Glaucoma refers to the optic nerve damage that is caused by a significant rise in intraocular pressure.

The
raised intraocular pressure is caused by a blockage in aqueous humour trying to escape the eye. There are two
types of glaucoma: open-angle and closed-angle.

Basic Anatomy and Physiology

The vitreous chamber of the eye is filled with vitreous humour.

The anterior chamber between the cornea and the iris and the posterior chamber between the lens and
the iris are filled with aqueous humour that supplies nutrients to the cornea.

The aqueous humour is produced by the ciliary body. The aqueous humour flows from the ciliary body,
around the lens and under the iris, through the anterior chamber, through the trabecular meshwork and into
the canal of Schlemm. From the canal of Schlemm it eventually enters the general circulation.
The normal intraocular pressure is 10-21 mmHg. This pressure is created by the resistance to flow through
the trabecular meshwork into the canal of Schlemm.

Pathophysiology
In open-angle glaucoma, there is a gradual increase in resistance through the trabecular meshwork. This
makes it more difficult for aqueous humour to flow through the meshwork and exit the eye. Therefore the
pressure slowly builds within the eye and this gives a slow and chronic onset of glaucoma.

In acute angle-closure glaucoma, the iris bulges forward and seals off the trabecular meshwork from
the anterior chamber preventing aqueous humour from being able to drain away. This leads to a continual
build-up of pressure. This is an ophthalmology emergency.

Increased pressure in the eye causes cupping of the optic disc. In the centre of a normal optic disc is the optic
cup. This is a small indent in the optic disc. It is usually less than half the size of the optic disc. When there is
raised intraocular pressure, this indent becomes larger as the pressure in the eye puts pressure on that indent
making it wider and deeper. This is called “cupping”. An optic cup greater than 0.5 the size of the optic disc is
abnormal.

Risk Factors
 Increasing age
 Family history
 Black ethnic origin
 Nearsightedness (myopia)

Presentation of Open-Angle Glaucoma

Often the rise in intraocular pressure is asymptomatic for a long period of time. It is diagnosed by routine
screening when attending optometry for an eye check.

Glaucoma affects peripheral vision first. Gradually the peripheral vision closes in until they experience tunnel
vision.

It can present with gradual onset of fluctuating pain, headaches, blurred vision and halos appearing around
lights, particularly at night time.
Measuring Intraocular Pressure
Non-contact tonometry is the commonly used machine for estimating intraocular pressure by opticians. It
involves shooting a “puff of air” at the cornea and measuring the corneal response to that air. It is less accurate
but gives a helpful estimate for general screening purposes.

Goldmann applanation tonometry is the gold standard way to measure intraocular pressure. This involves a
special device mounted on a slip lamp that makes contact with the cornea and applies different pressures to the
front of the cornea to get an accurate measurement of what the intraocular pressure is.
Diagnosis
Goldmann applanation tonometry can be used to check the intraocular pressure.

Fundoscopy assessment to check for optic disc cupping and optic nerve health.

Visual field assessment to check for peripheral vision loss.

Management of Open-Angle Glaucoma

Management of glaucoma aims to reduce the intraocular pressure. Treatment is usually started at an intraocular
pressure of 24 mmHg or above. Patients are followed up closely to assess the response to treatment.

Prostaglandin analogue eye drops (e.g. latanoprost) are first line. These increase uveoscleral outflow.
Notable side effects are eyelash growth, eyelid pigmentation and iris pigmentation (browning).

Other options:

 Beta-blockers (e.g. timolol) reduce the production of aqueous humour

 Carbonic anhydrase inhibitors (e.g. dorzolamide) reduce the production of aqueous humour
 Sympathomimetics (e.g. brimonidine) reduce the production of aqueous fluid and increase
uveoscleral outflow

Trabeculectomy surgery may be required where eye drops are ineffective. This involves creating a new
channel from the anterior chamber, through the sclera to a location under the conjunctiva. It causes a “bleb”
under the conjunctiva where the aqueous humour drains. It is then reabsorbed from this bleb into the general
circulation.
Acute angle-closure glaucoma occurs when the iris bulges forward and seals off the trabecular
meshwork from the anterior chamber preventing aqueous humour from being able to drain away. This leads
to a continual build-up of pressure in the eye. The pressure builds up particularly in the posterior chamber,
which causes pressure behind the iris and worsens the closure of the angle.

Acute angle-closure glaucoma is an ophthalmology emergency. Emergency treatment is required to prevent

permanent loss of vision.

Risk Factors
The risk factors are slightly different to open-angle glaucoma:

 Increasing age
 Females are affected around 4 times more often than males
 Family history
 Chinese and East Asian ethnic origin. Unlike open-angle glaucoma, it is rare in people of black ethnic
origin.
 Shallow anterior chamber

Certain medications can precipitate acute angle-closure glaucoma:

 Adrenergic medications such as noradrenalin

 Anticholinergic medications such as oxybutynin and solifenacin
 Tricyclic antidepressants such as amitriptyline, which have anticholinergic effects

Presentation
The patient will generally appear unwell in themselves. They have a short history of:
  Severely painful red eye
 Blurred vision
 Halos around lights
 Associated headache, nausea and vomiting

Examination
 Red-eye
 Teary
 Hazy cornea
 Decreased visual acuity
 Dilatation of the affected pupil
 Fixed pupil size
 Firm eyeball on palpation

Initial Management
NICE CKS 2019 say patients with potentially life-threatening causes of red eye should be referred for same-
day assessment by an ophthalmologist. If there is a delay in admission, whilst waiting for an ambulance:

 Lie patient on their back without a pillow

 Give pilocarpine eye drops (2% for blue, 4% for brown eyes)
 Give acetazolamide 500 mg orally
 Given analgesia and an antiemetic if required

Pilocarpine acts on the muscarinic receptors in the sphincter muscles in the iris and causes constriction of the
pupil. Therefore it is a miotic agent. It also causes ciliary muscle contraction. These two effects cause the
pathway for the flow of aqueous humour from the ciliary body, around the iris and into the trabecular
meshwork to open up.

Acetazolamide is a carbonic anhydrase inhibitor. This reduces the production of aqueous humour.
Secondary Care Management
Various medical options can be tried to reduce the pressure:

 Pilocarpine
 Acetazolamide (oral or IV)
 Hyperosmotic agents such as glycerol or mannitol increase the osmotic gradient between the blood
and the fluid in the eye
 Timolol is a beta-blocker that reduces the production of aqueous humour
 Dorzolamide is a carbonic anhydrase inhibitor that reduces the production of aqueous humour
 Brimonidine is a sympathomimetic that reduces the production of aqueous fluid and increase
uveoscleral outflow

Laser iridotomy is usually required as a definitive treatment. This involves using a laser to make a hole in the
iris to allow the aqueous humour to flow from the posterior chamber into the anterior chamber. The relieves
pressure that was pushing the iris against the cornea and allows the humour the drain.