Glaucoma

Question 1

What is the definition of glaucoma?

Answer 1

Glaucoma is an optic neuropathy, with characteristic optic nerve head changes (i.e. increased cup to disc ratio (C/D ratio)) (structural lesion) and a corresponding visual field defect (functional problem), which may or may not be associated with raised IOP.

Question 2

what is the definition of oculohypertension?

Answer 2

IOP > 21 mmHg, without detectable glaucomatous damag

Question 3

how does one screen for glaucoma?

Answer 3

• Gonioscopy – visualize the anterior chamber
• Dilated ophthalmoscopy – dilated eye, examining fundus and optic nerve head
• Automated perimetry – visual field testing, e.g. Humphrey (static perimetry)
• Tonometry – to check IOP (can be affected if corneal thickness differs from norm, see Imbert Fick Law, or can be increased when eye is dilated)

Question 4

who are the high risks groups who should be screened for glaucoma?

Answer 4

• Older individuals: Risk increases once you are above 50 years old
• Age > 40 + history of POAG in a close family member (strong FHx of glaucoma)
• PMHx of raised IOP
• FHx of POAG
• Asians are at a higher risk of angle-closure glaucoma, as compared to Caucasians
• High myopia (increased risk of POAG), high hypermetropia (increased risk of PACG)
• Other risk factors, e.g. smoking

Question 5

what is the main surgery for POAG?

Answer 5

Trabeculectomy

Question 6

what are the types of visual field defects that can occur with POAG?

Answer 6

• paracentral sctomas
• Nasal step
• temporal wedge
• arcuate scotoma ( beginning as downward/upward extensions of the blind spot)
• ring scotoma (when superior and inferior arcuate scotomas become continuous)
• end stage (small island of central vision + temporal island)

Question 7

what are the risk factors for normal tension glaucoma?

Answer 7

• Family history of glaucoma
• History of major blood loss or blood transfusion
• History of migraine
• History of Raynaud’s phenomenon- spasm of blood vessels leading to discolouration of fingers and toes.

Question 8

Definition of primary angle closure suspect (PACS)?

Answer 8

• Gonioscopy shows posterior meshwork iridotrabecular contact in 3 or more quadrants, but no peripheral anterior synechiae (PAS).
• Normal IOP, optic disc, and visual field.

Question 9

Definition of primary angle closure (PAC)?

Answer 9

• Gonioscopy shows 3 or more quadrants of iridotrabecular contact, with raised IOP and/or PAS.
• Normal optic disc and field.

Question 10

Definition of primary angle closure glaucoma (PACG)?

Answer 10

• ITC in 3 or more quadrants, with glaucomatous optic neuropathy.
• Optic nerve damage from an episode of severe IOP elevation, such as acute angle closure, may not appear as typical glaucomatous cupping.

Question 11

What are the mechanisms of angle closure

Answer 11

• Relative pupillary block
• non pupillary blcok (associated with deeper anterior chamber)
• lens induced angle closure (usually rapid progression of lens intumescence [phacomorphic glaucoma] or anterior lens subluxation)
• retrolenticular

Question 12

what are the risk factors for PACG?

Answer 12

• Age: elderly 🡪 more relative pupillary block
• Gender: F > M
• Race: Asian
• FHx: angle closure (anatomical predisposition)
• Refraction: eyes with pure pupillary block are typically hypermetropic
• Axial length: short eyes tend to have shallow AC
• Cataracts

Question 13

what is the presentation of a patients with PACG?

Answer 13

• Intermittent, mild symptoms of blurring (“smoke-filled room”) and haloes (“rainbow around lights”) due to corneal epithelial oedema, OR
• Acutely with markedly decreased vision, redness and ocular/periocular pain and headache

Question 14

what are the signs of chronic PACG?

Answer 14

• VA is normal unless damage is advanced

- AC is usually shallower in relative pupillary block than non-pupillary block

Question 15

what are the signs of acute PACG?

Answer 15

• VA is usually 6/60 to HM
• IOP is usually very high (50-100 mmHg)
• Conjunctival hyperaemia, with violaceous circum corneal injection
• Corneal epithelial oedema

Question 16

what is the management of primary angle closure suspect?

Answer 16

Laser iridotomy

Question 17

what is the management for acute primary angle closure?

Answer 17

Initial management (aim to break the attack – medical)

• Pt to assume supine position to encourage lens to shift posteriorly under the influence of gravity
• IV acetazolamide 500 mg (lowers IOP)
• Single dose apraclonidine 0.5% or 1% (lowers IOP), timolol 0.5% (lowers IOP), and prednisolone 1% or dexamethasone 0.1% (reduces inflammation) to affected eye, leaving 5 minutes between each
• Pilocarpine 2-4% (miotic) one drop to BOTH eyes (in fellow eye for prophylaxis), repeated after 30 minutes

Subsequent management – surgical (after attack is broken, i.e. clear cornea, normalised IOP)
- Subsequent management – surgical (after attack is broken, i.e. clear cornea, normalised IOP)

• Consider cataract surgery (because of possible lens involvement or contribution)

Question 18

what is the pathophysiology of acute angle closure glaucoma?

Answer 18

• Contact between pupil margin and anterior lens surface (in pre-existing narrow angle) -> resistance to aqueous outflow from post to ant chamber -> pressure differential builds up -> peripheral iris bows forward -> angle block -> aqueous outflow obstructed -> acute increase in IOP
• Pupillary block is 1’ cause of IOP, not the angle block

Question 19

what are the symptoms of acute angle closure glaucoma?

Answer 19

• sudden onset, usually unilateral, painful red eye, LOV, BOV
• A/w one-sided headache, N/V
• Pt may see coloured halos/rainbows around light
• Usually presents at night due to pupil dilation (radial muscles of the iris contract)

Question 20

what are the signs of acute angle closure glaucoma?

Answer 20

• Eye feels firm on palpation
• Conjunctival injection
• Hazy cornea (corneal oedema)
• Shallow AC (anterior chamber)
• High IOP
• ***Fixed, mid-dilated pupil that is unresponsive to light

Question 21

what is the pathogenesis of neovascular glaucoma?

Answer 21

• NVG occurs as a result of aggressive iris neovascularisation (rubeosis iridis). The most common aetiological cause is severe, diffuse, and chronic retinal ischaemia
• hypoxic retinal tissue produces angiogenic factors in an attempt to revascularize hypoxic areas; the most important of these is probably VEGF.
• The mediators induce both retinal and anterior segment neovascularisation, the latter initially impairing aqueous outflow in the presence of an open angle, with subsequent progression to typically severe and relentless secondary synechial angle closure glaucoma (when new blood vessels develops fibrosis 🡪 then the fibrovascular tissue contracts 🡪 closes the angle).

Question 22

what are the causes of neovascular glaucoma?

Answer 22

• Ischaemic central retinal vein occlusion (CRVO): Glaucoma typically occurs 3 months after the occlusive event (100-day glaucoma)
• Diabetes mellitus (DM)/diabetic retinopathy: Risk of glaucoma is decreased by panretinal photocoagulation (PRP)
• Arterial retinal vascular disease, e.g. central retinal arterial occlusion (CRAO)
• Others: Intraocular tumours, long-standing retinal detachment (RD), chronic intraocular inflammation

Question 23

what is management of neovascular glaucoma?

Answer 23

Rubeosis iridis: PRP, intravitreal anti-VEGF, treat underlying cause

Secondary open angle glaucoma

• Medical: IOP lowering agents, intravitreal anti-VEGF, topical steroids if significant inflammation is present
• PRP
• Surgical: cyclodiode (if medical IOP control not possible)

Secondary angle closure glaucoma

• Medical as above (intravitreal anti-VEGF will not reverse established angle closure)
• PRP
• Surgical: cyclodiode, endocyclodiode, drainage surgery (enhanced trabeculectomy or shunt)

Question 24

beta blockers

• examples
• mechanism
• c/i
• pros

Answer 24

• timolol
• Decrease pdtn
  (by non-pigmented ciliary epithelium, i.e. ciliary body)
• Asthma, bradycardia, heart block
• cheap + efficacious = 1st line

Question 25

carbonic anhydrase inhibitors - examples - mechanism - c/i - cons

Answer 25

acetazolamide, dorzolamide Inhibits CA which catalyses rxn that creates osmotic grad for passive flow of aqueous C/I - G6PD deficiency - Sulfonamides allergy - Sickle cell anaemia - Severe renal impairment/ - ESRF – metabolic acidosis cons - PO: LT use limited by S/E of malaise, fatigue, anorexia, depression - opical: S/E stinging sensation, cornea endothelium dysfunction

Question 26

prostaglandin analogues - examples - mechanism - pros - cons

Answer 26

latanoprost, travaprost increases uvoscleral outflow + relaxes ciliary body muscle and dilates spaces between ciliary body muscle bundles Pros: efficacious + ON dosing but more ex than BB = 2nd line Cons (S/E) - conjunctival hyperaemia, burning and stinging sensation - increased iris + around eye pigmentation - eyelash growth (hypertrichosis)

Question 27

a adrenergic agonists - examples - mechanism - c/i - cons

Answer 27

brimonidine Increases uvoscleral outflow Young children, due to potential to cross BBB, and respiratory depression increased incidence of allergic rxns

Question 28

miotics - examples - cons

Answer 28

physostigmine Ocular S/E: small pupils, myopia, increased subjective visual disturbance