Glaucoma refers to a collection of disorders resulting in progressive optic neuropathy in which raised intraocular pressure is typically a key factor.
Glaucoma is a common pathology affecting the eye that untreated can result in significant loss of vision. Worldwide it is the leading cause of irreversible blindness with 66 million affected, 12.5 million of whom are blind. In the UK it is responsible for around 10% of those registered blind. There are two major forms of glaucoma (and a related condition ocular hypertension):
In this note we will focus on the chronic form of primary open-angle glaucoma. POAG is by far the most common form of glaucoma. Its pathogenesis is poorly understood and onset often insidious.
When diagnosed, treatment typically involves topical therapies (e.g. topical beta blocker or prostaglandin analogue).
POAG affects around 2% of adults over the age of 40 in the UK.
Prevalence increases with advancing age with an estimated 8% of those aged 80 years affected. The gender ratio is balanced and it is more common in those of African heritage. Importantly the condition is thought to go unrecognised in up to 50% of people.
A number of risk factors have been associated with the development of POAG.
Aqueous humour is produced by epithelium covering the ciliary bodies in the posterior chamber of the eye.
The eye may be divided into three chambers:
The aqueous humour is produced and actively secreted by the ciliary epithelium located in the posterior chamber of the eye. It is a watery fluid with a similar make-up to plasma though with a far lower protein content.
NOTE: Inflammation of the uvea can lead to increased membrane permeability and therefore protein content in the aqueous humour. This can scatter light resulting in flare.
The aqueous humour passes through the pupil into the anterior chamber and drains at the anterior chamber angle (iridocorneal angle). There are two drainage pathways:
The pathogenesis of POAG remains unclear.
The pathogenesis of POAG is poorly understood. Raised IOP appears central too many cases though it is disputed as to whether this occurs due to increased production, reduced drainage, anatomical differences or a combination of factors.
Loss of axons of the optic nerve may occur due to elevated IOP. Other factors may also predispose individuals to this with a mix of systemic (e.g. microcirculatory damage) and genetic factors implicated.
Secondary open-angle glaucoma is relatively rare and normally occurs due to reduced drainage of aqueous humour and raised IOP. They occur secondary to defined processes, a few of these are described below:
POAG is asymptomatic until the late stages of disease.
Patients with POAG are largely asymptomatic. Though visual loss may occur, central vision is preserved until late in the disease. The peripheral visual loss often goes unnoticed and the other eye may somewhat compensate for the defect.
Diagnosis is therefore typically made during routine ophthalmic examination at optometrists. GP’s may also suspect the diagnosis after visualising ‘cupped discs’ during ophthalmoscopy. Formal ophthalmic review will include:
There is no formal screening programme for open angle glaucoma.
Despite this there are a number of ways signs indicative of glaucoma may be picked up. NICE CKS advise the following groups to be reviewed by optometrists:
Treatment is aimed at preventing visual loss.
Management of glaucoma is guided by ophthalmologists, each patients findings are reviewed to help decide upon management. Treatment is generally targeted at reducing IOP, a number of the options are discussed below:
Generally NICE advise treatment in patients with suspected chronic open angle glaucoma and an IOP of 24mmHg or greater. For these patients and patients with chronic open angle glaucoma a topical prostaglandin analogue (e.g. Latanoprost) is normally used as first line therapy.
In patients with advanced disease surgery with pharmacological augmentation (Mitomycin C) may be offered.
In those in whom IOP is not reduced enough with topical prostaglandin analogues (and good adherence) to prevent progressive visual loss, the following may be considered:
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