What is it?

The eye behaves as a closed structure, where IOP changes cannot be lessened, so they adversely affect the thickness and function of the RNFLs. This means that occipital interpretation of vision is reduced in the affected areas, with the most common loss being to peripheral vision, which may result in tunnel vision. It generally affects peripheral vision, and also central vision over time. However, in some types of glaucoma, the most common initial campimetry lesion involves the central 10º of the visual field, with the consequent early loss of visual function.

Any injury to the RNFL is irreversible, as we cannot restore its function once it has been altered, so if the nerve fibres of the optic nerve do not regenerate, early detection of this disease is important in order to treat it in time.

Risk factors

Elevated IOP: the most well-known risk factor is IOP (intraocular pressure), with the normal range being 10-21 mmHg. This pressure has no relation whatsoever to blood pressure.
IOP level is the primary known risk factor for the development of glaucoma and for progression of glaucoma. It is estimated that the risk of glaucoma with IOP ≥ 26 mmHg may be up to 12 times higher than in individuals with normal IOP. There is good evidence to show that lowering IOP acts as a major protective factor against lesions in the optic nerve (ON) in patients susceptible to glaucoma.

Old age: this is another significant risk factor in the diagnosis and progression of glaucoma. Epidemiological studies show that the prevalence of glaucoma increases exponentially with age.

Family history of glaucoma: this is a risk factor for glaucoma. In studies where siblings of patients diagnosed with glaucoma were examined alongside a control group, the probability of having POAG was 9.2 times higher for people who have a first-degree relative (sibling or parent) with confirmed POAG.

Race, ethnicity: racial-ethnic characteristics are an important risk factor for POAG, with a prevalence up to three times higher in African-American (West African and Afro-Caribbean) individuals compared to white individuals, and blindness due to glaucoma being at least six times more frequent in African-American individuals.

Central corneal thickness (CCT), Pachymetry: CCT thinner than the normal range is an independent risk factor associated with a higher probability of developing POAG.

Low ocular perfusion pressure: It has been observed that reduced ocular perfusion pressure may lead to changes in blood flow to the ONH and contribute to the progression of glaucomatous damage.

Type 2 diabetes mellitus: in the absence of conclusive data on the association between type 2 diabetes mellitus (DM) and POAG, there are population-based studies that support the evidence that it is an important risk factor for the development of POAG, relating it to microvascular changes in the ONH, with a higher probability of presenting lesions in the RNFL in people with type 2 DM.

Myopia: many epidemiological studies in different populations with a wide global geographical distribution suggest that people with myopia have a higher prevalence of POAG than people without myopia, and recent studies have also shown a relationship between long axial length (axial myopia) and a higher prevalence of POAG, based on the fact that it is associated with weaker scleral support, increasing the susceptibility of the ONH to glaucomatous damage.

Migraine, vasospasm: considered a risk factor for glaucomatous lesions due to autoregulation of blood flow to the ONH.

Genetic factors: we know that glaucoma can occur at any age, with typical Mendelian inheritance. Some genes have been identified in hereditary forms of glaucoma (e.g., MYOC, OPTN, WDR36, TBK1) and mutations have been found in the majority of these genes, which could lead to opening.

This type of glaucoma is more common with age, due to an increase in the volume of the crystalline lens (the lens where cataracts are formed), which could obstruct the passage of aqueous humour towards the front of the eye, pathologically pushing the iris forward and closing the angle.

It is also common in women and people of Asian descent. The latter sometimes suffer from a syndrome called "plateau iris", where the peripheral area of the iris is shaped in a particular way, blocking the angle to leave just a small slit. This disorder is not responsive to laser treatment (iridotomy).

In some cases the problem is that the periphery of the iris is too thick or it has been displaced forward because the ciliary processes (the area where the aqueous humour is produced, located behind the iris) are abnormally bulky and push it forward.

Other risk factors for angle closure include hyperopia and short-sightedness, as the lens volume becomes too large within a space that is smaller than normal.

This type of glaucoma is currently classified by the way in which the angular closure develops, rather than by symptoms (acute, subacute and chronic). As such, the mildest form would be in cases where we suspect that the angle formed by a patient’s iris and cornea may close (suspected primary angle closure), but their ocular pressure is still normal; this is known as an occludable angle.

In these cases, laser peripheral iridotomy will reduce the risk of closure and an increase in IOP.

Secondly, we have patients who suffer from angular closure, which means that the iris and the trabecular meshwork adhere together and the IOP is usually above normal, but the optic nerve is not yet damaged.

In some of these cases the IOP is intermittent. In these patients, iridotomy may or may not be effective, depending on the degree of angular closure, known as synechia.

Finally there is primary closed-angle glaucoma, which applies to cases with a closed angle, high IOP and signs of glaucomatous damage to the optic nerve.

In some cases the angular closure is acute, known as acute glaucoma attack, and in these cases the IOP is usually above 40 mmHg. These episodes are accompanied by symptoms such as pain, red eye, blurred vision and even nausea and vomiting. It is considered an emergency that should be treated as soon as possible, as it could lead to disastrous consequences for the patient’s vision.

Risk factors

This type of glaucoma is more common with age, due to an increase in the volume of the crystalline lens, which could obstruct the passage of aqueous humour towards the front of the eye, pathologically pushing the iris forward and closing the angle.

It is also common in women and people of Asian descent.

Other risk factors for angle closure include hyperopia and short-sightedness, as the lens volume becomes too large within a space that is smaller than normal.

This type of glaucoma is usually caused by multiple factors, where the IOP is not the most significant risk factor. Other relevant factors include vascular alterations, hereditary factors, and many others.

As with the more common types of glaucoma, it is essential that this illness be diagnosed as early as possible, to avoid severe or irreversible damage. Symptoms don’t usually appear until visual field loss occurs.

Since in 50% of cases the disease does not progress at 5 years without treatment, appropriate treatment should be provided once it has been shown that the disease is progressing, in young patients or patients suffering from advanced illness.

Given that there is also an associated vascular component involved, patients should also be advised to exercise regularly, control their cholesterol and avoid unhealthy habits, such as smoking, and, above all, any associated vascular disease should also be ruled out by performing an echo-Doppler analysis of the SAT and a respiratory test to rule out sleep apnoea syndrome (OSASH).

Congenital glaucoma encompasses various different glaucoma subtypes. The severity of the disorder depends on the age at which it is manifested, the level of aggressiveness and the presence of associated deformities.

The prevalence is 1 in 10.000 newborns.
There are different types according to the age at when it presents itself:

Primary congenital/infantile forms of glaucoma:
• Primary congenital glaucoma (PCG)
Neonatal or appearance after birth (0-1 month)
Early childhood onset (1 to 24 months)
Late onset or late diagnosis (> 2 years)
Non-progressive spontaneous cases with normal IOP, with typical signs of PCG
• Late-onset/early juvenile infantile open-angle glaucoma (onset in those over 2 years of age until puberty)
• Secondary infantile glaucoma

They usually have a poor visual prognosis, with deficits in visual function; the earlier they occur, the greater the prognosis.

Pigmentary glaucoma which occurs when the pigment granules in the iris break off into the eye fluid (aqueous humour) and block the eye’s drainage system.