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This document discusses the anatomy, physiology, and diseases of the lens. It provides details on:
- The structure of the lens, including its capsule, epithelium, fibers, and zonule.
- The metabolism and biochemical composition that allow the lens to remain transparent.
- The various types of cataracts including cortical, nuclear, complicated, and diabetic cataracts. Symptoms, signs, grading, and treatment are described for each type.
- Risk factors and pathophysiology involved in age-related cataract formation and progression. Stages of cortical cataract from lamellar separation to hypermature are outlined.
- Complications that can arise from cataracts
This document discusses the anatomy, physiology, and diseases of the lens. It provides details on:
- The structure of the lens, including its capsule, epithelium, fibers, and zonule.
- The metabolism and biochemical composition that allow the lens to remain transparent.
- The various types of cataracts including cortical, nuclear, complicated, and diabetic cataracts. Symptoms, signs, grading, and treatment are described for each type.
- Risk factors and pathophysiology involved in age-related cataract formation and progression. Stages of cortical cataract from lamellar separation to hypermature are outlined.
- Complications that can arise from cataracts
This document discusses the anatomy, physiology, and diseases of the lens. It provides details on:
- The structure of the lens, including its capsule, epithelium, fibers, and zonule.
- The metabolism and biochemical composition that allow the lens to remain transparent.
- The various types of cataracts including cortical, nuclear, complicated, and diabetic cataracts. Symptoms, signs, grading, and treatment are described for each type.
- Risk factors and pathophysiology involved in age-related cataract formation and progression. Stages of cortical cataract from lamellar separation to hypermature are outlined.
- Complications that can arise from cataracts
ANATOMY TRANSPARENT BICONVEX, CRYSTALLINE STRUCTURE PLACED BETWEEN IRIS & VITREOUS IN A SAUCER SHAPED DEPRESSION PATELLAR FOSSA POSTERIOR CAPSULE OF THE LENS IS ATTACHED WITH VITREOUS BY LIGAMENTUM HYALOIDEO CAPSULARE (WIEGER’S LIGAMENT) BERGER’S SPACE IS BETWEEN HYALOID FACE & LENS CAPSULE WEIGHT – 255 mg
RADIUS OF CURVATURE
>ANT SURFACE -10 mm
>POST SURFACE – 6 mm REFRACTIVE INDEX -1.39mm REFRACTIVE POWER -16 – 17 D STRUCTURE OF LENS LENS CAPSULE >Thickest basement membrane of the body > Thicker anteriorly than posteriorly > Stain positively with PAS > Highly elastic but not contain any elastic tissue ANTERIOR LENS EPITHELIUM SINGLE LAYER OF CUBOIDAL NUCLEATED EPITHELIUM METABOLIC, SYNTHETIC & TRANSPORT IN FUNCTION EQUATORIAL REGION IS COLUMNAR WHICH FORMS NEW LENS FIBRES NO POSTERIOR EPITHELIUM WHICH IS USED UP IN FILLING CENTRAL CAVITY OF LENS VESICLE LENS FIBRES FIRST FORMED FROM POSTERIOR EPITHELIUM & LATER FROM EQUATORIAL REGION HEXAGONAL IN CROSS SECTION BOUND TOGETHER BY GROUND SUBSTANCES ARRANGED IN THE FORM OF Y SHAPED SUTURES NUCLEUS > CENTRAL PART WITH OLDEST FIBRES CORTEX > PHERIPHERAL PART WITH YOUNGEST LENS FIBRES CILIARY ZONULE RUN FROM CILIARY BODY FUSE WITH OUTER LAYER OF LENS CAPSULE AROUND EQUATOR HOLD THE LENS IN POSITION ENABLE THE CILIARY MUSCLE TO ACT ON IT PHYSIOLOGY TRANSPARENCY OF THE LENS IS DUE TO > SPARSITY OF CELLS > SINGLE LAYER OF EPITHELIAL CELLS > CLOSE ALIGNMENT OF CELLS > SEMIPERMEABLE LENS CAPSULE > AVASCULARITY / SAME REFRCTIVE INDEX > PUMP MECHANISM OF LENS FIBRES > HIGH CONCENTRATION OF REDUCED GLUTATHIONE BIOCHEMICAL COMPOSITION WATER – 65% PROTEIN – 34% ( Insoluble – Albuminoid) (Soluble – Crystallines) AMINO ACIDS – No tryptophane,cystine, Hydroxy proline CARBOHYDRATES – Glucose, Fructose, LIPIDS – Lecithin ELECTROLYTES – Potassium inside the lens ASCORBIC ACID METABOLISM LENS EPITHELIUM GENERATES ENERGY FROM CARBOHYDRATE METABOLISM ANAEROBIC METABOLISM – 85% (EM Pathway) HMP SHUNT KREB’S CYCLE SORBITAL PATHWAY LENSEPITHELIUM MAINTAINS LOW CONCENTRATION OF Na/water WITHIN THE LENS BY Na-K –ATPase PUMP CATARACTOGENISIS RISK FACTORS > INCREASING AGE > U V RADIATION > DIETARY FACTORS – VIT A, C ,E Defi > SEVERE DIARRHOEA > DIABETES / HYPERTENSION / SMOKING > RENAL FAILURE > MYOPIA / GLAUCOMA > STEROIDS > GENETIC PATHOGENISIS OF CATARACT ANY OPACITY IN THE LENS OR ITS CAPSULE IS CALLED CATARACT THREE BASIC MECHANISMS > Damage to lens capsule > Changes in lens fibre protein synthesis > Increased lens hydration CORTICAL CATARACT AGING | LENS CAPSULE MORE PERMEABLE | ACCUMULATION OF Na ions& H2O | INCREASED HYDRATION DISRUPTION OF LENS FIBRE MEMBRANE | VACUOLES FORMATION | INCREASED RATIO OF INSOLUBLE TO SOLUBLE PROTEIN | OPACIFICATION NUCLEAR CATARACT U – V RADIATION | PHOTO OXIDATION OF AROMATIC AMINO ACIDS | BROWN PIGMENTATION | DEPOSITION OF ABNORMAL LIPOPROTEIN DECREASED REDUCED GLUTATHIONE | INCREASED INSOLUBLE PROTEIN | NUCLEAR CATARACT CLASSIFICATION CONGENITAL OR DEVELOPMENTAL TRAUMATIC > MECHANICAL > IRRADIATION > ELECTRIC SHOCK COMPLICATED SECONDARY TOXIC COMPLICATED CATARACT > ANTERIOR UVEITIS > HIGH MYOPIA > RETINAL DETACHMENT > RETINITIS PIGMENTOSA > GLAUKOM FLECKENS SECONDARY CATARACT > DIABETES > HYPOCALCAEMIA > MYOTONIC DYSTROPHY > ATOPIC DERMATITIS TOXIC CATARACT > CORTICOSTEROIDS > MIOTICS > CHLORPROMAZINE > GOLD SYNDROMES > DOWNE’S > LOWE’S > WILSON’S DISEASE > FABRY’S DISEASE > TREACHER COLLINS SENILE CATARACT AFTER THE AGE OF 50 BILATERAL – But develops earlier in one eye EQUAL IN MEN & WOMEN PRE SENILE CATARACT – Less than 50 yrs TYPES CORTICAL OR SOFT CATARACT (75-80%) NUCLEAR CATARACT OR HARD CATARACT (20 -25%) CORTICAL CATARACT HYDRATION FOLLOWED BY COAGULATION OF PROTEINS TWO TYPES 1) CUNEIFORM – Wedge shaped opacity at periphery 2) CUPLIFORM ( Posterior cortical cat ) Saucer shaped opacity at posterior cortex CUNEIFORM CATARACT SYMPTOMS > Painless progressive loss of vision > Uniocular diplopia or polyopia > Coloured halos > Black spots > Glare > Progressive decrease in peripheral field > White opacity inside the black of the eye STAGES STAGE OF LAMELLAR SEPARATION STAGE OF INCIPIENT CATARACT IMMATURE STAGE MATURE STAGE HYPERMATURE STAGE LAMELLAR SEPARATION Demarcation of cortical fibres by fluid Seen with S\L Invisible ophthalmoscopically Greyish in colour due to increase in reflection & scattering of light INCIPIENT CATARACT Wedge shaped spokes of opacities in periphery of the lens ( cuneiform opacities) commonly in lower nasal quadrant Sectorial alterations in the refractive indices of the lens fibres Irregular refraction & polyopia Greyish colour with oblique illumination Black against the red back ground with ophthalmoscope IMMATURE STAGE Diffuse opacification & irregular so that deeper layers of cortex become opaque & cloudy Progressive hydration of cortical layers Greyish or Greyish white colour Iris shadow present Fundal glow is faint 4th purkinje image distorted not absent IRIS SHADOW As long as any clear lens substance between pupilary margin of iris & the opacity as in IMC the iris throws a shadow upon the grey opacity when the light is cast upon the eye from one side INTUMESCENT CATARACT Progressive hydration of the cortical layers may cause swelling of the lens making anterior chamber shallow causing phacomorphic glaucoma MATURE STAGE White or pearly white No iris shadow Absent fundal glow Vn is HM or PL 4th purkinje image absent HYPERMATURE STAGE Cortex becomes disintegrated & is transformed into a pultaceous mass Lens becomes shrunken Anterior capsule becomes thickened Iris becomes tremulous AC becomes deep Degeneration of zonule leading to luxation of lens TWO TYPES A) MORGAGNIAN CATARACT B) SCLEROSIS ( shrunken cataract ) MORGAGNIAN CATARACT > Cortex becomes fluid > Nucleus sink to the bottom of the lens > liquefied cortex is milky > Nucleus is as a brown mass limited above by a semicircular line COMPLICATIONS SUBLUXATION OR DISLOCATION OF LENS LENS INDUCED GLAUCOMA LENS INDUCED UVEITIS ABSOLUTE GLAUCOMA ( No PL ) CUPLIFORM CATARACT Dense aggregations of opacities like a plaque just beneath the capsule Usually in the posterior cortex Cataract progresses towards the equator not axially towards the nucleus Seen as a yellow layer in S\L Markedly diminishes the vn Vn better in darkness NUCLEAR CATARACT Occur earlier than cortical cat (After 40) Blurs distant vn more than NV Tinted dark brown, dusky red, or even brown Colour is due to melanin deposition & photo oxidation of aromatic amino acids Progressive myopia due to increased RI Progression is very slow Hypermaturity never occurs SYMPTOMS Defective vn for distance Induced myopia Myopia neutralises plus power of presbyopia ( second sight ) Finally loss of vn SIGNS Vn is reduced to HM Yellow, brown, or black in colour Iris shadow is present Fundal glow is blackened GRADING GRADE 1 - Grey or Greenish yellow GRADE 2 - Yellow nucleus GRADE 3 - Amber GRADE 4 - Brown to black DIFF BET CORT & NUCL CAT CORTICAL CATARACT NUCLEAR CATARACT 1) Start at late 50 Earlier than cortical type 2) Uniocular diplopia, No such symptoms poyopia, halos 3)Index hypermetropia Index myopia 4)Greyish white to milky Yellow, brown or black white 5)Gradually progressive Slowly progressive Hypermaturity never ocurs COMPLICATED CATARACT Disturbances in nutrition of lens due to inflammation or degeneration CAUSES 1) IRIDOCYCLITIS 2) DEGEN MYOPIA 3) RETINITIS PIGMENTOSA 4) RETINAL DETACHMENT 5) ANTERIOR SEGMENT ISCHAEMIA FEATURES Opacification occurs in posterior cortex Ophthalmoscopically seen as dark area S/L – greyish white with irregular borders called as BREAD CRUMBS appearences Polychromatic lusture Remain stationary for long time VN much impaired as the opacity is in nodal point of the eye TREATMENT Control inflammation with local & systemic steroids IOL implantation DIABETIC CATARACT TWO TYPES 1 ) EARLY ONSET SENILE CATARACT 2 ) TRUE DIABETIC CATARACT FEATURES BILATERAL PROGRESS MORE RAPIDLY DEPEND ON DURATION OF DM INCREASED OXIDATIVE DAMAGE ANT OR POST SUB CAPSULAR REGION SNOW FLAKE CAT ( White dots ) mechanism Excessive glucose in lens | Metabolizes to sorbital | Increases osmolarity | Imbibition of H20 in to the lens form vacuoles | opacification GALACTOSAEMIA Autosomal Recessive Inherited congenital disease Inborn inability to metabolise galactose Classical – GPUT Deficiency Milder disorder – Galacto kinase deficiency Bilateral cataract , MR , Hepato spleenomegaly , failure to thrive in classical type MECHANISM Failure of conversion of Galactose to Glucose leads to increase in Galactose levels in blood & accumulation of Galactilol with in the lens Osmotic swelling of lens fibres FEATURES Bilateral cataract in early life Anterior & posterior sub capsular lamellar opacity first Later becomes total Regression occurs if milk & milk products are eliminated from the diet DIAGNOSIS REDUCING SUGAR IN URINE RBC ENZYME ASSAY TRAUMATIC CATARACT Due to penetrating injury Star shaped opacity in posterior cortex called Rosette HEAT CATARACT Prolonged exposure to IR rays Disc shaped opacity in posterior cortex True exfoliation of lens capsule IR rays absorbed by pigment of iris & CB Glass blowers cataract POSTERIOR CAPSULAR OPACIFICATION AFTER CATARACT OR SECONDARY CATARACT OPACITY WHICH FOLLOWS ECCE MECHANISM In IMC soft clear cortex sticks to the capsule Shut off by adhesion of the remains of anterior capsule to the posterior capsule Cuboidal cells that line the anterior capsule fullfil their function of forming new lens fibres Fibres are abortive & opaque as they are formed in abnormal conditions TYPES > CAPSULAR > CAPSULO LENTICULAR > PIGMENTARY or Hgic ELSCHNIG PEARLS Sub capsular cells proliferate & instead of forming lens fibres develops into large balloon like cells which fills the pupilary aperture SOMMERRING RING ENCLOSED BETWEEN TWO LAYERS OF LENS CAPSULE CAUSE TROUBLE BY BECOMING DISLOCATED INTO AC TREATMENT DISCISSION OR NEEDLING USING ZEIGLER’S KNIFE CAPSULECTOMY WITH FINE SCISSORS YAG LASER CAPSULOTOMY SUBLUXATION OF LENS Portion of zonule absent Lens is displaced sideways Remains behind the pupil DISLOCATION OF LENS Lens loses all zonular supports Lens moves either forwards in to AC or backwards into vitreous AETIOLOGY CONGENITAL ACQUIRED 1) Spontaneous – due to stretching > Buphthalmos > High myopia 2) Degenerative > Hypermature cataract 3) Trauma ECTOPIA LENTIS DEFINITION Congenital bilateral subluxation or dislocation of the lens usually upwards & bilateral CAUSES FAMILIAL SYSTEMIC DISEASES > Marfan’s syndrome > Homocystinuria SECONDARY TO EYE D > Uveitis > Hypermature cataract > Pseudo exfoliation TRAUMA SYMPTOMS In subluxation – lens becomes spherical producing myopic astigmatism In dislocation – Eye becomes hypermetropic with loss of accomodation Dislocated into AC or vitreous causes secondary glaucoma Uniocular diplopia & Glare SIGNS Irregular deep AC with tremulousness of iris & lens Dislocated lens appears in pupilary area as a dark cresent in oblique illumination Posterior dislocation into vitreous causes lens induced uveitis TREATMENT Anterior dislocation – Lens removal after controlling IOP Subluxation - Best possible correction with glasses through aphakic portion Posterior dislocation with uveitis – lens removal. With out uveitis no trt MANAGEMENT OF CATARACT MEDICAL TRT – NOT USEFUL SURGICAL TRT INDICATIONS OF SURGERY OPTICAL REASONS – No longer to carry out his day to day activities with best visual correction Medical reasons > phacolytic glaucoma > Secondary angle closure G due to intumescent cataract > Vitreoretinal diseases INVESTIGATION To detect underlying local or systemic pathology To prevent intra operative or post operative complications To calculate IOL power To predict the visual outcome after surgery HISTORY Any trauma or inflammation of the eye Any posterior segment disease like macular lesions, venous thrombosis, vitreous hge. Nature of glasses, using in the past DM, HT, Cardiac problems, bronchial asthma, dental & aural problems, etc. Drug allergy. LOCAL INVESTIGATIONS OCULAR EXAMINATION > Vn & Refraction of the eye to be operated > Perception of light ( PL ) > projection of rays ( PR ) > Pupilary reactions > S\L examination > IOP > Patency of lacrimal passages > Fundus examination IMPORTANCE OF PL &PR No PL – Visual improvement after surgery is nil Accurate PR – Excludes RD In accurate PR – In RD, Chorioretinal atrophy , Advanced stage of glaucoma SLIT LAMP EXAMINATION To evaluate the type & extent of cataract To evaluate the health of cornea To find out the evidences old iridocyclitis To find out any pathology of anterior segment of the other eye Conjunctival swab for culture & sensitivity Calculation of IOL Power Macular function tests B – scan Systemic investigations IOL POWER CALCULATION 1) Based on basic refraction > P = 19D +[R X 1.25 ] 2) Using S R K regression formula > keratometry > USG – A scan MACULAR FUNCTION TESTS Two point discrimation test Maddox rod test Colour vision test Pupillary light reflex Purkinje’s entoptic view of retina Blue field entoptoscopy Amsler’s Grid test Photo-stress test Laser interferometry & PAM Foveal ERG VER USG –B Scan Specular microscopy SYSTEMIC INVESTIGATION Blood pressure Blood sugar (pp) Dental check up ENT check up Urine examination X-ray chest, ECG, Cardiological evaluation SURGICAL TECNIQUES ICCE ECCE WITH IOL PHACO EMULSIFICATION WITH IOL GLAUCOMA SURGERY WITH CATARACT SURGERY KERATOPLASTY WITH CATARACT SURGERY ( Triple procedure ) ECCE Excision of central part of anterior capsule Expression of nucleus Cortical cleaning Posterior capsule, equatorial region & peripheral part of anterior capsule are intact MERITS Chances of vitreous loss is minimal Vitreous related ant segment complication are negligible Less chance of CME due to intact capsule Intact PC guards against infection for prolonged period DEMERITS Difficult microsurgical procedure Costly & takes time to master PCO is common Can’t be done in dislocated lens & is difficult in subluxated lens ICCE Whole crystalline lens including the capsule is removed leaving a clear pupillary area MERITS Simple, quick, cheap, & suitable for camp surgery No chance of after cataract No possibility of developing uveitis & secondary glaucoma Cosmetically looks better DEMERITS Not safe below 35 yrs IOL implantation impossible Vitreous related AC problem is higher Incidence of CME is higher Incidence of aphakic RD is high Corneal astigmatism is more as limbal section is larger PHACO EMULSIFICATION Basically ECCE with phacoemulsifier which is sophisticated instrument Lens nucleus & cortical matter are emulsified by ultrasonic vibration (1mm titanium needle vibrating 40,000 times/sec Removed by simultaneous controlled irrigation & aspiration Whole pc & part of AC are left intact MERITS Sutureless cataract surgery More rapid wound healing Shorter convalescence Early stabilisation of refraction with minimum or no astigmatism DEMERITS The equipment is expensive More difficult technique High incidence of complications by the beginers Difficult to perform in white mature cataract & Grade 4 nuclear cataract COMPLICATIONS LOCAL ANAESTHESIA > RBH > PERFORATION OF GLOBE > OCULOCARDIAC REFLEX > INTRACRANIAL SPREAD OF DRUGS OPTICAL REHABILITATION SPECTACLE CONTACT LENS IOL DURING SURGERY Injury to cornea – DM detachment Damage to endothelium Vitreous loss PC rent Nucleus drop Expulsive hge EARLY PO COMPLICATION ( First 3 wks ) Iris prolapse Flat or shallow AC (wound leak or choroidal detachment) Pupilary block glaucoma Residual lens matter Secondary glaucoma Po iridocyclitis Endophthalmitis LATE COMPLICATIONS CME PCO RD ENDOTHELIAL DECOMPENSATION SUN SET SYNDROME ( Inferior subluxation ) SUN RISE SYN ( Sup subluxation ) WIND SHIELD WIPER SYNDROME IOL - MATERIALS IDEAL MATERIAL SHOULD BE > High optical quality > Light wt > Resistant to bio degradation > Lack of inflammatory reaction > Lack of antigenicity > Lack of carcinogenicity PARTS OF IOL OPTIC – Non foldable – PMMA Foldable – Silicone & Hydrogel HAPTICS – poly propylene PC IOL – 10 degree anterior angulation of haptics AC IOL - Posterior angulation of haptics SHAPE – ROUND OR OVAL EDGE – SQUARE OR ROUNDED TYPES OF IOL Three piece lens Optic & the haptic made of different or same material One piece lens Optic & the haptic made of the same material SIZE OF OPTIC 5 – 6mm in diameter TOTAL DIAMETER 13.5 – 14 mm