OPH - Glaucoma

Question 1

Basic Anatomy and Physiology of the Eye

Chambers in the Eye
Aqueous Humour
Intraocular Pressure
Optic Disc and Cup

Answer 1

1. ) Eye Chambers - anterior, posterior, vitreous
   - anterior: cornea –> iris, filled w/ aq humour
   - posterior: iris –> lens, also filled w/ aq humour
   - vitreous: posterior lens –> retina, the largest chamber filled with vitreous humour
2. ) Aqueous Humour - nourishes the lens and cornea as they are avascular so they can remain transparent
   - produced by the ciliary body, flows around the lens and under the iris, through the anterior chamber
   - flows through the trabecular meshwork and into the canal of Schlemm into the episcleral veins
   - 4-20% drained via unconventional uveoscleral route (across the ciliary body into the suprachoroidal space)
3. ) Intraocular Pressure - normal IOP is 10-21mmHg
   - created by the resistance to flow through the trabecular meshwork into the canal of Schlemm
   - the balance between the rate of production and drainage of aq humour
   - measured using tonometry which can be affected by corneal thickness (higher thickness = higher pressure) which needs correction
4. ) Optic Disc and Cup - round spot on the retina
   - small indent in the centre of the disc is the optic cup
   - ↑IOP creates a larger indent in the optic disc making it wider and deeper thus ‘cupping’
   - optic cup > 50% of the optic disc is abnormal.

Question 2

Open-Angle (Chronic) Glaucoma

Pathophysiology
Clinical Features
Investigations
Management

Answer 2

1. ) Pathophysiology - ↑IOP –> damage to optic nerve
   - trabecular meshwork deteriorates w/ age, gradually increasing resistance through the trabecular meshwork
   - this reduces drainage of aq humour –> slow ↑IOP
   - risk factors: ↑age, FH, myopia (shortsightedness), black ethnic origin,
   - normal-tension glaucoma also exists but the cause is unknown, it is optic nerve damage without raised IOP
2. ) Clinical Features
   - often asymptomatic, picked up on screening
   - loss of peripheral vision –> tunnel vision
   - fluctuating pain, headaches, blurred vision
   - halos appearing around lights, particularly at night
3. ) Investigations
   - Goldmann applanation tonometry: measure IOP
   - fundoscopy: optic disc cupping, optic nerve health
   - visual field assessment: peripheral visual field loss, central scotoma in advanced disease
4. ) Management - start treatment once IOP >24mmHg
   - main cause of irreversible blindness if not treated
   - annual screening for >40s w/ positive FH

Question 3

Acute-Angle (Acute) Glaucoma

Pathophysiology
Risk Factors
Clinical Features
Initial Management

Answer 3

1. ) Pathophysiology - ↑IOP –> damage to optic nerve
   - iris bulges forward and seals off the trabecular meshwork from the anterior chamber
   - this prevents drainage of aq humour –> fast ↑IOP
2. ) Risk Factors
   - ↑age, females, FH, hyperopia (shallow anterior chamber)
   - Chinese and East Asian, rare in black ethnic origin
   - medication: noradrenaline, anticholinergics (oxybutynin etc…), cyclopentolate, TCAs, steroids
3. ) Clinical Features
   - painful red eye, blurred vision, halos around lights
   - teary, hazy cornea, ciliary injection, ↓visual acuity
   - associated headache, nausea and vomiting
   - fixed and dilated pupil
   - firm eyeball on palpation
4. ) Initial Management - ophthalmic emergency
   - lie the patient on their back without a pillow
   - pilocarpine eye drops (2% for blue, 4% for brown): pupil constriction and ciliary muscle contraction open up flow of aq humour into the trabecular meshwork
   - PO/IV acetazolamide 500mg: carbonic anhydrase inhibitor (CAi) which ↓production of aqueous humour
   - analgesia and antiemetic if required

Question 4

Medications (Eye Drops) Used in Managing Glaucoma

Prostaglandin Analogues
Pilocarpine
Alpha Agonist
Beta Blockers
Carbonic Anhydrase Inhibitors

Answer 4

1. ) Prostaglandin Analogues - eg. latanoprost, travoprost bimatoprost, nightly (ON), 1° for chronic glaucoma
   - increases uveoscleral outflow of aqueous humour
   - side effects: eyelash growth, eyelid pigmentation, iris pigmentation (browning), contact dermatitis
2. ) Beta-Blockers - e.g. timolol, carteolol, OD-BD
   - reduces the production of aqueous humour
   - used second line for chronic glaucoma and can also be used in acute glaucoma
   - side effects: bradycardia
3. ) Alpha-Agonist - e.g. brimonidine, apraclonidine, BD
   - ↓aq fluid production and small ↑uveoscleral outflow
   - can be used for chronic or acute glaucoma
4. ) Carbonic Anhydrase Inhibitors (CAi) - e.g. dorzolamide, brinzolamide, used TDS
   - reduces the production of aqueous humour
   - acetazolamide is systemic (PO/IV) and only used in the initial management of acute glaucoma
   - common side effect is a metallic taste
5. ) Pilocarpine - miotic (parasympathomimetic)
   - QDS (monotherapy), 2% for blue, 4% for brown eyes
   - stimulates muscarinic receptors in sphincter muscles
   - pupil constriction and ciliary muscle contraction ↑ aq humour outflow into the trabecular meshwork
   - only used for initial management of acute glaucoma
   - side effects: blurred vision, headaches in younger

Question 5

Surgical Management for Glaucoma

Trabeculectomy 
Laser Iridotomy (peripheral iridectomy)

Answer 5

1. ) Trabeculectomy - first line if eligible for surgery
   - creates a new channel from the anterior chamber, through the sclera to a location under the conjunctiva
   - creates a ‘bleb’ where aq humour drains
   - complications: iritis, blebitis, sudden ↑/↓in IOP, can heal up so can stop working
2. ) Laser Iridotomy - definitive for acute glaucoma
   - a hole in the iris allowing aq humour to flow from the posterior chamber into the anterior chamber
   - it relieves pressure that was pushing the iris against the cornea and allowed the humour to drain
   - completed in both eyes prophylactically