Glaucoma affects over 100,000 Australians, with approximately 2.3% of people over the age of 55 affected. This statistic increases to as many as one in ten people 80 years or above. Despite significant public awareness campaigns, many who have glaucoma are unaware that they have the disease. It is estimated that 50% of glaucoma sufferers are currently undiagnosed.
Glaucoma is caused by excessive pressure within the eye, which in turn places pressure on the delicate nerve fibres that form the optic nerve (the pathway for visual information linking the eye to the brain). A rise in the normal fluid pressure within the eye (“Intraocular Pressure” or IOP) can significantly damage the optic nerve with loss of peripheral vision (visual field). There is no absolute threshold of pressure to indicate glaucoma is present.
Damage to the optic nerve is unfortunately irreversible and treatment is aimed at preventing further damage.
What Causes Glaucoma?
"Aqueous humor" is the name given to the fluid naturally and continuously being produced by the eye. This fluid exits the eye at the angle where the cornea and iris meet, via a drainage system called the trabecular meshwork.
If the aqueous humor is not able to be drained from the eye at the same rate as it is produced, intraocular pressure increases leading to damage of the optic nerve (glaucoma).
The most common form of glaucoma is Primary Open-Angle Glaucoma. This is a chronic condition. It is important to realise that there are no symptoms of raised intraocular pressure with this condition. Therefore it is important to have regular eye tests to assess the intraocular pressure and optic nerve. If left untreated, peripheral vision begins to decrease first, and can progress until the entire visual field is affected, and blindness ensues.
Acute Angle Closure Glaucoma, however, may cause symptoms such as severe eye pain, nausea, vomiting, blurred vision, halos around lights and a red eye. This type of glaucoma is uncommon.
Automated perimetry is used to detect the presence of retinal nerve damage caused by glaucoma.
Types of Glaucoma
Primary Open-Angle Glaucoma (POAG)
Here, the trabecular meshwork at the angle at which the aqueous humor is filtered out of the eye is poorly functioning and therefore, decreases the filtration rate out of the eye and thus increases the pressure within the eye. If untreated, this can cause permanent damage to the optic nerve over months or years. As the pressure build up is slow, there are no symptoms until the very late stages of the disease.
Acute Angle-Closure Glaucoma
This is where the iris bulges and physically blocks the angle where the aqueous humor is supposed to drain. A block in the drainage system causes the intraocular pressure to build-up dramatically and rapidly. This form of glaucoma can cause redness of the eye, blurred vision, nausea and intense pain and must be treated immediately as this can cause blindness in just a day or two.
Low-Tension or Normal-Tension Glaucoma
Similar to Primary Open-Angle Glaucoma except that the intraocular pressure is measured as being similar to that of a normal eye. The examination of the eye and investigations confirms the presence of glaucoma, but the intraocular pressure is “normal”. This may be due to an abnormally sensitive optic nerve. People who have low blood pressure or poor circulation are more at risk of this form of glaucoma.
Where an ocular defect is present at birth which restricts the fluid drainage system. Surgery is required to limit damage to the eyes.
Glaucoma can be caused by other eye conditions. Such conditions include trauma and inflammation. Pigmentary glaucoma is secondary to the pigment particles of the iris causing a blockage to the drainage system. Pseudoexfoliation is a similar condition where particles from within the eye block the drainage system. Use of corticosteroids (prednisone) for treatment of ocular or systemic inflammation can result in glaucoma. The most severe secondary glaucoma is neovascular glaucoma which can be caused by diabetes or vascular insufficiency of the retina.