Contents
Introduction
Definition of glaucoma – gradual death of the optic nerve often associated with high intraocular pressure. Increased intraocular pressure is usually due to an imbalance in aqueous humour production and drainage.
The Aqueous pathway
Aqueous humour – is a fluid produced by the ciliary body which helps to maintain the shape of the eye and nourishes the avascular lens and cornea. The fluid fills both the anterior and posterior chamber and is drained out of the eye via the irido-corneal angle in the anterior chamber. The aqueous humour filters back into the blood and circulation through the trabecular meshwork into the canal of Schlemm. Pressure is therefore maintained by a balance between aqueous production and egress.
Lets take a look at some eye anatomy. The anterior chamber and posterior chamber are both contained within the anterior compartment of the eye. The posterior compartment is taken up by the vitreous humour. Increased intraoccqular pressure occurs either when the aqueous humour can’t drain away properly through the trabecular meshwork and into the canal of Schlemm. More rarely, it is a problem with aqueous humour production.
This increased pressure caused by the fluid of the aqueous humour puts pressure on the vitreous humour in the posterior chamber, and in turn this presses onto the retina and optic nerve.
Damage first occurs to the peripheral retina, and later, to the optic nerve itself. Often peripheral visual symptoms go unnoticed by patients.
Now let’s look at the flow of aqueous humour. This fluid is produced by the ciliary processes in the posterior chamber. It then flows through the pupil and out through the trabecular meshwork and into the canal of Schlemm.
There are two main types of glaucoma – closed angle, and open angle. The angle referred to is the iridocorneal angle – this is the angle between the iris and the cornea.
In open angle glaucoma (usually chronic) the angle is not affected, but instead there is a defect of the trabecular meshwork which slows down the flow of aqueous humour.
In closed angle glaucoma (aka acute angle closure glaucoma – hint – usually its acute!) the ingle becomes narrowed (“closed”) and it is this narrowing that prevents aqueous from flowing correctly into the trabecular meshwork. Some individuals are genetically predisposed to acute angle closure due to purely the shape of their eye – they naturally already have a more shallow angle.
Open Angle Glaucoma
- Most common type
- Most patients >40 years old
- Usually chronic / slow onset
- Slow deterioration of peripheral vision
- Central vision usually normal
- In early disease – often no signs or symptoms
- Strongly familial
Major risk factors
- Family history
- Age
- Race- African Americans
- Thin cornea
- Large vertical nerve cupping
- High eye pressure
Mechanism
- Degeneration / clogging of the trabecular meshwork results in aqueous build up and chronically elevated eye pressure.
- The prolonged high pressure has been proposed to lead to optic nerve atrophy by;
- stretching
- vascular compromise
- alteration of glutamate transmitter pathways
- Progressive destruction of optic nerve results in gradual vision loss
- Because the vision loss occurs gradually patient don’t realise they have the disease until it is far advanced.
Screening
- Should start at age 30 and continue every 2 years if strong FHx
- Otherwise, recommended every 5 years if over 40 and every 2 years if over 60
Presentation
Usually there are three main examination findings:
- Elevated pressure
- Optic disc changes
- Visual loss (peripheral)
Elevated eye pressure
- (Normal pressure – 10-22mmHg)
- Measured with tonometer
- How much force it takes to flatten a 3mm diameter of cornea
- Pressure affected by corneal thickness
- Thin cornea = pressure reading lower than actual value
- Thick cornea = pressure reading higher than actual value
- Fluctuate throughout the day – typically highest in the morning
- NB – ‘normal pressure’ DOES NOT rule out glaucoma and ‘high pressure’ does not always indicate glaucoma
Optic disc changes
Seen on ophthalmoscopy Optic disc (normal indentation or cup which is less than 1/3rd of disc diameter)
- increased cupping
- fewer nerves course through optic disc
- Cup: disk ratio > 0.4-0.7
- vertical thinning and notching of neural rim
- Neural rim= space between inner cup and surrounding disc
- Normal neural rim follows the “ISNT” rule
- Haemorrhage at disc
- Disc vessels displaced nasally
- Optic atrophy – optic disc becomes pale as damage progresses
“ISNT RULE”
- Inferior rim Thickest
- Superior rim
- Nasal rim
- Temporal rim Thinnest
NB – In glaucoma the ISNT rule is lost
Visual loss
- Occurs in characteristic pattern…
- Central vision typically SPARED e.g. late stage patients may have 20/20 central vision but peripheral blindness
Treatment
It is only possible to treat the risk factors i.e. lower the intraocular pressure to 20mmHg or lower
Medical
- Topical β-blockers – decrease aqueous production at ciliary body
- Prostaglandin analogues – increase aqueous humour outflow
- Others – topical carbonic anhydrase inhibitors, alpha agonists
Surgical
- Trabeculectomy – creation of tract between anterior chamber to space under the conjunctiva. Apply antimetabolites like mitomycin C to avoid re-closure by scar formation
- Plastic tube shunt insertion into anterior chamber
- Laser procedure
- Argon laser trabeculoplasty used to burn portions of trabecular meshwork which increases outflow.
- Laser can also be used to burn portions of ciliary body to decrease aqueous production.
Acute Glaucoma (aka closed–angle glaucoma)
This is a MEDICAL EMERGENCY!
Mechanism
Pupillary block
- The lens pushes up against the back of iris blocking flow of aqueous humour through the pupil
- This resistance to aqueous flow produces a pressure-gradient across the iris
- Iris and lens are forced to move anteriorly
- Forward movement closes the irido-corneal angle and blocks the trabecular meshwork
- This causes build up of the aqueous fluid = RAPID RISE in eye pressure
- Increased pressure damages the retina due to stretching and decreased blood supply
Closure of outflow angle in
- Hyperopic eyes which have naturally shallow anterior chambers
- When the pupil dilates the iris gets thicker and the irido-corneal angle becomes smaller and is more likely to close spontaneously
- Medications that cause pupil dilatation – antihistamines and medications for colds
Presentation
- Extremely red and painful eye often associated with nausea and vomiting
- Patient may describe ‘halo around lights’
- this is due to swelling of the cornea as water is pushed into
- the cornea stroma by the high pressure
On examination
- Sluggish and dilated pupil
- High pressure – often > 60 mmHg
- Eye feels rock hard to palpation
Treatment
- Decrease eye pressure QUICKLY – many treatments at once
- Topical B-blockers (Timolol) – decrease aqueous production
- Carbonic anhydrase inhibitor (Acetazolamide) – decreases aqueous production
- Osmotic agents (oral glycerin + IV mannitol)
- Miotic (pilocarpine) – constrict pupil to open outflow angle
- Ultimately need Surgical treatment
- High intensity laser treatment – burn hole through the iris to create communication between the anterior and posterior chambers. This relieves the pressure gradient across the iris and moves it back to its normal position. The trabeuclar meshwork is re-opened and the aqueous fluid can drain out.
- It is typically done on both eyes, even when only one eye is affected at the initial presentation
References
- Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
- Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.
- Beers, MH., Porter RS., Jones, TV., Kaplan JL., Berkwits, M. The Merck Manual of Diagnosis and Therapy
- Lichen planus – dermnetnz
- Lichen Planus – patient.info