GLAUCOMA

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1- Definition

Glaucoma refers to a group of ophthalmic disorders

characterized by neuropathy of the optic nerve and progressive loss of retinal ganglion cells,

which leads to permanent deterioration of the visual field eventually lead to blindness.

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2- Classification

Glaucoma can be classified as the following :

A- Primary glaucoma:(NOT attributed to a pre-existing ocular or systemic disease).

includes 1-Primary open-angle glaucoma (POAG)

2-Primary angle-closure glaucoma (PACG)

3-Congenital glaucoma.

B- Secondary glaucoma:(attributed to preexisting ocular or systemic disease).

e.g. Pigmentary glaucoma, Neovascular glaucoma,

Traumatic glaucoma, and Pseudoexfoliative glaucoma.

most common types of glaucoma

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Aqueous Humor

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Intraocular Pressure• IOP is dependent upon the balance between

aqueous humor production and outflow.

• The normal range of IOP is 10 to 21 mm Hg.

• IOP is clinically measured by Tonometry.

• Caution should be used in assigning this range as being “normal” for IOP ………. WHY ?

• IOP is NO longer used as a diagnostic criterion for glaucoma, because optic neuropathy can be present in the normal range and can be absent at higher IOPs.

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3- Risk factors POAG

1.Family history. 2.Age. 3.Race. 4.central

corneal thickness (CCT ).

5.Elevated IOP.

PACG1.Hyperopia. 2.Gender.3.Eskimo or

Asian ethnicity.

4.Family history.

5.Age.

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4- PathophysiologyA- POAG :

• Increased IOP causes retinal ganglion cell axons to undergo mechanical stress, alters axonal protein transport, and decreases blood supply to the retina and the optic nerve leading to tissue ischemia.

• The level of IOP is related to the death of retinal ganglion cell and optic nerve fibers.

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4- PathophysiologyB- PACG :

Involves Two major mechanisms of Mechanical obstruction of trabecular meshwork by the peripheral iris include 1- Pupillary block (more common) .

2- Iris plateau.

• Both of these mechanisms result in the occlusion of aqueous humor outflow causing IOP elevation at extreme levels that can lead to vision loss in hrs to days.

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5- Clinical Presentation

A- POAG:General

• POAG is usually bilateral with asymmetric disease progression.

Symptoms: Pts e’ severe disease progression may report :

1. Loss of peripheral vision.

2. Presence of scotomata (blind spots) in vision field.

Signs: Ophthalmoscopic examination may reveal :

3.Optic nerve head (optic disc) cupping.

4.Large cup-to-disc ratio.

5.Notching of the optic nerve head rim.

6.Splinter hemorrhages (using a slit-lamp biomicroscope) 9

5- Clinical PresentationB- PACG:(Medical emergency due to high risk of vision loss)

General

• Unilateral in presentation,the other eye is at risk.

Symptoms

1. Ocular pain.2. Red eye.

3. Blurry vision.

4. Halos around lights.

Systemic symptoms

• Nausea/vomiting.

• Headache / Diaphoresis.

Signs

1. Cloudy cornea

2. Conjunctival hyperemia.

3. Pupil semidilated and fixed to light

4. Eye will be harder on palpation.

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6- Diagnostic Tests (POAG)1. Gonioscopy (measure anterior-chamber

angles).

2. Applanation tonometry ( measure IOP).

3. Pachymetry (measures central corneal thickness).

4. Automated perimetry (evaluates visual fields).

6- Diagnostic Tests (PACG)1.Gonioscopy.

2.Applanation tonometry.

3.Slit-lamp biomicroscopy.

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7- Management A- Desired outcome:1. Prevent further loss of visual function.

2. Maintain IOP at or below a pressure at which further optic nerve damage is unlikely to occur.

3. Manage an acute attack of angle closure.

4. Reverse or prevent angle closure.

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B-Treatment:

1- Non pharmacologic treatment:

a)Laser trabeculoplasty.b)Trabeculectomy.c) Cyclodestructive surgery.

Primary angle closure glaucoma (PACG) has Special treatment:

1- Drug therapy to decrease IOP (CAIs –Acetazolamide).2- Laser therapy (laser iridotomy).3- Incisional iridectomy.4- Topical corticosteroids.

2- Pharmacotherapy14

Ophthalmic Drugs for Glaucoma

Lowering IOP by

1-Reducing production of aqueous humor: β-Blockers. α2Adrenergic Agonists. Carbonic Anhydrase Inhibitors.

2-Decreasing the resistance to outflow of aqueous humor through trabecular meshwork: CHOLINERGICS AND CHOLINESTERASE INHIBITORS.

3-Improving the outflow of aqueous humor: PROSTAGLANDINS (uveoscleral outflow).

SYMPATHOMIMETICS (trabecular meshwork and the

uveoscleral outflow).

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A.Topical β-ADRENERGIC BLOCKING DRUGS

-Includes:1. Non-selective: Timolol, Levobunolol, Metipranolol & Carteolol.

2. β1-Selective: Betaxolol.

-Dosing: 1 drop BID-Side effects:1- Bronchospasm.

2- Bradycardia.

3- Hypotension.

4- CHF exacerbation.

5- Mask hypoglycemia.

6- Tachyphylaxis (20% to 50% of pts).

-Nasolacrimal occlusion is a technique to decrease amount of drug absorbed systemically and decrease the incidence of side effects and improve medication effectiveness.

- Contraindications1- Asthma 2- COPD 3- Sinus bradycardia 4- 2nd or 3rd degree heart failure

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Betaxolol can be used

B. α2-ADRENERGIC AGONISTS

-Includes: Brimonidine(more selective) & Apraclonidine.-Brimonidine:(Effective long-term monotherapy / adjunctive therapy)

- Apraclonidine(Short-term use only due to high rate of tachyphylaxis)

Used for prevention & ttt of postsurgical IOP elevations.-Dosing: 1 drop BID to TID.-Side effects:1-Blepharoconjunctivitis.

2-Foreign body sensation.

3-Papillary mydrasis (Apraclonidine).

4-Eyelid retraction(Apraclonidine).

5-Mild systemic hypotension and lethargy. ( Brimonidine pass BBB ). 17

C. CARBONIC ANHYDRASE INHIBITORS

1- Topical agents :

-Includes: Dorzolamide and Brinzolamide.

-Dosing: 1 drop BID with beta blockers or TID alone.

-Combination of Timolol+Dorzolamide is commonly used

-Side effects:1-Burning.2-Stinging.3-Itching.4-Dry eyes.5-Conjunctivitis

-Contraindicationspatients with history of hypersensitivity to sulphonamides.

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C. CARBONIC ANHYDRASE INHIBITORS

2- Orally-administered CAIs:-Includes: Acetazolamide , Dichlorphenamide, and Methazolamide.

-Side effects:1-Paresthesia of hands and feet.2-Hypokalemia and hyponatremia.3-Nephrolethiasis and renal failure.4-Hepatic insufficiency.5-Blooddyscrasias from bone marrow suppression. -Contraindications1-Hypokalemia. 2-Hyponatremia.

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D. CHOLINERGICS AND CHOLINESTERASE INHIBITORS

1- CHOLINERGICS:

-Includes: Pilocarpine and Carbachol.

-Dosing:1–2 drops TID or QID.

-Used with caution for closed angle

-Side effects:(due to miosis)1-Brow ache and headache.2-Affect night vision.3-Bradycardia at high conc.4-Retinal detachment.5-Iris cysts and Ciliary spasm. 6-Lacrimation, myopia, blurred vision.

-Contraindications:Severe myopia to

avoid retinal detachment

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D. CHOLINERGICS AND CHOLINESTERASE INHIBITORS

2- CHOLINESTERASE INHIBITORS:

-Includes: Echothiophate iodide &Demecarium bromide.

-Irreversible AchE inhibitors e’ long durations of action.

-Stop at least 1 week before general surgical procedure.

-Dosing: 1 drop BID.

-Side effects:1- Depletion of systemic cholinesterase and pseudocholinesterase.

2- Cataracts: occur in 30–50% of elderly patients using these drugs

for at least 6 months.21

E. PROSTAGLANDINS

-Includes: Latanoprost, Bimatoprost, Travoprost.-First-line alternatives to topical β-blockers.

-Patients required to lower IOP by greater than 25%.

-Lower IOP by 25% to 35% (Lower nocturnal IOP).

-Dosing: 1 drop once a day at bedtime

-Side effects:1- Conjunctival hyperemia.

2- Stinging on instillation.

3- Inc. in iris pigmentation.

4- Hypertrichosis.

5- Eyelashes darkening.

6- Worsen anterior uveitis & herpetic keratitis.22

F. SYMPATHOMIMETICS-includes: DIPIVEFRIN HCL , EPINEPHRINE.

-IOP is reduced by 20–25%.

-Last line agents due to their systemic S.E. profile.

-Dosing:1 drop BID.

-Intolerance to ocular adverse effects leads to discontinuation of epinephrine in 80% of patients.

-Side effects:

1-Burning, tearing.2-Reactive conjunctival hyperemia.3-Allergic blepharoconjunctivitis.4-Mydriasis Blurring of vision.

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G. HYPEROSMOTICS -Includes: Glycerin, Isosorbide and Mannitol-Dosing: Glycerin 1 – 1.5 g/kgIsosorbide 1.5 - 2 g/kgMannitol (20%) 1-2 g/kg (i.v.) over 45 min.

-(No Vomiting) Glycerin and Isosorbide can be given orally.

-(Vomiting) Mannitol (20%) can be given IV.-used e’ caution for patients with renal or C.V. diseases.-Side effects:1-Headache.2-Diuresis / Thirst.3-CNS dehydration.4-Coma.

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8-OUTCOME EVALUATION

• Evaluate patients 2 to 4 weeks after the initiation or alteration of medical therapy.

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Optic nerve head evaluation and visual field testing

Patients at target IOP and have no disease progression

every 6 to 18 months

Patients NOT at target IOP or have disease progression

every 2 to 12 monthsevery 1 to 6 months

9-Application of Ophthalmic medications1. Clean hands with soap and water.

2. Avoid touching the dropper tip with your fingers.

3. Shake dropper bottle if product is a suspension.

4. Tilt head back; pull down the lower eye lid with index finger.

5. Hold the dropper bottle with other hand as close as possible without touching the eye.

6. Gently squeeze the bottle so that one drop is placed into the pocket.

7. Close your eye for 2 to 3 minutes to allow for the maximum corneal penetration of drug.

8. Use a tissue to wipe away any excess liquid.

9. Replace and retighten the cap to the dropper bottle.

10.Wait at least 5 minutes before instilling another ophthalmic drug preparation.

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Patient caseM.H., a 52-year-old African American woman with brown eyes, presented for routine ophthalmic examination. Tonometry measured an IOP of 36 mmHg in both eyes. Ophthalmoscopy revealed physiologic cupping of the optic discs in both eyes, and visual field examination revealed a nerve fiber bundle defect consistent with glaucoma. and gonioscopy indicated that anterior chamber angles were open in both eyes. There were no signs of cataract formation. M.H. related a positive family history for glaucoma and presently is being treated for hypertension, CHF, and asthma.What is the best initial therapeutic treatment in M.H.?A. Timolol.B. Betaxolol.C. Apraclonidine.D. Dipivefrin.

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B

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Thank you