ARI SURYA

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.

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

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

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

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

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

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

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

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

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

SOAG 2. Lens-Induced Glaucoma

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

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

SOAG- Lens Induced Gl Phacolytic glaucoma

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

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

SOAG- Lens Induced Gl Lens Particle glaucoma

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

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

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

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

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

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

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

SOAG-Accidental & Surgical Trauma Hyphema

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

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

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

SOAG-Accidental & Surgical Traumatic / angle recession gl

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

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

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

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

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