Monday, June 8, 2009

Symptoms and clinical signs of glaucoma

A patient with primary open angle glaucoma (also known as chronic open angle glaucoma) may not notice any symptoms until severe visual damage has occurred. This is because the rise in intraocular pressure and consequent damage occurs so slowly that the patient has time to compensate. In contrast, the clinical presentation of acute angle closure glaucoma is well known, as the intraocular pressure rises rapidly and results in a red, painful eye with disturbance of vision.

Raised intraocular pressure

Most patients with raised intraocular pressure (IOP) are unaware that they have a problem. Raised IOP is detected most commonly through screening as part of a routine eye test by an optometrist. The IOP is determined by the balance between aqueous production inside the eye and aqueous drainage out of the eye through the trabecular meshwork. Each normal eye makes about 2 l of aqueous a minute¡ªthat is, about 70 litres during the course of a lifetime. In a British Caucasian population, 95% of people have an IOP between 10 and 21 mm Hg, but IOP can drop as low as 0 mm Hg in hypotony and can exceed 70 mm Hg in some glaucomas.

The rate at which raised IOP causes optic nerve damage depends on many factors, including the level of IOP and whether glaucomatous damage is early or advanced. In general, raised IOPs in the 20-30 mm Hg range usually cause damage over several years, but very high IOPs in the 40-50mm Hg range can cause rapid visual loss and also precipitate retinovascular occlusion.

Haloes around lights and a cloudy cornea

The cornea is kept transparent by the continuous removal of fluid by the endothelial cells. If the pressure rises slowly, this process takes longer to fail. When the pressure rises quickly (acute closed angle glaucoma) the cornea becomes waterlogged, causing a fall in visual acuity and creating haloes around lights (like looking at a light through frosted glass).

Pain

If the rise in pressure is slow, pain is not a feature of glaucoma until the pressure is extremely high. Pain is not characteristically a feature of primary open angle glaucoma.

Visual field loss

Pressure on the nerve fibres and chronic ischaemia at the optic nerve head cause damage to the retinal nerve fibres and usually results in characteristic patterns of field loss (arcuate scotoma).

However, this spares central vision initially, and the patient does not notice the defect. Sophisticated visual field testing techniques are required to detect early visual field defects. The terminal stage of glaucomatous field loss is a severely contracted field, because only a few fibres from the more richly innervated macula area survive. Even at this stage (tunnel vision) the vision may still be 6/6.

Optic disc changes

The optic disc marks the exit point of the retinal nerve fibres from the eye. With a sustained rise in IOP the nerve fibres atrophy, leaving the characteristic sign of chronic glaucoma¡ªthe cupped, pale optic disc.

Venous occlusion

Raised IOP can impede blood flow in the low pressure venous system, increasing the risk of retinal venous occlusion.

Enlargement of the eye

In adults no significant enlargement of the eye is possible because growth has ceased. In a young child there may be enlargement of the eye (buphthalmos or ¡°ox-eye¡±). This tends to occur with raised IOP in children under the age of three years. These children may also be photophobic and have watering eyes and cloudy corneas.


Enlarged watering eyes
with cloudycorneas in a child with glaucoma