorenal)-inborn error of amino acid metabolism Cataract + microphakia 28 +Congenital glaucoma Chromosomal abnormalities association cataract: -Down syndrome: Cataract occur in 5% of patients Opacity usually symmetrical and occur in late childhood Complications of congenital cat: Unilateral cat Strabismus Defective of (amblyopia) Bilateral cat Nystagmus Defective of vision Management of congenital cataract: Timing of surgery: Critical period for vision →up to 4 months of age(foveal fixation reflex develop between 2-4 months after birth) Remove visually significant cataract as early as possible Bilateral cataract 29 -Bilateral significant cataract---remove early (first 6wks)within few days of each other—to prevent amblyopia -Partial opacity→if good vision → glasses or mydriatics(for central opacity)→follow up →If poor vision →surgery Unilateral cataract: -Dense opacity→surgery as early as possible-within days(if after 4 months of age prognosis poor) -Partial opacity-follow up with glasses and Mydriatics and treat amblyopia--- surgery Assessment of visual function in child: 30 -VER(---Visual evoked response)-record electrical activity of visual cortex in response to light stimulation of the eye -Catford drum -Preferential looking Assessment of cataract density Direct ophthalmoscope -Dense opacity-fundus cannot be seen with either direct or indirect ophthalmoscopy -Partial opacity-fundus seen with at least indirect ophthalmoscopy Systemic investigations Particularly for bilateral cataract Includes: 31 -Serological tests –TORCH(Toxoplasma-Rubella-Cytomegalovirus-Herpes virus) -Urine –for galactosaemia and Lowe syndrome -Need pediatrician referral if suspect systemic disease Types congenital cataract surgery Post-operative complications : Posterior capsular opacifications(PCO) Is nearly universal if the posterior capsule is retained(or opacification of anterior hyloid face if no anterior vitrectomy done) Visual rehabilitation i-Spectacles –older children with bilateral aphakia ii-CL-for unilateral and bilateral aphakia→Difficult for child iii-IOL-in young children---infant? iv-Occlusion therapy—to prevent amblyopia 32 DISPLACEMENT OF LENS Lens dislocation or subluxation due to rupture of zonules Causes: 1-Congenital i -Marfan syndrome(AD-abnormality of CT) lens subluxation is bilateral, symmetric ,non-progressive and upward i-Homocysteinuria(AR)-lens subluxation typically downward 2-Acquired i-Traumatic-blunt trauma ii-hypermature cat iii-large eye(high myopia-buphthalmos) Types of lens displacement: 33 Symptoms- 1-Blurred vision due to refractive error i-Posterior dislocation(aphakia) cause hypermetropia ii-Subluxation cause astigmatism and myopia 2-Uniocular diplopia if edge of the lens crosses the pupil in subluxation. Signs- 1-Iridodonesis 2-Edge of lens visible in subluxation 3-U/S show lens if posterior dislocation in vitreous 4-Dislocation in A/C visible by naked eye or slit lamp : i-If transparent lens—spherical shape like large drop of oil ii-If cataractous lens---as opaque mass Complications of A/C dislocation -Secondary glaucoma due to angle closure or pupil block 5-Posterior dislocation in vitreous- -Signs of aphakia -Lens if opaque seen by ophthalmoscope -U/S confirm diagnosis Fate of posterior dislocated lens: 1-May remain quite in vitreous 34 2-Complications→ 2-Complications→ -Secondary glaucoma → -Pupil block by vitreous or phacolytic glaucoma -lens induced uveitis Indication for removal of ectopia lens- -Secondary glaucoma (pupil block by lens/ vitreous or phacolytic) -Uniocular diplopia -Lens induced uveitis I-Treatment of A/C dislocation— 1-Immediate removal 2-Diamox to decrease IOP 3-Lens extraction by cryoprop plus anterio vitrectomy + PI+ A/C IOL II-Treatment of posterior dislocation If quiet and no complications consider IOL If complication—remove via limbal inscion APHAKIA Absence of crystalline lens from the eye Causes: 1-Post traumatic→posterior dislocation 2-Post operative→ -after cat extraction -refractive surgery(clear lens extraction in high myopia) 3-congenital -very rare Surgical aphakia:post cat extraction: Signs→- -limbal scar -deep AC -iridodonesis,the pupil may be round(with or without PI)or distorted with broad iridectomy -black jet pupil. -The eye usually hypermetropic 35 D/D of Surgical aphakia →Posterior dislocation i-Trauma ii-Congenital.. Signs -No operation -No limbal scar -no PI -Fundus exam—show lens in vitreous -US—confirm presence of lens in vit. Optical problems of Aphakia Aphakia → Hypermetropia (loss of +18 D From refractive power of the eye) Ammatropia depend on previous state of refraction -Emmetrope become hypermetrope of +10.00D -Hypermetrope become hypermetrope of > +10.00D -simple myope become less myopic or hypermetrop < +10.00 -High myope >-25.00D become emmetrope. Unilateral aphakia causing anisometropia(refraction of BE show considerable difference of > 4D) Optical rehabilitation of aphakia: -Bilateral aphakia – secondary IOL or pairs of glasses(spherical convex lens) -Unilateral aphakia— Secondary AC IOL,CL(less image magnification--5%). No glass for unilateral aphakia (with the fellow eye emmetrope)because in previously emmetrope or hypermetrope the aphakic eye will need large plus lens 36 which will magnify its retinal image by 30%,resulting in aniseikonia with difficult in fusion and binocular diplopia will result. Pseudophakia:Presence of IOL A/C IOL→ optic and haptic of IOL could be seen in A/C P/C IOL→ mirror reflection 37