OCU DIS II

• Aqueous humor flows from the posterior chamber via the pupil in the anterior chamber
• Aqueous exits the anterior chamber via:

  • Trabecular meshwork: about 90% aqueous flows through this route
  • Uveoscleral pathway: about 10% aqueous flows via the uveoscleral pathway
  • Iris: some aqueous also drains via the iris
• Anatomy of aqueous outflow includes:

  • Uveal meshwork
  • Corneoscleral meshwork
  • Schwalbe line
  • Schelmm canal
  • Collector channels
  • Longitudinal muscle of ciliary body
  • Scleral spur
• Physiology of aqueous outflow includes:

  • Conventional outflow
  • Uveoscleral outflow
  • Iris outflow
• Classification of secondary glaucoma:

  • Open-angle:
  • Pre-trabecular: membrane over trabeculum
  • Trabecular: 'clogging up' of trabeculum
  • Angle-closure:
  • With pupil block: seclusio pupillae and iris bombe
  • Without pupil block: peripheral anterior synechiae
• Tonometers:

  • Goldmann:
  • Single or triple mirror
  • Contact surface diameter 12 mm
  • Coupling substance required
  • Suitable for ALT
  • Not suitable for indentation gonioscopy
  • Zeiss:
  • Four mirror
  • Contact surface diameter 9 mm
  • Coupling substance not required
  • Not suitable for ALT
  • Suitable for indentation gonioscopy
• Indentation gonioscopy differentiates 'appositional' from 'synechial' angle closure
• Shaffer grading of angle width:

  • Grade 4 (35° - 45°): ciliary body easily visible
  • Grade 3 (25° - 35°): at least scleral spur visible
  • Grade 2 (20°): only trabeculum visible, angle closure possible but unlikely
  • Grade 1 (10°): only Schwalbe line and perhaps top of trabeculum visible, high risk of angle closure
  • Grade 0 (0°): iridocorneal contact present, apex of corneal wedge not visible, use indentation gonioscopy
• Primary open-angle glaucoma:

  • Definition and risk factor
  • Theories of glaucomatous damage
  • Optic disc cupping
  • Visual field defects
  • Medical therapy
  • Laser trabeculoplasty
  • Trabeculectomy:
  • Indications
  • Technique
  • Filtration blebs
  • Complications
• Risk factors of primary open-angle glaucoma:

  • Age: most cases present after age 65 years
  • Race: more common, earlier onset, and more severe in blacks
  • Inheritance:
  • Level of IOP, outflow facility, and disc size are inherited
  • Risk is increased by x2 if parent has POAG
  • Risk is increased by x4 if sibling has POAG
  • Myopia
• Theories of glaucomatous damage:

  • Concentric excavation:
  • Diffuse loss of nerve fibers
  • Excavation enlarges concentrically
  • Initially may be difficult to distinguish from large physiological cup
  • Compare with previous record
  • Localized cupping:
  • Focal loss of nerve fibers
  • Notching at superior or more commonly inferior poles
  • Excavation becomes vertically oval
  • Double angulation of blood vessels ('bayoneting sign')
• Progression of nerve fiber damage

  End-stage damage

  Progression of glaucomatous cupping
• Visual field defects:

  • Early
  • Progression
  • Advanced
• Drugs to treat glaucoma:

  • Beta blockers
  • Sympathomimetics
  • Miotics
  • Prostaglandin analogues
  • Carbonic anhydrase inhibitors:
  • Topical
  • Systemic
• Laser trabeculoplasty:

  • Failed medical therapy
  • Primary therapy in non-compliant patients
• Trabeculectomy:

  • Indications:
  • Failed medical therapy and laser trabeculoplasty
  • Lack of suitability for trabeculoplasty:
  • Poor patient cooperation
  • Inability to adequately visualize trabeculum
  • As primary therapy in advanced disease
  • Technique
• Filtration blebs:

  • Type 1: thin and polycystic, good filtration
  • Type 2: flat, thin, and diffuse, relatively avascular, microcysts present, good filtration
  • Type 3: flat, engorged surface vessels, no microcysts, no filtration
  • Encapsulated: localized, firm cyst, engorged surface vessels, no filtration
• Treatment options for failed trabeculectomy:

  • Digital massage
  • Laser suture lysis
  • Topical steroids
  • Subconjunctival injection of 5-FU
  • Re-operation
  • Re-commence medical therapy
• Shallow anterior chamber

  Late bleb infection:

  • Predispositions:
  • Thin-walled, cystic bleb
  • Use of adjunctive antimetabolites
  • Bleb trauma
• Primary angle-closure glaucoma:

  • Pathogenesis
  • Classification:
  • Latent: asymptomatic
  • Subacute: intermittent angle closure
  • Acute:
  • Congestive: sudden total angle closure
  • Post congestive: follows acute attack
  • Chronic: 'creeping or latent' angle closure
  • Absolute: no PL following acute attack
• Intermittent angle-closure glaucoma

  Acute congestive angle-closure glaucoma

  Treatment of acute congestive angle-closure glaucoma
• Chronic angle-closure glaucoma

  Congenital glaucoma:

  • Primary
  • Iridocorneal dysgenesis:
  • Axenfeld-Rieger Anomaly
  • Peters Anomaly
  • Aniridia
  • In phacomatoses:
  • Sturge-Weber Syndrome
  • Neurofibromatosis-1
• Primary congenital glaucoma (PCG):

  • Rare disease due to genetically determined abnormalities in the trabecular meshwork and anterior chamber angle resulting in elevated intraocular pressure (IOP), without other ocular or systemic developmental anomalies
  • Commonly presents between the ages of 3-9 months, but the most severe form is the newborn onset
  • Elevated IOP is associated with the classic triad of symptoms (photophobia, epiphora, and blepharospasm)
• • If Haab striae and buphthalmos are seen without elevated IOP, optic nerve cupping, or corneal edema, then the patient has spontaneously arrested PCG
  • 1:10,000 births, 65% boys
  • Most sporadic, 10% autosomal recessive
  • Absence of angle recess with iris inserted directly into trabeculum
• Clinical features of primary congenital glaucoma:

  • Depend on the age of onset
  • Bilateral in 75% but frequently asymmetrical
• Management of primary congenital glaucoma

  Axenfeld Anomaly

  Rieger Anomaly

  Rieger Syndrome

  Peters Anomaly

  Aniridia

  Systemic implications of aniridia
• RS ANOMALY:

  • Usually sporadic
  • Bilateral in 80%
  • Glaucoma in 50%
• ANIRIDIA:

  • AN-1: 85%
  • Autosomal dominant
  • Isolated
  • AN-2 (Miller Syndrome): 13%
  • Deletion of short arm of chromosome 11
  • Wilms tumor, genitourinary anomalies, and mental handicap
  • AN-3 (Gillespie Syndrome): 2%
  • Autosomal recessive
  • Mental handicap and cerebellar ataxia
• GLAUCOMA IN STURGE-WEBER SYNDROME
• GLAUCOMA IN NEUROFIBROMATOSIS-1
• SECONDARY GLAUCOMAS:

  1. Pseudoexfoliation glaucoma

  2. Pigmentary glaucoma

  3. Neovascular glaucoma

  4. Inflammatory glaucoma

  5. Phacolytic glaucoma

  6. Post-traumatic angle recession glaucoma

  7. Iridocorneal endothelial syndrome

  8. Glaucoma associated with iridoschisis
• PSEUDOEXFOLIATION GLAUCOMA:

  • Secondary trabecular block open-angle glaucoma
  • Affects elderly, unilateral in 60%
  • Prognosis less good than in POAG
• PIGMENTARY GLAUCOMA:

  • Bilateral trabecular block open-angle glaucoma
  • Typically affects young myopic males
  • Increased incidence of lattice degeneration
• NEOVASCULAR GLAUCOMA:

  • Common, secondary angle-closure glaucoma without pupil block
  • Caused by rubeosis iridis associated with severe, chronic, diffuse retinal ischemia
  • Signs of advanced neovascular glaucoma
• TREATMENT OPTIONS OF NEOVASCULAR GLAUCOMA:

  • Topical:
  • Atropine and steroids to decrease inflammation
  • Beta-blockers
• INFLAMMATORY GLAUCOMA
• PHACOLYTIC GLAUCOMA
• POST-TRAUMATIC ANGLE RECESSION GLAUCOMA
• CLASSIFICATION OF IRIDOCORNEAL ENDOTHELIAL SYNDROME:

  • Proliferation of abnormal corneal endothelial cells
  • Typically affects one eye of a young to middle-aged woman
  • Three syndromes with certain overlap:

  1. Progressive Iris Atrophy

  • Iris atrophy in 100%

  2. Iris Naevus (Cogan-Reese) Syndrome

  • Iris atrophy in 50%

  3. Chandler Syndrome

  • Iris atrophy in 40%
  • Corneal changes predominate
• ABNORMALITIES OF LENS SHAPE:

  1. Coloboma

  2. Lenticonus

  3. Small lens