CVL: Glaucoma Flashcards
Definition of glaucoma
Optic neuropathy caused by raised IOP (>30mmHg, Normal: 12-22mmHg), leading to optic nerve damage and visual field loss
Pathogenesis of glaucoma
Imbalance between production and outflow
- Aqueous humor is produced by the ciliary body, flows through the pupil, reaching the angle of the anterior chamber, draining through trabecular meshwork into canal of Schlemm
- Blockage results in IOP building up behind the iris, becoming inappropriately high
- Prolonged/ repeated contact between iris and angle of anterior chamber leads to scarring of trabecular meshwork
- In AACG: Pupillary block due to dilation of pupil can cause iris to come into contact with angle of ant chamber
- Optic nerve damaged due to raised IOP compressing on it
- Resultant visual field loss from peripheral to central (Tunnel Vision)
Types of glaucoma
Primary
1. Primary open angle glaucoma: obstruction within trabecular meshwork and drainage to Schlemm’s canal
- Primary angle closure glaucoma:
- Acute angle closure glaucoma
- Chronic angle closure glaucoma
Secondary glaucoma
3. Neovascular glaucoma: DM or central retina vein occlusion
4. Inflammation: Uveitis
5. Compression: SOL/ Cataract/ Traumatic/ Hyphema/ Hemorrhages
6. Steroid-induced
7. Lens-induced glaucoma
- Congenital glaucoma
- Shallow Anterior Chamber
- Thick lens
Acute angle closure glaucoma
- Lens is located too far forward anatomically and rests against the iris
- Pressure builds up behind the iris > anterior chamber, causing the peripheral iris to bow forward and cover all or part of the anterior chamber angle
- In acute conditions, pupillary block due to dilation of pupil can cause iris to come into contact with angle of ant chamber
- Crowding of angle of anterior chamber
- If the entire angle is blocked suddenly, as occurs in complete pupillary block, the IOP rises rapidly, and acute symptoms can occur
Risk factors of AACG
Systemic
- FHx of acute PACG
- Increasing age: >50y/o
- Female gender
- Chinese
Ocular
- Hyperopia/ Hypermetropia
- Shallow anterior chamber depth
- Increased lens vault (Thick lens and/or anteriorly positioned lens)
- Thicker peripheral lens
- Ocular hypertension
Clinical features of AACG
Acute, sudden onset
Unilateral
Painful red eye
Frontal headache
N&V
BoV/Loss of vision
Preceding intermittent glare and haloes (coloured)
Raised IOP = Eye feels hard
Photophobia
Clinical signs of AACG
Perform anterior segment eye examination
- Oblique torch light test: Shallow anterior chamber (+ve eclipse sign)
- Gonioscopy showing closed angle in both eyes
- Goldmann applanation tonometry: Marked ↑ IOP (eye feels hard on palpation
- Fixed mid-/semi dilated non-reactive pupil
- Red eye with circumciliary injection
- Cloudy hazy oedematous cornea
- Increased cup-to-disc ratio
Management of AACG
!Ocular emergency!
- Reduce IOP ASAP
- Lie patient flat, press down on eyeball for few seconds and release, can force chamber open and ↓ pressure
Medical
2. Topical IOP-lowering drugs:
Aqueous suppressants
- Alpha agonist: Brimonidine
- Beta-blocker: Timolol
- Carbonic anhydrase inhibitor: IV acetazolamide
Increase aqueous outflow into uvea-scleral
- (muscurinic agonist) Pilocarpine eyedrops to miose pupil and reverse pupillary block
- Prostaglandin analogue: Latanoprost
- Definitive treatment
- Laser peripheral iridoplasty then do laser peripheral iridotomy
- Prophylactic LPI to other eye
- Offer cataract surgery to elderly (deepens anterior chamber) - Monitor for progression to CCAG
- Anterior segment imaging
- Visual fields
- Optic nerve head imaging (Heidelberg retina tomogram and optical coherence tomography of optic nerve head)
Chronic angle closure glaucoma
- Only a portion of the angle is blocked at a time and develops scarring
- Angle may become progressively more closed
Clinical features of POAG/COAG
- Initially asymptomatic
- Gradual, painless loss of vision
- Loss of peripheral vision (“tunnel vision”)
- Coloured halos
- Eye pain
- Headache
“Silent thief of eyesight”, may cause blindness if not detected and controlled early
Triad of ocular signs seen chronic glaucoma (POAG/CACG)
- Structural damage of optic nerve: Glaucomatous optic neuropathy
- Functional damage: Visual field defect
- Assessed using Humphrey’s perimetry - Increase IOP (*main risk factor)
- Measured using Goldmann applanation tonometry
Management of POAG/CACG
Aim: Preserve existing vision and prevent progression
- IOP is only modifiable risk factor
1st line Medical: decrease IOP using topical eyedrops
- Prostaglandin Analogues (Latanoprost - Xalatan)*
- Alpha agonist: Brimonidine
- Beta Blockers (Timolol)
- Carbonic Anhydrase Inhibitors (Acetazolamide/ Dorzolamide)
- Miotic (Pilocarpine)
RECHECK IOP AFTER MEDICATIONS
-> Trial max 3 types of eye drops first
Laser:
- Laser Trabeculoplasty: laser treatment of trabecular meshwork to ↑ aqueous
humour outflow
Surgical:
- Trabeculectomy
- Glaucoma Drainage Device: Tube Shunts
**For CACG, offer prophylactic laser peripheral iridotomy on top of topical meds because CACG are always at risk of developing AACG
Offer cataract surgery for elderly patient as it can help to deepen anterior chamber
How is anterior chamber angle assessed?
Slit lamp gonioscopy
What is primary open angle glaucoma?
Trabecular meshwork is an active process that absorbs aqueous humour via pinocystosis.
POAG involves degeneration of the trabecular meshwork filter, usually by unknown causes, that leads to aqueous backup and chronically elevated eye pressure
Risk factors of POAG
Major
- Family history of POAG (2–3x increased risk)
- Increased intraocular pressure
- Increased age
Minor
- Myopia
- Hypertension
- Diabetes
