Glaucoma Aryanti Ibrahim aDefinition: It is a heterogenous group of diseases in which damage to the optic nerve(optic neuropathy) is usually caused

by raised ocular pressure (normal IOP is 15.5 mmHg) acting on the nerve head.range (11-21) Basic physiology of aqueous humour: 1. Conventional pathway 2. Uveo-scleral pathway LOP: Depends on the balance between production and removal of aqueous humour 1. Conventional Pathway: 2. Uveo-scleral pathway Mechanism of Optic nerve fiber damage Mechanical damageTo optic nerve axons by the raised IOP Ischemia of nerve fibers caused by impaired perfusion pressure (reducing blood flow at optic nerve head) Classification of Glaucoma: 1. Primary glaucoma: 1. Chronic open angle 2. Acute and chronic closed angle 2. Congenital glaucoma: 1. Primary 2. Rubella 3. Seconday to other inherited ocular disorders (e.g. an-iridia; absense of iris) 3. Secondary glaucoma (causes): 1. trauma 2. Ocular surgery

3. Associated with other ocular diseases (uveitis) 4. Raised episcleral venous pressure 5. Steroid induced Primary Glaucoma: Primary OPEN angle glaucoma Pathogenesis: Resistance of drainage of aqueous through the Trabecular meshwok, due to:

1. Thickening of Trabecular lamellae (reduces pore size). 2. Reduction in number of lining Trabecular cells. 3. Increased extracellular material in the Trabecular meshwork spaces. Primary OPEN angle glaucoma: It is the most common type of glaucoma It is the 3rd cause of blindness in the UK. It is also called chronic open angle glaucoma. It causes SLOW damage to the optic nerve, causing gradual loss of vision. The patient first loses the peripheral visual field then it progress to total blindness if left untreated. Primary OPEN angle glaucoma (cont.) Symptoms:

1. Because the vision loss is gradual, the patient usually present when severe damage has occurred. 2. Most patients are detected by optometrist routine examination. Risk groups:

1. Affects 1 in 200 of population over the age of 40. 2. Males and females are equally affected. 3. The prevalence increase with age to nearly 10% in the over 80 population. 4. There maybe family history but the exact mode of inheritance is not clear.

Normal tension glaucoma: Some open angle glaucoma have normal intra-ocular pressure called low-tension or normaltension glaucoma.(glucomatous change) In these cases, there will be damage to the optic nerve even though the intra-ocular pressure is within normal range. The eyes of the normal tension glaucoma have normal angles, so its features are similar to that of primary open angle glaucoma. The causes of normal tension glaucoma is still unknown. The optic nerve is susceptible to damage even from normal IOP. Normal-tension glaucoma is thought to be related, at least in part, to poor blood flow to the optic nerve.

Normal tension glaucoma (cont.): Risk factors:

1. Family history of glaucoma. 2. Cardiovascular diseases. Treatment: 1. Even though the IOP is normal but medication to decrease IOP as much as possible are used. Acute angle closure glaucoma: The condition occurs in small eyes (as in hyperopoia) with shallow anterior chambers. Normally there is some resistance between the pupil margin and the lens. But sometimes. Acute angle closure glaucoma (cont.): Symptoms: 1. The eyes becomes red and painful due to rapid increase in IOP. Acute angle closure glaucoma (cont.): 2. Blurred vision; because the cornea becomes edematous. Acute angle closure glaucoma (cont.):

3. Patient may notice haloes (circles of light) around light due to dispersed light in waterlogged cornea. Acute angle closure glaucoma (cont.): They may have similar symptoms in the past that are aborted by going to sleep, because sleeping constricts the pupils pulling it from the lens. 7. Medical management of glaucoma Goal of treatment: - lowest risk - fewest side effect - least disruption of patients life Target IOP: - severity of the damage - life expectancy - associated risk factor Medical agents: 1. Beta-adrenergic antagonists 2. Parasympathomimetic ( miotic ) agent 3. Carbonic anhydrase inhibitors 4. Adrenergic agonist 5. Hypotensive lipids 6. Combination medications 7. Hyperosmotic agents 7. Medical management of glaucoma 1. Beta-adrenergic antagonists: - inhibiting cAMP production in ciliary epithelium => decrease aqueous humor secretion 20-50 % => decrease IOP 20-30 % - peak 2-3 hours - non selective beta-antigonist: carteolol, levobunolol, timolol maleate selective beta1 antigonist: betaxolol

- side effect: bronchospasm, bradycardia, heart block, lower BP CNS depression, punctate keratitis, impotence, allergy 7. Medical management of glaucoma 2. Parasympathomimetic agents: - Direct-acting cholinergic agents: affect the motor endplates pilocarpine Indirect-acting cholinergic agents:inhibit enzyme acethylcholinesterase echothiophate iodide - Contraction of the longitudinal ciliary muscle => increase outflow => decrease IOP 15-25 % - Reduced uveoscleral outflow - Disrupt the blood-aqueous barrier - associated retinal detachment - induced myopia 7. Medical management of glaucoma 3. Carbonic anhydrase inhibitors: - Direct antagonist activity on ciliary epithelial carbonic anhydrase => decrease aqueous humor - Systemic CAI: Acetazolamide ( 62.5 mg gid ) decrease IOP 15-20 %

Methazolamide ( 25-30 mg bid,tid ) side effect: ( dose relate ) acidosis, depression, numbness, renal stone, hypokalemia bone marrow depression - Topical CAI:

Dorzolamide, Brinzolamide, Sulfonamide decrease IOP 14-17 % side effect: bitter taste, punctate keratopathy 7. Medical management of glaucoma 4. Adrenergic agonist: - Nonselective Alpha agonist : epinephrine Dipivefrin increase conventional and uveoscleral outflow decrease IOP 15-20 % side effect: headache, increase BP, tachycardia, arrhythmia adrenocchrome depositsat the conjunctival and cornea pupillary dilation, allergic blepharoconjunctivitis cystoid macular edema - Relative selective Alpha agonist : Alpraclonidine Brimonidine decrease aqueous production increase uveoscleral outflow decrease IOP 20-30 % 7. Medical management of glaucoma 5. Hypotensive lipids: - increase uveoscleral outflow 50 % Latanoprost, Travoprost, Bimatoprost Unoprostone decrease IOP 25-32 % decrease IOP 13-18 %

- side effect: darkening of the iris and periocular skin conjunctival hyperemia, hypertrichosis

Herpes keratitis, cystoid macular edema uveitis 6. Combined medication: - Cosopt: timolol maleate 0.5% + dorzolamide 2% - Advantage: less confusion increase compliance 7. Medical management of glaucoma 7. Hyperosmotic agents: - Osmotic gradient => drawing water from the vitreous cavity - effect are transient => rebound elevation IOP - oral glycerine, intravenous manitol - side effect: headache mental confusion acute congestion heart failure myocardial infarction 8. Surgical theraphy for glaucoma Open angle glaucoma: Trabeculectomy: - Indication: - Failed maximum medication - progressive glaucomatous optic neuropathy - Relative contraindication: - blind eye - rubeosis iridis - active iritis - Less successful in younger, aphakia, pseudophakia uveitis glaucoma, black, previously failed filtering

8. Surgical theraphy for glaucoma Open angle glaucoma: Trabeculectomy Complication Early infection hypotony flat anterior chamber aqueous misdirection hyphema cataract Late leakage failure cataract blebitis endophthalmitis dysesthetic bleb

cystoid macular edema hypotony maculopathy choroidal effusion suprachoroidal hemorrhage loss of vision 8. Surgical theraphy for glaucoma Angle closure glaucoma: 1. Laser iridectomy: indication: pupillary block

bleb migration hypotony

contraindication: active rubeosis iridis systemic anticoagulants complication: focal lens or corneal damage retinal detachment bleeding IOP spike 2. Peripheral iridoplasty 3. Cataract extraction 8. Surgical theraphy for glaucoma Congenital glaucoma: Goniotomy: clear cornea

Trabeculotomy: cloudy cornea indication: childhood glaucoma

contraindication: - unstable health - multiple anomalies with poor prognosis complication: - hyphema

- infection - lens damage - uveitis