ARI SURYA Definition Glaucoma refers to a group of diseases that have in common a characteristic optic Neuropathy with associated visual field loss for.

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2 ARI SURYA

3 Definition Glaucoma refers to a group of diseases that have in common a characteristic optic Neuropathy with associated visual field loss for which elevated intraocular pressure (IOP) is one of the primary Risk factors.

4 Definition…  Primary glaucoma = are not associated with known ocular or systemic disorders that cause in creased resistance to aqueous out flow = both eye = inherited  Secondary glaucoma  associated with ocular or systemic disorders. = Unilateral = familial occurance is less common

5 CLASSIFICATION OPEN ANGLE GLAUCOMA Primary open angle glaucoma Normal tension glaucoma Juvenile open angle glaucoma Glaucoma suspect Secondary open angle glaucoma

6 CLASSIFICATION OPEN ANGLE GLAUCOMA Primary open angle glaucoma Normal tension glaucoma Juvenile open angle glaucoma Glaucoma suspect Secondary open angle glaucoma

7 CLASSIFICATION… Secondary open angle glaucoma ↑ resistensi to TM outflow ~other condition Pigmentary gl Phacolytic gl Steroid induced gl Exfolia tion Angle recession g l ↑ post TM resist to outflow secondary Carotid cavernous sinus fistula

8 Secondary Open – Angle Glaucoma 1. Exfoliation Syndrome (Pseudoexfoliation)  Characterized by the deposition of a distinctive fibrillar material in the anterior segments of the eye  Histochemical : elastic microfibrils &extracelluler matrixs  Origin materials :? Basement membrane disorder  Monocular/binocular

9 SOAG Exfoliation Syndrome (Pseudoexfoliation)  Founds : ○ Lens Epithelium & capsule >> ant lens capsule  dilated pupil ○ Pupilliary margin ○ Ciliary epithelium, ○ Iris pigmen epithelium, iris stroma, iris blood vessels ○ Subconjunctiva tissue ○ Zonulla fibers of the lens ○ Corneal endothelium ○ Anterior hyaloid  for aphakic

10  A central area and a peripheral zone of deposition are usually separated by an intermediate clear area

11 SOAG Exfoliation Syndrome (Pseudoexfoliation)  Examination Chamber angle narrow  ant movement lens-iris diaphragma related to zonular weakness TM : heavily brown pigmented SL : Sampaolesi line Pupil : dilated poorly Phacodonesis & Iridodonesis  zonular weakness

12 SOAG Exfoliation Syndrome (Pseudoexfoliation)  Threatment : Laser trabeculoplasty Response may not last Trabeculectomy Increase in postoperative inflammation

13 SOAG 2. Lens-Induced Glaucoma

14 SOAG- Lens Induced Gl Phacolytic glaucoma mature or hypermature cataractthe leakage of lens protein through the capsuleInflammatory debris/ macrophage obstruct TMPhacolytic glaucoma

15 SOAG- Lens Induced Gl Phacolytic glaucoma  Clinically: Elderly with history of poor vision Sudden onset of pain Conjungtival hyperemia Markedly elevated IOP Microcystic corneal edema Cell & flare without KP Open anterior chamber angle  Th/ cataract extraction with medications to control IOP before surgery

16 SOAG- Lens Induced Gl Phacolytic glaucoma

17 SOAG- Lens Induced Gl Lens Particle glaucoma  If lens cortex particles obtruct TM after cataract extraction, capsulotomy, ocular trauma( penetrating lens)  Depend on - quantity of lens material released Degree of inflammation Ability of TM to clear lens material Functional status of the ciliary body  Occur >> within weeks of the initial surgery/trauma

18 SOAG- Lens Induced Gl Lens Particle glaucoma  Clinical findings: Free cortical material in anterior chamber IOP ↑ Moderate anterior chamber reaction Microcystic corneal edema Posterior synechiae & PAS  Th/ - medical th to control IOP  material resorbs ○ Mydriatics ○ Topical steroid ○ Surgical removal of the lens material

19 SOAG- Lens Induced Gl Lens Particle glaucoma

20 SOAG Intraocular Tumors Mechanism depens on size, type & location  direct tumor invasion of the anterior chamber angle  angle closure by rotation of the ciliary body / ant displacement of the lens-iris diaphragma  intraocular hemorrhage  neovascularization of the angle  deposition of tumor cells, inflammatory cells, & celluler debris on TM

21 SOAG Ocular Inflammation Mechanisms:  Edema of TM  TM endothelial cell dysfunction  Blockage of TM by fibrin & inflammatory cells  Prostaglandin – mediated breakdown of the blood-aqueous barrier  Blockage of Schlemm’s canal by inflammatory cells  Steroid induced reduction in aqueous outflow through TM

22 SOAG- Ocular Inflammation…  >> anterior uveitis idiopathic : herpes zoster iridocyclitis, herpes simplex keratouveitis, toxoplasmosis, rhematoid arthritis, pars planitis  Clinical finding: KP Precipitates on TM PAS / post sinechiae with iris bombe  angle closure

23 SOAG- Ocular Inflammation…  Th/ complicated Corticosteroid ↑IOP Miotic :avoid in iritis  aggravate inflammation, post sinechiae Prostaglandin analog  exacerbate inflammation

24 SOAG Accidental & Surgical Trauma  k/ Non penetrating trauma : Hyphema Angle recession Iridodialysis Iris sphincter tear Cyclodialysis Lens subluxation

25 SOAG-Accidental & Surgical Trauma Hyphema  ↑ IOP : recurrent hemorrhage / rebleeding ○ Obstruction RBCs, inflammatory cell, debris & fibrin on TM or direct injury to TM  Rebleeding following hyphema ± 5-10% ○ Within 3-7 days of the initial hyphema  Sickle cell hemoglobinopathies: ○ >> ↑ IOP after hyphema ○ RBCs tend to sickle in AC ~ acidity of the stagnant aqueous ○ Rigid cell  difficult pass TM ○ Optic nerve >> senstitive to ↑ IOP & ischemic injury  AION & CRAO as a result of compromised microvascular perfusion

26 SOAG-Accidental & Surgical Trauma Hyphema  th / uncomplicated hyphema ; Conservative : eye shield, limited activity & head elevation Topical & sistemic corticosteroid ~inflammation Cycloplegic if ciliary spasm / photophobia(+)  Th / if ↑↑ IOP aqueous suppressant & hyperosmotic agent ○ CAI avoid in sickle cell  CAI ↑ aqueous acidity Surgical ○ I/ obstruct vision, early in very young children ○ Washout procedure + iridectomy / trabeculectomy Total hyphema  pupillary block Uncontrolled IOP

27 SOAG-Accidental & Surgical Trauma Hyphema

28 SOAG-Accidental & Surgical Traumatic / angle recession gl  Tear in ciliary body between longitudinal and circular muscle fiber  Clinical : Brown colored, broad angle recess Absent or torn iris proceses White, glistening scleral spur Depression in the overlying TM PAS at the border of the recession  Th/ aqueous suppressant, prostaglandin analog, trabeculectomy

29 SOAG-Accidental & Surgical Traumatic / angle recession gl  Pathogenesis (glaucoma dx &management, Gork) Impact aqueous forced laterally&posteriorly againt iris&angle  hydrodynamic force cause tear between longitudinal & the connecting circular and oblique muscle  disrupt branches of anterior or posterior ciliary arteries  bleeding in AC

30 In years following trauma, inner circular radial muscle  degeneratif change  scarring, fibrosis&obliteration of the intertrabecular spaces & schlemm’s canal-  decreased outflow facility Damage of the ciliary muscle disrupts the tension exerted on the TM  reduce the functional capacity of TM

31 SOAG-Accidental & Surgical Traumatic / angle recession gl

32 SOAG-Accidental & Surgical Surgical trauma  ↑ IOP post procedure: Cataract extraction Filtering surgery Corneal transplantation Laser surgery  Mechanisme ?: Pigment release Inflammatory cell & debris Mechanical deformation of TM Agent OVD higher molecular weight

33 SOAG-Accidental & Surgical Surgical trauma  Implantation of IOP -  secondary glaucoma Uveitis- glaucoma –hyphema (UGH)syndrome Secondary pigmentary glaucoma Pseudophakic pupillary block

34 SOAG-Accidental & Surgical Surgical trauma UGH  chafting of the iris by the IOL  Clinically: Chronic inflammation, secondary iris neovascularization recurrent hyphema  Th/ lens repositioning

35 SOAG Drug & Glaucoma  Corticosteroid-induced glaucoma : Prolonged use of topical, periocular, intravitreal, inhaled, systemic Increase resistance to aqueous outflow in TM Prednisolone & dexamethason >> fluorometholone, rimexolone,  Cycloplegic drug can ↑ IOP in open angle Risk>> POAG, exfoliation, pigment dispersion, on miotic therapy

36 THANK YOU