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What should IOP (intraocular pressure) be?

11-21 mmHg


How is IOP measured

with a tonometer
force needed to flatten the corneal surface


What is ocular HTN

raised IOP (>21mmHg) without developing the changes of glaucoma.


define the anterior chamber of the eye

between the iris and the cornea's innermost surface, the endothelium.


How is aqueous humour made

produced by the ciliary bodies


Describe the passage of aqueous humour through the anterior chamber

made in ciliary body
passes posterior to iris, anterior to the lens, and then through pupil
flows out via trabecular meshwork
then canal of Schlemm
then episcleral vessels
then systemic venous circulation

also the uveoscleral route:
instead drains into root of iris/ciliary muscle before draining into scleral vascular system


What is acute angle closure glaucoma

there is a junction between the iris and cornea at the periphery of the anterior chamber = the anterior chamber angle.

the iris can become apposed to the trabecular meshwork and so block off the aqueous drainage.


What is the difference between primary and secondary angle closure glaucoma

primary = as a consequence of the anatomy of the eye: some people's angles are naturally very narrow which makes the angle more vulnerable to blocking off. Severe hypermetropes, advanced age, asian

secondary = as a result of forces exerted on the iris either anteriorly or posteriorly (eg, the lens bulging forward as a result of swelling) or blockage, as a result of the trabecular meshwork being blocked by matter such as blood (from a hyphaema), blood vessels (from poorly controlled advanced diabetic eye disease) or proteins (as seen in hypertensive uveitis).


Describe the control of aqueous humour production

autonomic - adrenergic

alpha 2 - stimulation reduces aqueous production and increases uveoscleral outflow, leading to fall in IOP

beta 2 - stimulation increases aqueous producion adn therefore increases IOP


What are the symptoms of acute angle closure glaucoma

Pain - this is severe and rapidly progressive.
Blurred vision (rapidly progressing to visual loss).
Coloured haloes around lights.


What situations can precipitate acute angle closure? Why?

during a moment of stress or excitement,
whilst watching TV in dim lighting conditions
after topical mydriatics or systemic anticholinergics.

due to pupillary block. - The mid-dilated pupil snags on to the lens, so causing a build-up of aqueous beneath it which further pushes the iris forward, so eventually blocking off the trabecular meshwork.


Give some signs of acute angle closure glaucoma

generally unwell.
red eye - more marked around the periphery of the cornea.
There is a hazy cornea
non-reactive (or minimally reactive) mid-dilated pupil.
Globe hard on palpation


What is the diagnostic criteria for angle closure glaucoma

History of at least 2 of:

Ocular pain.
History of intermittent blurring of vision with haloes

at least three of the following signs:
IOP greater than 21 mm Hg (clinically this can mean a stony hard pupil).
Conjunctival injection.
Corneal epithelial oedema.
Mid-dilated non-reactive pupil.
Shallow chamber in the presence of occlusion.


How is angle closure glaucoma managed pharmacologically

give all topical glaucoma medications that are not contra-indicated in the patient, together with intravenous acetazolamide. Patients are lain supine.

Topical agents inlude:
Beta-blockers - eg, timolol, cautioned in asthma.
Steroids - prednisolone 15 every 15 minutes for an hour, then hourly.
Pilocarpine 1-2% (in patients with their natural lens).
Phenylephrine 2.5% (in patients who do not have their own lens).
Acetazolamide is given intravenously (500 mg over 10 minutes) and a further 250 mg slow-release tablet after one hour - check for sulfonamide allergy and sickle cell disease/trait.

Offer systemic analgesia ± antiemetics.


Describe the mechanism of action of beta blockers on the eye eg. timolol

reduce production of aqueous by ciliary body


Describe the mechanism of action of alpha agonists on the eye eg. apraclonidine

reduced production of aqueous by ciliary body
increased outflow via uveoscleral tract


Describe the mechanism of action of prostaglandin analogues on the eye eg. latanoprost

increase uveoscleral outflow


Describe the mechanism of action of carbonic anhydrase inhibitors on the eye eg. acetazolamide

decrease production aqueous


Describe the mechanism of action of parasympathomimetics on the eye eg. pilocarpine

increases outflow of aqueous by ciliary muscle contraction, opening trabecular network


How is angle closure glaucoma managed surgically

Peripheral iridotomy (PI) - this refers to (usually two) holes made in each iris with a laser, usually at around the 11 and 2 o'clock positions. This is to provide a free-flow transit passage for the aqueous. Both eyes are treated, as the fellow eye will be predisposed to an AAC attack too

Surgical iridectomy - this is carried out where PI is not possible.

Lensectomy - one of the few situations where cataract surgery is performed on an urgent basis is when the cataractous lens has swollen to precipitate an attack of AAC. The lens is extracted at the earliest opportunity.


Give some complications of angle closure glaucoma

permanent loss of vision,
repetition of the acute attack,
attack in the fellow eye
central retinal artery or vein occlusion


Give some risk factors for open angle glaucoma

age >65
Family history
Race - it is three to four times more common in Afro-Caribbean people
Ocular hypertension
myopia (short-sightedness)
retinal disease (eg, central retinal vein occlusion, retinal detachment and retinitis pigmentosa)
Diabetes a
systemic hypertension


Describe briefly the pathophysiology of open angle glaucoma

The primary problem in glaucoma is disease of the optic nerve.
there is a progressive loss of retinal ganglion cells and their axons. (optic neuropathy)
associated with a raised IOP
flow is reduced through the trabecular meshwork


How does open angle glaucoma present?

most people are asymptomatic, because initial visual loss is to peripheral vision and the field of vision is covered by the other eye,

patients do not notice visual loss until severe and permanent damage has occurred, often impacting on central (foveal) vision.

Open-angle glaucoma may be detected on checking the IOPs and visual fields of those with affected relatives.

Suspicion may arise if abnormal discs, IOPs or visual fields are noted.


How is the eye examined for potential open angle glaucoma

Gonioscopy - used to measure the angle between the cornea and the iris

Corneal thickness - this influences the IOP reading. If it is thicker than usual, it will take greater force to indent the cornea and an erroneously high reading will be obtained.


Optic disc examination - this is a direct marker of disease progression. Optic disc damage is assessed by looking at the cup:disc ratio: normal is 0.3, although it can be up to 0.7 in some normal people: Glaucoma is suggested by an increase in cupping with time, rather than by cupping alone.

Visual fields


Hoe is the cupping of the optic disc measured?

cup = bright bit in middle
disc = dark bit around it

cup radius:disc radius

increased = more than 0.3


Do I need to inform the DVLA if my patient has glaucoma

The onus is on the patient to inform the DVLA (and it is important to document that you have advised them of this).

It is the DVLA (and approved opticians) who will assess the visual fields and decide whether a patient can continue to drive.

If you are concerned that the patient should not drive and has not told the DVLA (despite your clear advice to do so), it may be appropriate to inform the DVLA medical advisors


What treatments are available for open angle glaucoma

drugs to reduce IOP - beta blockers, alpha agonists, sympathomimetics, carbonic anhydrase inhibitors, miotics

laser - Argon laser trabeculoplasty (ALT) (lasering to the trabecular meshwork in the iridocorneal angle, so enhancing aqueous outflow), Selective laser trabeculoplasty (SLT)

surgery - trabeculectomy, artificial shunt, canaloplasty


What is AMD

age-related macular degeneration
changes, which occur in the central area of the retina (macula) in people aged 55 years and above.
without any other obvious precipitating cause,


What are the key findings on examination of the retina in AMD


dry - hypo/hyperpigmentation of RPE, geographic atropy
wet - neovascularisation