Anterior eye structures disorders
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  • 1. EyeAnteriorStructuresPathlogiesandDisorders
    Fielmann
    Optometrist
    IrinaJagilovich
    e-mail: irina.jagilovica@gmail.com
  • 2. DISORDERS OF LASHES
    1. Trichiasis
    2. Metaplastic lashes
    3. Distichiasis
    4. Phthiriasispalpebrarum
    5. Madarosis
    6. Poliosis
  • 3. MadarosisDecrease in number or complete loss of lashes
    Local causes
    • Chronic anterior
    lid margin disease
    • Infiltrating tumours
    • 4. Burns, radiotherapy
    or cryotherapy
  • 5. Poliosis
    Premature localized whitening of hair
    Ocular associations
    Chronic anterior blepharitis
    Sympathetic ophthalmitis
    Systemic associations
    Vogt-Koyanagi-Harada
    syndrome
    Waardenburg syndrome
  • 6. Distichiasis
    • Second row of lashes arising from meibomian gland orifices
    • 7. Congenital
  • Trichiasis
    Most frequently affects lower lidof normal lashes
    Most frequently affects lower lid
    Inferior punctateepitheliopathy
  • 8. Phthiriasispalpebrarum
    Infestation of lashes by pubic crab louse and its ova (nits)
    Typically affects children in poor hygenic conditions
  • 9. Staphylococcal blepharitis
    Chronic irritation worse in mornings
    Hyperaemia and telangiectasia of anterior
    lid margin
    Scarring and hypertrophy if longstanding
    Scales around base of lashes
    (collarettes)
  • 10. Complications of staphylococcal blepharitis
    poliosis
    madarosis
    trichiasis
    Recurrent styes
    Marginal keratitis
    Tear film instability
  • 11. Seborrhoeicblepharitis
    Shiny anterior lid margin
    Greasy scales
    Hyperaemia of lid margin
    Lashes stuck together
  • 12. Meibomianitis
    Inflamed and blocked
    meibomiangland orifices
    Meibomian cyst formation
  • 13. Meibomianseborrhoea
    Oil globules over meibomian gland orifices
    Oily and foamy tear film
  • 14. Herpes simplex
    Signs
    • Crops of small vesicles
    • 15. Rupture and crust
    • 16. Heal without scarring
    after 7 days
    Complications
    • Follicular conjunctivitis
    • 17. Keratitis
    Treatment - topical
    antivirals
  • 18. BENIGN EYELID LESIONS
    1. Nodules
    • Chalazion
    • 19. Acute hordeola
    Molluscumcontagiosum
    Xanthelasma
    2. Cysts
    3. Tumours
  • Signs of chalazion (meibomian cyst)
    Painless, roundish, firm lesion
    within tarsal plate
    May rupture through conjunctiva
    and cause granuloma
  • 29. Molluscumcontagiosum
    Painless, waxy, umbilicated nodule
    May be multiple in AIDS patients
    Chronic follicular conjunctivitis
    Occasionally superficial keratitis
  • 30. Xanthelasma
    Common in elderly or those withhypercholesterolaemia
    Yellowish, subcutaneous plaques containing cholesterol and lipid
    Usually bilateral and located medially
  • 31. Eyelid cysts
    Cyst of Moll
    Translucent
    On anterior lid margin
    Cyst of Zeis
    Opaque
    On anterior lid margin
  • 32. Viral wart (squamous cell papilloma)
    Most common benign lid tumour
    Raspberry-like surface
  • 33. Keratoses
    Seborrhoeic
    Actinic
    Common in elderly
    Affects elderly, fair-skinned individuals
    Discrete, greasy, brown lesion
    Most common pre-malignant skin lesion
    Flat ‘stuck-on’ appearance
    Rare on eyelids
    Flat, scaly, hyperkeratotic lesion
  • 34. Keratoacanthoma
    Uncommon, fast growing nodule
    Acquires rolled edges and keratin-filled crater
    Involutes spontaneously within 1 year
  • 35. Naevi
    Elevated
    Flat, well-circumscribed
    Has both intradermal
    and junctional
    components
    May be non-pigmented
    Pigmented
    No malignant potential
    Low malignant potential
  • 36. MALIGNANT EYELID TUMOURS
    1. Basal cell carcinoma
    2. Squamous cell carcinoma
    3. Meibomian gland carcinoma
    4. Melanoma
    5. Kaposi sarcoma
  • 37. Basal Cell Carcinoma - Important Facts
    1. Most common human malignancy
    2. Usually affects the elderly
    3. Slow-growing, locally invasive
    4. Does not metastasize
    5. 90% occur on head and neck
    6. Of these 10% involve eyelids
    7. Accounts for 90% of eyelid malignancies
  • 38. Nodular basal cell carcinoma
    Shiny, indurated nodule
    Slow progression
    Surface vascularization
    May destroy large portion of eyelid
  • 39. Ulcerative basal cell carcinoma(rodent ulcer)
    Chronic ulceration
  • 40. Sclerosing basal cell carcinoma
    Indurated plaque with loss of lashes
    Spreads radially beneath normal
    epidermis
    May mimic chronic blepharitis
  • 41. Squamous cell carcinoma
    Nodular
    Ulcerative
    Less common but more aggressive than BCC
    No surface vascularization
  • 42. Meibomian gland carcinoma
    Hard nodule; may
    mimic chalazion
    Very large tumour
    Diffuse thickening of lid margin and loss of lashes
    Conjunctival invasion; may
    mimic chronic conjunctivitis
  • 43. Melanoma
    Plaque with irregular
    outline
    Blue-black nodule with
    normal surrounding skin
    May be non-pigmented
    Variable pigmentation
  • 44. Kaposi sarcoma
    Vascular tumour occurring in patients with AIDS
    Usually associated with advanced disease
    Very sensitive to radiotherapy
  • 45. Entropion & ectropion
  • 46. Horner syndrome
    Caused by oculosympatheticpalsy
    Usually unilateral mildptosis and miosis, anisocoria
    Normal pupillary reactions
  • 47. Important causes of Horner syndrome
    Central
    (first order neurone)
    Posterior hypothalamus
    • Brainstem disease
    (vascular, demyelination)
    • Spinal cord disease
    (syringomyelia, tumours)
    Pre-ganglionic
    (second order neurone)
    Superior cervical
    ganglion
    • Intrathoracic lesions
    (Pancoasttumour, aneurysm)
    • Neck lesions
    (glands, trauma)
    Post-ganglionic
    (third order neurone)
    • Internal carotid artery disease
    Ciliospinal centre of
    Budge( C8 - T2 )
    • Cavernous sinus mass
  • Simple bacterial conjunctivitis
    Subacute onset of mucopurulent
    discharge
    Crusted eyelids and conjunctival
    injection
  • 48. Signs of conjunctivitis
    Usually bilateral, acute watery
    discharge and follicles
    Subconjunctivalhaemorrhages and
    pseudomembranes if severe
  • 49. Signs of keratitis
    Focal, subepithelialkeratitis
    Focal, epithelial keratitis
    May persist for months
    Transient
  • 50. Progression of vernal conjunctivitis
    Diffuse papillary hypertrophy, most marked on superior tarsus
    Formation of cobblestone papillae
  • 51. Limbal vernal
    Trantas dots
    Mucoid nodule
  • 52. CONJUNCTIVAL TUMOURS
    1. Benign
    2. Pre-malignant
    • Primary acquired melanosis ( PAM )
    • 56. Intraepithelial neoplasia (carcinoma in situ)
    3. Malignant
  • Naevus
    Most frequently juxtalimbal
    Presents in first two decades
    Sharply demarcated and slightly
    elevated
    30% are almost non-pigmented
  • 60. Melanoma
  • 61. Papilloma
    Pedunculated
    Sessile
    • Presents in middle age
    • 62. Presents in childhood or early adulthood
    • 63. Not caused by infection
    • 64. Infection with papilloma virus
    • 65. Single and unilateral
    • 66. May be multiple and bilateral
  • Epibulbardermoid
    Signs
    Association
    • Presents in childhood
    • 67. Occasionally Goldenhar
    syndrome
    • Smooth, soft mass
    • 68. Usually juxtalimbal
  • Lipodermoid
    • Presents in adulthood
    • 69. Soft, movable, subconjunctival mass
    • 70. Most frequently at outer canthus
  • Intraepithelial neoplasia
    (carcinoma in situ)
    Signs
    Progression
    • May become vascular and extend onto
    cornea
    • Presents in late adulthood
    • 71. Juxtalimbal fleshy avascular mass
    • 72. Malignant transformation is uncommon
  • Primary acquired melanosis (PAM)
    Signs
    Types
    PAM without atypia is benign
    Presents in late adulthood
    Unilateral, irregular areas of flat,
    brown pigmentation
    PAM with atypia is pre-malignant
    May involve any part of conjunctiva
  • 73. Conjunctival melanoma
    From naevus
    Primary
    From PAM with atypia
    Very rare
    Most common type
    Solitary nodule
    Sudden appearance of
    nodules in PAM
    Frequently juxtalimbal
    but may be anywhere
    Sudden increase in size
    or pigmentation
  • 74. Squamous cell carcinoma
    Progression
    Signs
    • Arises from intraepithelial
    neoplasia or de novo
    • Slow-growing
    • 75. May spread extensively
    • 76. Presents in late adulthood
    • 77. Rarely metastasizes
    • 78. Frequently juxtalimbal
  • Kaposi sarcoma
    • Affects patients with AIDS
    • 79. Vascular, slow-growing tumour of low malignancy
    • 80. Very sensitive to radiotherapy
    • 81. Most frequently in inferior fornix
  • Lymphoma
    • Usually presents in adulthood
    • 82. Benign or malignant
    • 83. Salmon-coloured, subconjunctival infiltrate
  • PERIPHERAL CORNEAL INFLAMMATION
    1. Marginal keratitis
    2. Rosaceakeratitis
    3. Phlyctenulosis
    4. Acute stromalkeratitis
  • 84. Marginal keratitis
    Progression
    Subepithelial infiltrate
    separated by clear zone
    Vascularization
    followed by resolution
    Circumferential spread
  • 85. Rosaceakeratitis
    • Affects 5% of patients with acne rosaeca
    • 86. Bilateral and chronic
    Progression
    Peripheral inferior
    vascularization
    Subepithelial infiltration
    Thinning and
    perforationif severe
  • 87. Phlyctenulosis
    • Uncommon, unilateral - typically affects children
    • 88. Severe photophobia, lacrimation and blepharospasm
    Conjunctivalphlycten
    Corneal phlycten
    • Small pinkish-white nodule
    near limbus
    • Usually transient and resolves
    spontaneously
    • Starts astride limbus
    • 89. Resolves spontaneously or extends
    onto cornea
  • 90. Acute stromalkeratitis
    • Uncommon, usually unilateral
    • 91. Associated with non-necrotizing scleritis
    Progression
    Superficial or mid-stromal infiltration
    Opacification and vascularization
  • 92. CORNEAL INFECTIONS
    1. Bacterial keratitis
    2. Fungal keratitis
    3. Acanthamoebakeratitis
    4. Infectious crystalline keratitis
    Herpes simplex keratitis
    -Epithelial
    -Disciform
    6. Herpes zoster keratitis
  • 93. Bacterial keratitis
    • Contact lens wear
    • 94. Chronic ocular surface disease
    • 95. Corneal hypoaesthesia
    Expanding oval, yellow-white,
    dense stromal infiltrate
    Stromal suppuration and
    hypopyon
  • 96. Fungal keratitis
    Frequently preceded by ocular trauma with organic matter
    Greyish-white ulcer which may be
    surrounded by feathery infiltrates
    Slow progression and occasionally
    hypopyon
  • 97. Acanthamoebakeratitis
    • Contact lens wearers at particular risk
    • 98. Symptoms worse than signs
    Perineuralinfiltrates
    (radial
    keratoneuritis)
    Small, patchy
    Anteriorstromal
    infiltrates
    Ulceration, ring
    abscess& small,
    satellite lesions
    Stromal
    opacification
    Treatment
  • 99. Infectious crystalline keratitis
    • Very rare, indolent infection (Strep. viridans)
    • 100. Usually associated with long-term topical steroid use
    • 101. Particularly following penetrating keratoplasty
    White, branching, anterior stromal crystalline deposits
  • 102. Herpes simplex epithelial keratitis
    • Dendritic ulcer with terminal
    bulbs
    • May enlarge to become
    geographic
    • Stains with fluorescein
  • Herpes simplex disciformkeratitis
    Signs
    Associations
    Central epithelial and stromaloedema
    Occasionally surrounded by
    Wesselyring
    Folds in Descemet membrane
    Small keratic precipitates
  • 103. Herpes zoster keratitis
    Nummular keratitis
    Acute epithelial keratitis
    Develops in about 50% within
    2 days of rash
    Develops in about 30% within
    10 days of rash
    Small, dendritic or stellate
    epithelial lesions
    Multiple, fine, granular deposits
    just beneath Bowman membrane
    Tapered ends without bulbs
    Halo of stromal haze
    May become chronic
    Resolves within a few days
  • 104. CORNEAL DEGENERATIONS
    1. Age-related
    2. Lipid keratopathy
    3. Band keratopathy
    4. Spheroidal degeneration
    5. Salzmann nodular degeneration
  • 109. Arcussenilis
    • Innocuous and extremely common in elderly
    • 110. Occasionally associated with hyperlipoproteinaemia
    • 111. Peripheral border separated
    from limbus by clear zone
    • Bilateral, circumferential bands
    of lipid deposits
    • Diffuse central and sharp
    peripheral border
    • Clear zone may be thinned
    ( senile furrow)
  • 112. Vogt white limbal girdle
    Innocuous and very common in elderly
    Bilateral
    White, crescentic line along nasal and
    temporal limbus
    Type 1 - separated from limbus by clear zone
    Type 2 - not separated by clear zone
  • 113. Crocodile shagreen
    • Uncommon and innocuous
    • 114. Usually bilateral
    Polygonal stromal opacities separated by
    clear space
    Most frequently involve anterior stroma
    (anterior crocodile shagreen)
    Occasionally involve posterior stroma
    (posterior crocodile shagreen)
  • 115. Cornea guttata
    • Common, bilateral and usually innocuous
    • 116. Rarely progression to Fuchs dystrophy
    Tiny dark spots on central endothelium
  • 117. Lipid keratopathy
    Primary
    Secondary
    Common, secondary to previous
    disciformkeratitis
    Rare, occurs spontaneously in
    avascular cornea
    Unilateral stromal deposits with
    vascularization
    Usually unilateral stromal deposits
    without vascularization
  • 118. Band keratopathy
    • Common, unilateral or bilateral depending on cause
    • 119. Subepithelial calcification
    Progression
    Central spread of calcification
    Interpalpebrallimbalopacification
    Small holes within calcified area
    Separated by clear zone
  • 120. CORNEAL DYSTROPHIES
    1. Anterior
    • Cogan microcystic
    ..
    2. Stromal
    • Lattice I, II, III
    • 123. Granular I, II, III (Avellino)
    • 124. Macular
    3. Posterior
    • Fuchs endothelial
    • 125. Posterior polymorphous
  • Cogan microcystic dystrophy
    • Most common of all dystrophies
    • 126. Neither familial nor progressive
    • 127. Recurrent corneal erosions in about 10% of cases
    Dots
    Cysts
    Fingerprints
    Maps
  • 128. Signs of Cogan dystrophy
    Microcysts
    Dots
    Maps
    Fingerprints
  • 129. Reis-Bucklers dystrophy
    ..
    Onset - early childhood with recurrent corneal erosions
    Honeycomb appearance
    Superficial polygonal opacities
    keratoplastyif severe
  • 130. Meesmann dystrophy
    Onset - first decade with mild visual symptoms
    • Tiny, epithelial cysts, maximal centrally
    • 131. Clear in retroillumination
    • 132. Grey in direct illumination
    Treatment- not required
  • 133. Schnyder dystrophy
    Onset - second decade with visual impairment
    Subepithelial ‘crystalline’ opacities
    Treatment- excimer laser keratectomy
  • 134. Lattice dystrophy type I
    Onset - late first decade with recurrent corneal erosions
    Progression
    Fine, spidery, branching lines within
    stroma
    Later general haze may submerge
    lesions
    Treatment - penetrating keratoplasty if severe
  • 135. Granular dystrophy type I
    Onset - first decade with recurrent corneal erosions
    Progression
    Eventual confluence
    Initial superficial and
    central crumb-like opacities
    Later deeper and
    peripheral spread but
    limbus spared
    Treatment - penetrating keratoplasty if severe
  • 136. Fuchs endothelial dystrophy
    Onset - old age
    Progression
    Eventually bullous
    keratopathy
    Later central stromal
    oedema
    Gradual increase in
    cornea guttata with
    peripheral spread
    Treatment- penetrating keratoplasty if advanced
  • 137. CORNEAL ECTASIAS
    1. Keratoconus
    2. Keratoglobus
    3. Pellucid marginal degeneration
  • 138. Morphological classification of keratoconus
    Nipple cone
    Oval cone
    Globus cone
    Small and steep curvature
    Larger and ellipsoidal
    Largest
  • 139. Signs of keratoconus
    Bilateral in 85% but asymmetrical
    Prominent corneal nerves
    Oil droplet reflex
    Vogt striae
    Bulging of lower lids
    on downgaze
    Munson sign
    Fleischer ring & scarring
    Acute hydrops
  • 140. Keratoglobus
    Onset usually at birth
    Bilateral protrusion and thinning of entire cornea
    Associations - Leber congenital amaurosis and blue sclera
  • 141. Pellucid marginal degeneration
    • Onset between 20 and 40 years
    • 142. Bilateral crescent-shaped inferior corneal thinning
  • EPISCLERITIS AND SCLERITIS
    1. Episcleritis
    2. Anterior scleritis
    • Non-necrotizing diffuse
    • 144. Non-necrotizing nodular
    • 145. Necrotizing with inflammation
    • 146. Necrotizing without inflammation
    ( scleromalaciaperforans )
    3. Posterior scleritis
  • 147. Applied anatomy of vascular coats
    Scleritis
    Episcleritis
    Normal
    • Maximal congestion of
    deep vascular plexus
    • Radial superficial
    episcleralvessels
    • Maximal congestion
    of episcleral vessels
    • Deep vascular plexus
    adjacent to sclera
    • Slight congestion of
    episcleral vessels
  • 148. Simple episcleritis
    • Common, benign, self-limiting but frequently recurrent
    • 149. Typically affects young adults
    Simple sectorialepiscleritis
    Simple diffuse episcleritis
    • Seldom associated with a systemic disorder
  • Nodular episcleritis
    • Less common than simple episcleritis
    • 150. May take longer to resolve
    • 151. Treatment - similar to simple episcleritis
    Localized nodule which can be moved
    over sclera
    Deep scleral part of slit-beam
    not displaced
  • 152. Diffuse anterior non-necrotizing scleritis
    • Relatively benign - does not progress to necrosis
    • 153. Widespread scleral and episcleral injection
  • Complications of uveitis
    Posterior synechiae - 30%
    Cataract -20%
    Glaucoma due to PAS - 15%
    Band keratopathy - 10%
  • 154. UVEAL TUMOURS
    1. Iris melanoma
    2. Iris naevus
    3. Ciliary boy melanoma
    4. Choroidal melanoma
    5. Choroidalnaevus
    6. Choroidalhaemangioma
    7. Choroidal metastatic carcinoma
    8. Choroidal osseous choristoma
    9. Melanocytoma
  • 156. Iris Melanoma
    1. Very rare - 8% of uveal melanomas
    2. Presentation - fifth to sixth decades
    3. Very slow growth
    4. Low malignancy
    5. Excellent prognosis
  • 157. Iris melanoma
    Usually pigmented nodule at
    least 3 mm in diameter
    Invariably in inferior half of iris
    Occasionally non-pigmented
    Surface vascularization
    Angle involvement may
    causeglaucoma
    Pupillarydistortion, ectropion
    uveaeand cataract
  • 158. Differential diagnosis of iris melanoma
    Adenoma of pigment
    epithelium
    Large iris naevus distorting
    pupil
    Leiomyoma
    Ciliary body melanoma
    eroding iris root
    Metastasis to iris
    Primary iris cyst
  • 159. Iris naevus
    Diffuse
    Typical
    • Pigmented, flat or slightly elevated
    • 160. May cause ipsilateralhyperchromic
    heterochromia
    • Diameter usually less than 3 mm
    • 161. Occasionally mild distortion of pupil
    anectropionuvea
    • May be associated with
    Cogan-Reese syndrome
  • 162. Ciliary body melanoma
    • Rare - 12% of uveal melanomas
    • 163. Presentation - 6th decade
    • 164. May be discovered by chance
    • 165. Prognosis - guarded
  • Anterioruveitis
    Symptoms:acute iritis causes a sudden onset of unilateral photophobia, redness, pain and blurred vision. In chronic anterior uveitis symptoms may initially be absent or mild.
    Signs:Circumcorneal injection and a small pupil in acute iritis.
    Keratic precipitates may be small in acute iritis or large and mutton fat in granulomatous inflammation. Hypopyon and a fibrinousexudate.
  • 166. Anterioruveitis
    Posterior synechiae
    Hypopyon
  • 167. Acute anterior uveitis in young adults
    • Majority are men
    • 168. 45% are positive for HLA-B27
    • 169. Initially no systemic disease
    • 170. Minority subsequently develop ankylosing spondylitis
    Fibrinousexudate
    Residual pigment on lens
  • 171. 4. Behçet disease
    5.Vogt-Koyanagi-Harada syndrome
    7. Tubulointerstitialnephritis
    5
    5
    IMPORTANT SYSTEMIC ASSOCIATIONS OF UVEITIS
    1. Spondylarthropathies
    2. Juvenile idiopathic arthritis
    3. Sarcoidosis
    6. Inflammatory bowel disease
    • Ulcerative colitis
    • 175. Crohn disease
  • ACQUIRED CATARACT
    1. Classification of age-related cataract
    • Morphological
    • 176. According to maturity
    2. Other causes of cataracts
    3. Surgery
    • Large incision extracapsular extraction
    • 182. Phacoemulsification
  • Classification of Age-related Cataract
    According to Morphology
    1. Subcapsular
    2. Nuclear
    3. Cortical
    4. Christmas tree
  • 184. Subcapsular cataract
    Anterior
    Posterior
  • 185. Nuclear cataract
    Progression
    • Exaggeration of normal nuclear
    ageing change
    • Increasing nuclear opacification
    • 186. Causes increasing myopia
    • 187. Initially yellow then brown
  • Cortical cataract
    Progression
    Progressive radial spoke-like opacities
    Initially vacuoles and clefts
  • 188. Christmas tree cataract
    Polychromatic, needle-like opacities
    May co-exist with other opacities
  • 189. Classification according to maturity
    Immature
    Mature
    Hypermature
    Morgagnian
  • 190. Other causes of cataract - diabetes
    Juvenile
    Adult
    • Cortical and subcapsular
    opacities
    • White punctate or snowflake
    posterior or anterior opacities
    • May progress more quickly
    thanin non-diabetics
    • May mature within few days
  • Other causes of cataract - atopic dermatitis
    • Cataract develops in 10%
    of cases between 15-30 years
    • Anterior subcapsular plaque
    (shield cataract)
    • Bilateral in 70%
    • 191. Wrinkles in anterior capsule
    • 192. Frequently becomes mature
  • Causes of traumatic cataract
    Concussion
    ‘Vossius’ ring from
    imprinting of iris pigment
    Flower-shaped
    Penetration
    Other causes
  • Drugs
    Chlorpromazine
    Systemic or topical steroids
    - initially posterior subcapsular
    - central, anterior capsular granules
    • Long-acting miotics
    Other drugs
  • Secondary (complicated) cataract
    Posterior subcapsular
    Glaukomflecken
    • Chronic anterior uveitis
    • 196. Follows acute angle-closure glaucoma
    • 197. High myopia
    • 198. Central, anterior subcapsular
    opacities
    • Hereditary fundus dystrophies
  • Lenticonus
    Posterior
    Anterior
    • Posterior axial bulge
    • 199. Anterior axial bulge
    • 200. Unilateral - usually sporadic
    • 201. Associated with Alport syndrome
    • 202. Bilateral - familial or in Lowe
    syndrome
  • 203. ECTOPIA LENTIS
    1. Acquired
    2. Isolated familial ectopialentis
    3. Associated with systemic syndromes
    • Marfan syndrome
    • 204. Weill-Marchesani syndrome
    • 205. Homocystinuria
    4. Treatment options
  • 206. Acquired ectopialentis
    Stretched zonules
    Trauma
    Anterior uvealtumours
    Degenerate eye
  • 208. Ocular features of Marfan syndrome
    Upward subluxation
    Lattice
    degeneration
    Axial myopia
    Zonuleusually intact
    Angle anomaly and
    glaucoma
    Blue sclera
    Cornea plana
  • 209. Weill-Marchesani syndrome
    Ocular features
    Systemic features
    Short stature
    Microspherophakia
    Short stubby fingers (brachydactyly)
    Usually anterior lens subluxation
    Mental handicap
    Angle anomaly and glaucoma
  • 210. Homocystinuria
    • Defect in cystathio beta-synthase
    Systemic features
    Ocular features
    Malarflush and fine, fair hair
    Downward lens subluxation
    Marfanoidhabaitus
    Disintegration of zonule
    Increased platelet stickiness
    Mental handicap
  • 211. Treatment Options for EctopiaLentis
    1. Spectacle correction
    • For induced astigmatism
    • 212. For aphakic portion
    2. Nd:YAG laser zonulysisto displace lens out of visual axis
    3. Surgical removal
    • Associated cataract
    • 213. Lens-induced glaucoma
    • 214. Endothelial touch
    • 215. When other methods are inappropriate
  • Refrerencfes
    Jack J Kanski. ClinicalOphtalmology. A Systemicapproach
    Jack J Kanski. IllustratedTutorials