Glaucoma is the name given to a number of conditions in
which the optic nerve is damaged where it leaves the eye. This type of damage
has characteristic features and effects on vision. There are many types of
glaucoma, but for the purposes of this article we shall concentrate on those
types that are associated with uveitis.
Up to 20% of patients with uveitis will develop glaucoma.
Glaucoma caused by uveitis, is called a secondary glaucoma. In uveitis
patients, glaucoma is normally the result of a rise in pressure (intraocular
pressure) inside the eye. . This will be explained below after a
look at the parts of the eye involved. At this point it is worth pointing out
that, often, raised intraocular pressure (IOP) is taken to be the same thing
as glaucoma. This is not the case, they are actually quite different.
It is just that a raised IOP will lead to glaucoma if not treated.

Anatomy of the eye in relation to Glaucoma
The space in front of the lens contains watery fluid, the
aqueous and behind the lens, the rest of the eye is filled with a clear jelly,
the vitreous. The watery compartment is divided into two, the anterior
chamber, which is in front of the iris and the posterior chamber behind the
iris but in front of and at the side of the lens. (The vitreous compartment is
often mistakenly thought to be the posterior chamber). Watery fluid is
secreted into the posterior chamber by special cells covering the inner
surface of the ciliary body and passes through the pupil into the anterior
chamber where, in the angle of the anterior chamber, it is normally able to
drain through a special sieve-like tissue called the trabecular meshwork
leading to a circular drainage canal from which it passes back into the blood
stream (trabecular flow). A balance between the fluid entering and leaving the
eye determines the pressure within it - the intraocular pressure. This
pressure maintains the shape of the eye, a little like air pressure in a
balloon.
Raised Intraocular pressure and glaucoma.
There are several different ways in which this pressure can
be raised and it can happen slowly (chronic) or occasionly quickly (acute).
The upper limit of ‘normal’ is generally taken to be 21 mmHg. and is
measured very simply. If the IOP is above 21mmHg but there is no damage to the
optic nerve then the term ocular hypertension is used.
The increased pressure, in time, will damage the end of the
optic nerve by affecting the blood supply to the nerve or by directly damaging
the nerve endings .. It is this damage which is called glaucoma. The
damage to the optic nerve has characteristic effects on the vision. This is
why it is important to be able to distinguish between a raised IOP and
glaucoma.
How does glaucoma affect vision?
In most people glaucoma will develop slowly, that is, it is
chronic. Eventually the damage to the optic nerve will affect the
peripheral part of vision. It will not affect the central vision where our
reading, recognising faces and small detail goes on. There are blind areas in
the ‘side vision’. By the time this has occurred the damage to the optic
nerve is advanced. The classic description of vision loss in glaucoma is ’tunnel
vision’. In this chronic form there is rarely any pain.
Although much less common, more of a concern is when the
glaucoma is acute, that is it comes on very quickly. This often is
painful and ‘haloes’ of light may be seen. Occasionally, abdominal pain
and nausea may be present.
As glaucoma is preceded by a rise in IOP, then the best way
to prevent glaucoma is by regular monitoring. One fortunate aspect for
uveitis patients is that their intraocular pressures are likely to be
monitored very regularly.
Glaucoma associated with uveitis
The inflammation that occurs with uveitis results in blood
cell debris and ‘sticky’ protein leaking out of blood vessels into the
clear, aqueous. This can lead to a rise in intraocular pressure in a number
of ways:

1. Open Angle
The angle made between the iris and the cornea (see diagram
2 above) is normal or ’open’. However the trabecular meshwork, the
drainage system through which the fluid in the eye escapes, becomes blocked by
debris as a result of the inflammation. This results in a rise of intraocular
pressure.
This type is the most common and develops gradually.

2. Closed angle. There are two ways in which the
angle is closed or narrowed.
a) Posterior synechiae (see diagram 3 above)
Sometimes, as a result of the inflammation in uveitis, the
iris sticks to the lens which is sitting close behind it. It may do so in
isolated ‘spots’, but if extensive these posterior synechiae, may obstruct
the flow of aqueous through the pupil and out through the drainage system (see
diagram). The resulting rise in IOP, may be slow but it potentially can be
very rapid if the iris becomes ’bowed’ forward to ’close’ the angle of
the anterior chamber. As the angle is narrowed or closed it can be seen in the
diagram that the drainage system will be become closed off.
b) Anterior synechiae (not shown on diagram).
Sometimes the front surface of the iris becomes ‘stuck’
to the cornea or sclera. These anterior synechiae can also bow for ward the
iris and close the angle.
3. Steroid Usage
Steroid drops used to treat uveitis sometimes cause the IOP
to rise. This seems to happen in a minority of susceptible patients. This rise
is usually gradual and normally occurs within a month or two of starting the
drops, but can occur much later.
Stopping or reducing the drops will lower the pressure, but
eliminating inflammation, by vigorous treatment when necessary, is far more
important in the long run and so the pressures are monitored and treated as
necessary. The treatment of uveitis always involves this balance between
treating vigorously to completely remove any inflammation whilst overall,
using the minimum of drugs long term.
4). Other rare types
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Fuch's heterochromic uveitis in which a mild
inflammation is associated with loss of pigment from the iris of the
affected eye which becomes blue, if previously brown. Symptoms are
often absent in the early stages but a raised pressure and cataract
changes may occur later and affect vision.
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Posner Schlossman syndrome or glaucomatocyclitic
crisis when the patient may see rainbow coloured haloes due to a
sudden marked rise of eye pressure but the signs of uveitis are
minimal and may be localised to the trabecular meshwork.
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Rubeotic glaucoma, in which new blood vessels grow
on to the iris, following retinal ischaemia. These vessels can block
the trabecular meshwork.
Treatment of Glaucoma
As glaucoma is a risk factor to people with uveitis, the
best approach is always prevention.
The best means of preventing glaucoma are:
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vigorous treatment of any inflammation to
prevent the scarring and debris which is the commonest cause of the
rise in intraocular pressure.
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Preventing the iris sticking to the lens
(posterior synechiae). This is done with the use of mydriatic drops.
Examples are tropicamide, cyclopentolate and atropine.
Treatment works on a sliding scale from milder cases to the
more severe.
Eye drops are all that are usually required.
Examples are: betoptic, timoptol and trusopt.
Tablets may be used for more severe cases. A drug
called diamox is used , usually for short spells.
Laser . This usually involves a short, simple
treatment which is carried out at the eye clinic. The aim is to open new
channels fro the fluid to pass through.
Surgery If these treatments are unable to keep the
pressures in the normal range, then the next stage may be surgery. The
most common type of surgery is a procedure called a trabeculectomy. This
involves cutting a small flap under the white of the eye, to allow a
little fluid to escape and thus reduce the pressure.
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Summary
Glaucoma is damage to the optic nerve which
can affect vision
intraocular pressure (IOP) is the pressure
within the eye and if raised for long, it can cause glaucoma.
Up to 20% of people with uveitis may get
glaucoma.
Glaucoma may come on gradually (chronic) and
have no symptoms, or it may, less often, come on suddenly
(acute) and be painful and cause some loss of vision and
possibly haloes of light are seen.
Eye pressure must be monitored regularly when
under treatment for uveitis and any sudden onset of symptoms
suggesting an acute attack must be reported straight away.
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